[{"extern":"1","citation":{"ama":"Barton NH. Appendix to “A simulation study of multilocus clines” by S J E Baird. <i>Evolution</i>. 1995;49(6):1038-1045. doi:<a href=\"https://doi.org/10.1111/j.1558-5646.1995.tb04431.x\">10.1111/j.1558-5646.1995.tb04431.x</a>","apa":"Barton, N. H. (1995). Appendix to “A simulation study of multilocus clines” by S J E Baird. <i>Evolution</i>. Wiley. <a href=\"https://doi.org/10.1111/j.1558-5646.1995.tb04431.x\">https://doi.org/10.1111/j.1558-5646.1995.tb04431.x</a>","short":"N.H. Barton, Evolution 49 (1995) 1038–1045.","chicago":"Barton, Nicholas H. “Appendix to ‘A Simulation Study of Multilocus Clines’ by S J E Baird.” <i>Evolution</i>. Wiley, 1995. <a href=\"https://doi.org/10.1111/j.1558-5646.1995.tb04431.x\">https://doi.org/10.1111/j.1558-5646.1995.tb04431.x</a>.","ieee":"N. H. Barton, “Appendix to ‘A simulation study of multilocus clines’ by S J E Baird,” <i>Evolution</i>, vol. 49, no. 6. Wiley, pp. 1038–1045, 1995.","ista":"Barton NH. 1995. Appendix to ‘A simulation study of multilocus clines’ by S J E Baird. Evolution. 49(6), 1038–1045.","mla":"Barton, Nicholas H. “Appendix to ‘A Simulation Study of Multilocus Clines’ by S J E Baird.” <i>Evolution</i>, vol. 49, no. 6, Wiley, 1995, pp. 1038–45, doi:<a href=\"https://doi.org/10.1111/j.1558-5646.1995.tb04431.x\">10.1111/j.1558-5646.1995.tb04431.x</a>."},"doi":"10.1111/j.1558-5646.1995.tb04431.x","quality_controlled":"1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["1558-5646"]},"year":"1995","intvolume":"        49","page":"1038 - 1045","oa":1,"issue":"6","type":"journal_article","_id":"4298","article_processing_charge":"No","publication":"Evolution","oa_version":"Published Version","date_created":"2018-12-11T12:08:07Z","author":[{"orcid":"0000-0002-8548-5240","full_name":"Barton, Nicholas H","first_name":"Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","last_name":"Barton"}],"day":"01","status":"public","title":"Appendix to \"A simulation study of multilocus clines\" by S J E Baird","volume":49,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1111/j.1558-5646.1995.tb04431.x"}],"month":"12","date_published":"1995-12-01T00:00:00Z","article_type":"original","publisher":"Wiley","publist_id":"1773","date_updated":"2022-06-28T07:47:30Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published"},{"_id":"4428","type":"dissertation","article_processing_charge":"No","extern":"1","citation":{"ieee":"P. Ho, “Automatic analysis of hybrid systems,” Cornell University, 1995.","ista":"Ho P. 1995. Automatic analysis of hybrid systems. Cornell University.","mla":"Ho, Pei. <i>Automatic Analysis of Hybrid Systems</i>. Cornell University, 1995, pp. 1–188.","apa":"Ho, P. (1995). <i>Automatic analysis of hybrid systems</i>. Cornell University.","chicago":"Ho, Pei. “Automatic Analysis of Hybrid Systems.” Cornell University, 1995.","short":"P. Ho, Automatic Analysis of Hybrid Systems, Cornell University, 1995.","ama":"Ho P. Automatic analysis of hybrid systems. 1995:1-188."},"oa_version":"Published Version","date_created":"2018-12-11T12:08:48Z","author":[{"first_name":"Pei","last_name":"Ho","full_name":"Ho, Pei"}],"language":[{"iso":"eng"}],"day":"01","year":"1995","status":"public","title":"Automatic analysis of hybrid systems","main_file_link":[{"url":"https://hdl.handle.net/1813/7193","open_access":"1"}],"page":"1 - 188","supervisor":[{"orcid":"0000-0002-2985-7724","full_name":"Henzinger, Thomas A","first_name":"Thomas A","id":"40876CD8-F248-11E8-B48F-1D18A9856A87","last_name":"Henzinger"}],"month":"08","date_published":"1995-08-01T00:00:00Z","oa":1,"degree_awarded":"PhD","abstract":[{"text":"Hybrid systems are real-time systems that react to both discrete and continuous activities (such as analog signals, time, temperature, and speed). Typical examples of hybrid systems are embedded systems, timing-based communication protocols, and digital circuits at the transistor level. Due to the rapid development of microprocessor technology, hybrid systems directly control much of what we depend on in our daily lives. Consequently, the formal specification and verification of hybrid systems has become an active area of research. This dissertation presents the first general framework for the formal specification and verification of hybrid systems, as well as the first hybrid-system analysis tool--HyTech. The framework consists of a graphical finite-state-machine-like language for modeling hybrid systems, a temporal logic for modeling the requirements of hybrid systems, and a computer procedure that verifies modeled hybrid systems against modeled requirements. The tool HyTech is the implementation of the framework using C++ and Mathematica.\r\n\r\nMore specifically, our hybrid-system modeling language, Hybrid Automata, is an extension of timed automata with discrete and continuous variables whose dynamics are governed by differential equations. Our requirement modeling language, ICTL, is a branching-time temporal logic, and is an extension of TCTL with stop-watch variables. Our verification procedure is a symbolic model-checking procedure that verifies linear hybrid automata against ICTL formulas. To make HyTech more efficient and effective, we use model-checking strategies and abstract operators that can expedite the verification process. To enable HyTech to verify nonlinear hybrid automata, we introduce two translations from nonlinear hybrid automata to linear hybrid automata. We have applied HyTech to analyze more than 30 hybrid-system benchmarks. In this dissertation, we present the application of HyTech to three nontrivial hybrid systems taken from the literature.","lang":"eng"}],"publisher":"Cornell University","publist_id":"304","date_updated":"2022-06-28T07:30:34Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published"},{"oa":1,"abstract":[{"text":"Hybrid automata model systems with both digital and analog components, such as embedded control programs. Many verification tasks for such programs can be expressed as reachability problems for hybrid automata. By improving on previous decidability and undecidability results, we identify the precise boundary between decidability and undecidability of the reachability problem for hybrid automata.\r\n\r\nOn the positive side, we give an (optimal) PSPACE reachability algorithm for the case of initialized rectangular automata, where all analog variables follow trajectories within piecewise-linear envelopes and are reinitialized whenever the envelope changes. Our algorithm is based on the construction of a timed automaton that contains all reachability information about a given initialized rectangular automaton. The translation has practical significance for verification, because it guarantees the termination of symbolic procedures for the reachability analysis of initialized rectangular automata. The translation also preserves the omega-languages of initialized rectangular automata with bounded nondeterminism.\r\n\r\nOn the negative side, we show that several slight generalizations of initialized rectangular automata lead to an undecidable reachability problem. In particular, we prove that the reachability problem is undecidable for timed automata augmented with a single stopwatch.","lang":"eng"}],"month":"01","date_published":"1995-01-01T00:00:00Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","publisher":"ACM","publist_id":"228","date_updated":"2022-06-09T14:40:29Z","main_file_link":[{"open_access":"1","url":"https://dl.acm.org/doi/10.1145/225058.225162"}],"page":"373 - 382","day":"01","year":"1995","publication_identifier":{"isbn":["9780897917186"]},"language":[{"iso":"eng"}],"title":"What's decidable about hybrid automata?","status":"public","doi":"10.1145/225058.225162","citation":{"short":"T.A. Henzinger, P. Kopke, A. Puri, P. Varaiya, in:, Proceedings of the 27th Annual ACM Symposium on Theory of Computing, ACM, 1995, pp. 373–382.","chicago":"Henzinger, Thomas A, Peter Kopke, Anuj Puri, and P. Varaiya. “What’s Decidable about Hybrid Automata?” In <i>Proceedings of the 27th Annual ACM Symposium on Theory of Computing</i>, 373–82. ACM, 1995. <a href=\"https://doi.org/10.1145/225058.225162\">https://doi.org/10.1145/225058.225162</a>.","apa":"Henzinger, T. A., Kopke, P., Puri, A., &#38; Varaiya, P. (1995). What’s decidable about hybrid automata? In <i>Proceedings of the 27th annual ACM symposium on Theory of computing</i> (pp. 373–382). Las Vegas, NV, United States of America: ACM. <a href=\"https://doi.org/10.1145/225058.225162\">https://doi.org/10.1145/225058.225162</a>","mla":"Henzinger, Thomas A., et al. “What’s Decidable about Hybrid Automata?” <i>Proceedings of the 27th Annual ACM Symposium on Theory of Computing</i>, ACM, 1995, pp. 373–82, doi:<a href=\"https://doi.org/10.1145/225058.225162\">10.1145/225058.225162</a>.","ieee":"T. A. Henzinger, P. Kopke, A. Puri, and P. Varaiya, “What’s decidable about hybrid automata?,” in <i>Proceedings of the 27th annual ACM symposium on Theory of computing</i>, Las Vegas, NV, United States of America, 1995, pp. 373–382.","ista":"Henzinger TA, Kopke P, Puri A, Varaiya P. 1995. What’s decidable about hybrid automata? Proceedings of the 27th annual ACM symposium on Theory of computing. STOC: Symposium on the Theory of Computing, 373–382.","ama":"Henzinger TA, Kopke P, Puri A, Varaiya P. What’s decidable about hybrid automata? In: <i>Proceedings of the 27th Annual ACM Symposium on Theory of Computing</i>. ACM; 1995:373-382. doi:<a href=\"https://doi.org/10.1145/225058.225162\">10.1145/225058.225162</a>"},"date_created":"2018-12-11T12:09:11Z","quality_controlled":"1","oa_version":"Published Version","article_processing_charge":"No","_id":"4502","type":"conference","publication":"Proceedings of the 27th annual ACM symposium on Theory of computing","extern":"1","author":[{"last_name":"Henzinger","first_name":"Thomas A","id":"40876CD8-F248-11E8-B48F-1D18A9856A87","orcid":"0000−0002−2985−7724","full_name":"Henzinger, Thomas A"},{"full_name":"Kopke, Peter","first_name":"Peter","last_name":"Kopke"},{"last_name":"Puri","first_name":"Anuj","full_name":"Puri, Anuj"},{"last_name":"Varaiya","first_name":"P.","full_name":"Varaiya, P."}],"conference":{"location":"Las Vegas, NV, United States of America","end_date":"1995-06-01","start_date":"1995-05-29","name":"STOC: Symposium on the Theory of Computing"},"acknowledgement":"We thank Howard Wong-Toi for a careful reading.\r\n"},{"abstract":[{"lang":"eng","text":"Taking advantage of the restricted expression of metabotropic glutamate receptor subtype 6 (mGIuR6) in retinal ON bipolar cells, we generated knockout mice lacking mGIuR6 expression. The homozygous mutant mice showed a loss of ON responses but unchanged OFF responses to light. The mutant mice displayed no obvious changes in retinal cell organization nor in the projection of optic fibers to the brain. Furthermore, the mGIuR6-deficient mice showed visual behavioral responses to light stimulation as examined by shuttle box avoidance behavior experiments using light exposure as a conditioned stimulus. The results demonstrate that mGIuR6 is essential in synaptic transmission to the ON bipolar cell and that the OFF response provides an important means for transmitting visual information."}],"oa":1,"page":"757 - 765","external_id":{"pmid":["7889569"]},"intvolume":"        80","pmid":1,"year":"1995","publication_identifier":{"issn":["0092-8674"]},"language":[{"iso":"eng"}],"acknowledgement":"We thank Drs. N. Mizuno, M. Iso, M. Tachibana, A. Kaneko, M. Tessier-Lavigne, and T. Hensch for useful advice and A. Uesugi for photographic assistance. This work is supported by grants in aid for specially promoted research, for scientific research on priority areas, and for scientific research (A) from the Ministry of Education, Science, and Culture in Japan and by grants from the Ministry of Health and Welfare of Japan, the Sankyo Foundation, and the Senri Life Science Foundation.","quality_controlled":"1","citation":{"mla":"Masu, Masayuki, et al. “Specific Deficit of the ON Response in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” <i>Cell</i>, vol. 80, no. 5, Cell Press, 1995, pp. 757–65, doi:<a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">10.1016/0092-8674(95)90354-2</a>.","ieee":"M. Masu <i>et al.</i>, “Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene,” <i>Cell</i>, vol. 80, no. 5. Cell Press, pp. 757–765, 1995.","ista":"Masu M, Iwakabe H, Tagawa Y, Miyoshi T, Yamashita M, Fukuda Y, Sasaki H, Hiroi K, Nakamura Y, Shigemoto R, Takada M, Nakamura K, Nakao K, Katsuki M, Nakanishi S. 1995. Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. Cell. 80(5), 757–765.","short":"M. Masu, H. Iwakabe, Y. Tagawa, T. Miyoshi, M. Yamashita, Y. Fukuda, H. Sasaki, K. Hiroi, Y. Nakamura, R. Shigemoto, M. Takada, K. Nakamura, K. Nakao, M. Katsuki, S. Nakanishi, Cell 80 (1995) 757–765.","chicago":"Masu, Masayuki, Hideki Iwakabe, Yoshiaki Tagawa, Tomomitsu Miyoshi, Masayuki Yamashita, Yutaka Fukuda, Hitoshi Sasaki, et al. “Specific Deficit of the ON Response in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” <i>Cell</i>. Cell Press, 1995. <a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">https://doi.org/10.1016/0092-8674(95)90354-2</a>.","apa":"Masu, M., Iwakabe, H., Tagawa, Y., Miyoshi, T., Yamashita, M., Fukuda, Y., … Nakanishi, S. (1995). Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">https://doi.org/10.1016/0092-8674(95)90354-2</a>","ama":"Masu M, Iwakabe H, Tagawa Y, et al. Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. <i>Cell</i>. 1995;80(5):757-765. doi:<a href=\"https://doi.org/10.1016/0092-8674(95)90354-2\">10.1016/0092-8674(95)90354-2</a>"},"doi":"10.1016/0092-8674(95)90354-2","extern":"1","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","date_updated":"2022-06-28T13:27:50Z","publist_id":"4339","publisher":"Cell Press","article_type":"original","date_published":"1995-02-10T00:00:00Z","month":"02","main_file_link":[{"url":"https://www.sciencedirect.com/science/article/pii/0092867495903542","open_access":"1"}],"title":"Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene","volume":80,"status":"public","day":"10","author":[{"first_name":"Masayuki","last_name":"Masu","full_name":"Masu, Masayuki"},{"full_name":"Iwakabe, Hideki","first_name":"Hideki","last_name":"Iwakabe"},{"last_name":"Tagawa","first_name":"Yoshiaki","full_name":"Tagawa, Yoshiaki"},{"last_name":"Miyoshi","first_name":"Tomomitsu","full_name":"Miyoshi, Tomomitsu"},{"full_name":"Yamashita, Masayuki","last_name":"Yamashita","first_name":"Masayuki"},{"first_name":"Yutaka","last_name":"Fukuda","full_name":"Fukuda, Yutaka"},{"full_name":"Sasaki, Hitoshi","first_name":"Hitoshi","last_name":"Sasaki"},{"full_name":"Hiroi, Kano","last_name":"Hiroi","first_name":"Kano"},{"last_name":"Nakamura","first_name":"Yasuhisa","full_name":"Nakamura, Yasuhisa"},{"orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto"},{"full_name":"Takada, Masahiko","last_name":"Takada","first_name":"Masahiko"},{"first_name":"Kenji","last_name":"Nakamura","full_name":"Nakamura, Kenji"},{"full_name":"Nakao, Kazuki","first_name":"Kazuki","last_name":"Nakao"},{"last_name":"Katsuki","first_name":"Motoya","full_name":"Katsuki, Motoya"},{"first_name":"Shigetada","last_name":"Nakanishi","full_name":"Nakanishi, Shigetada"}],"date_created":"2018-12-11T11:58:23Z","oa_version":"Published Version","publication":"Cell","issue":"5","_id":"2559","type":"journal_article","article_processing_charge":"No"},{"main_file_link":[{"url":"https://dl.acm.org/doi/10.5555/313651.313712","open_access":"1"}],"page":"312-321","scopus_import":"1","date_published":"1995-01-01T00:00:00Z","month":"01","abstract":[{"lang":"eng","text":"We present a model with restricted randomness for edge updates in dynamic graph algorithms and a general technique\r\nfor analyzing the expected running time of an update operation. This model is able to capture the average case in many applications, since (1) it allows restrictions on the set of edges which can be used for insertions and (2) the type (insertion or deletion) of each update operation is arbitrary, i.e., not random. We use our technique to analyze existing and new dynamic algorithms for maximum cardinality matching, minimum spanning forest, connectivity, 2-edge connectivity,\r\nk-edge connectivity, k-vertex connectivity, and bipartiteness. Given a random graph G with mo edges and n vertices and\r\na sequence of 1 update operations such that the graph contains rni edges after operation i, the expected time for performing the updates for any 1 is O(1 logn + n xi=, l/fii) in the case of minimum spanning forests, connectivity, 2-\r\nedge connectivity, and bipartiteness. The expected time per update operation is O(n) in the case of maximum matching. For k-edge and k-vertex connectivity we also give improved bounds. Additionally we give an insertions-only algorithm for maximum cardinality matching with worst-case O(n) amortized time per insertion. "}],"oa":1,"date_updated":"2023-02-21T16:24:58Z","publisher":"Society for Industrial and Applied Mathematics","publication_status":"published","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","extern":"1","publication":"6th Annual ACM-SIAM Symposium on Discrete Algorithms","_id":"11928","type":"conference","article_processing_charge":"No","oa_version":"Published Version","date_created":"2022-08-19T07:10:23Z","quality_controlled":"1","citation":{"ama":"Alberts D, Henzinger MH. Average case analysis of dynamic graph algorithms. In: <i>6th Annual ACM-SIAM Symposium on Discrete Algorithms</i>. Society for Industrial and Applied Mathematics; 1995:312-321.","ista":"Alberts D, Henzinger MH. 1995. Average case analysis of dynamic graph algorithms. 6th Annual ACM-SIAM Symposium on Discrete Algorithms. SODA: Symposium on Discrete Algorithms, 312–321.","ieee":"D. Alberts and M. H. Henzinger, “Average case analysis of dynamic graph algorithms,” in <i>6th Annual ACM-SIAM Symposium on Discrete Algorithms</i>, San Francisco, CA, United States, 1995, pp. 312–321.","mla":"Alberts, David, and Monika H. Henzinger. “Average Case Analysis of Dynamic Graph Algorithms.” <i>6th Annual ACM-SIAM Symposium on Discrete Algorithms</i>, Society for Industrial and Applied Mathematics, 1995, pp. 312–21.","apa":"Alberts, D., &#38; Henzinger, M. H. (1995). Average case analysis of dynamic graph algorithms. In <i>6th Annual ACM-SIAM Symposium on Discrete Algorithms</i> (pp. 312–321). San Francisco, CA, United States: Society for Industrial and Applied Mathematics.","short":"D. Alberts, M.H. Henzinger, in:, 6th Annual ACM-SIAM Symposium on Discrete Algorithms, Society for Industrial and Applied Mathematics, 1995, pp. 312–321.","chicago":"Alberts, David, and Monika H Henzinger. “Average Case Analysis of Dynamic Graph Algorithms.” In <i>6th Annual ACM-SIAM Symposium on Discrete Algorithms</i>, 312–21. Society for Industrial and Applied Mathematics, 1995."},"conference":{"location":"San Francisco, CA, United States","start_date":"1995-01-22","end_date":"1995-01-24","name":"SODA: Symposium on Discrete Algorithms"},"author":[{"full_name":"Alberts, David","first_name":"David","last_name":"Alberts"},{"last_name":"Henzinger","first_name":"Monika H","id":"540c9bbd-f2de-11ec-812d-d04a5be85630","full_name":"Henzinger, Monika H","orcid":"0000-0002-5008-6530"}],"related_material":{"record":[{"status":"public","id":"11680","relation":"later_version"}]},"publication_identifier":{"isbn":["0898713498"]},"language":[{"iso":"eng"}],"day":"01","year":"1995","status":"public","title":"Average case analysis of dynamic graph algorithms"},{"author":[{"orcid":"0000-0002-0977-7989","full_name":"Sazanov, Leonid A","id":"338D39FE-F248-11E8-B48F-1D18A9856A87","first_name":"Leonid A","last_name":"Sazanov"},{"last_name":"Jackson","first_name":"Julie","full_name":"Jackson, Julie"}],"publication":"FEBS Letters","_id":"1949","issue":"2-3","type":"journal_article","article_processing_charge":"No","oa_version":"Published Version","date_created":"2018-12-11T11:54:52Z","status":"public","title":"Proton translocating transhydrogenase and NAD- and NADP-linked isocitrate dehydrogenases operate in a substrate cycle which contributes to fine regulation of the tricarboxylic acid cycle activity in mitochondria","volume":344,"day":"16","main_file_link":[{"url":"https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2894%2900370-X","open_access":"1"}],"date_updated":"2022-06-09T13:21:50Z","publist_id":"5134","publisher":"Elsevier","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_type":"original","date_published":"1994-05-16T00:00:00Z","month":"05","acknowledgement":"LAS is grateful to the Wellcome Trust for a fellowship. We should like to thank Prof. R.M. Denton for discussion.","extern":"1","quality_controlled":"1","doi":"10.1016/0014-5793(94)00370-X","citation":{"ama":"Sazanov LA, Jackson J. Proton translocating transhydrogenase and NAD- and NADP-linked isocitrate dehydrogenases operate in a substrate cycle which contributes to fine regulation of the tricarboxylic acid cycle activity in mitochondria. <i>FEBS Letters</i>. 1994;344(2-3):109-116. doi:<a href=\"https://doi.org/10.1016/0014-5793(94)00370-X\">10.1016/0014-5793(94)00370-X</a>","mla":"Sazanov, Leonid A., and Julie Jackson. “Proton Translocating Transhydrogenase and NAD- and NADP-Linked Isocitrate Dehydrogenases Operate in a Substrate Cycle Which Contributes to Fine Regulation of the Tricarboxylic Acid Cycle Activity in Mitochondria.” <i>FEBS Letters</i>, vol. 344, no. 2–3, Elsevier, 1994, pp. 109–16, doi:<a href=\"https://doi.org/10.1016/0014-5793(94)00370-X\">10.1016/0014-5793(94)00370-X</a>.","ieee":"L. A. Sazanov and J. Jackson, “Proton translocating transhydrogenase and NAD- and NADP-linked isocitrate dehydrogenases operate in a substrate cycle which contributes to fine regulation of the tricarboxylic acid cycle activity in mitochondria,” <i>FEBS Letters</i>, vol. 344, no. 2–3. Elsevier, pp. 109–116, 1994.","ista":"Sazanov LA, Jackson J. 1994. Proton translocating transhydrogenase and NAD- and NADP-linked isocitrate dehydrogenases operate in a substrate cycle which contributes to fine regulation of the tricarboxylic acid cycle activity in mitochondria. FEBS Letters. 344(2–3), 109–116.","chicago":"Sazanov, Leonid A, and Julie Jackson. “Proton Translocating Transhydrogenase and NAD- and NADP-Linked Isocitrate Dehydrogenases Operate in a Substrate Cycle Which Contributes to Fine Regulation of the Tricarboxylic Acid Cycle Activity in Mitochondria.” <i>FEBS Letters</i>. Elsevier, 1994. <a href=\"https://doi.org/10.1016/0014-5793(94)00370-X\">https://doi.org/10.1016/0014-5793(94)00370-X</a>.","short":"L.A. Sazanov, J. Jackson, FEBS Letters 344 (1994) 109–116.","apa":"Sazanov, L. A., &#38; Jackson, J. (1994). Proton translocating transhydrogenase and NAD- and NADP-linked isocitrate dehydrogenases operate in a substrate cycle which contributes to fine regulation of the tricarboxylic acid cycle activity in mitochondria. <i>FEBS Letters</i>. Elsevier. <a href=\"https://doi.org/10.1016/0014-5793(94)00370-X\">https://doi.org/10.1016/0014-5793(94)00370-X</a>"},"intvolume":"       344","pmid":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0014-5793"]},"year":"1994","external_id":{"pmid":["8187868"]},"page":"109 - 116","abstract":[{"lang":"eng","text":"H+-transhydrogenase (H+-Thase) and NADP-linked isocitrate dehydrogenase (NADP-ICDH) are very active in animal mitochondria but their physiological function is only poorly understood. This is especially so in the case of the heart and muscle, where there are no major consumers of NADPH. We propose here that H+-Thase and NADP-ICDH have a combined function in the fine regulation of the activity of the tricarboxylic acid (TCA) cycle, providing enhanced sensitivy to changes in energy demand. This is achieved through cycling of substrates by NAD-linked ICDH, NADP-linked ICDH and H+-Thase. It is proposed that NAD-ICDH operates in the forward direction of the TCA cycle, but NADP-ICDH is driven in reverse by elevated levels of NADPH resulting from the action of the transmembrane proton electrochemical potential gradient (Δp) on H+-Thase. This has the effect of increasing the sensitivity to allosteric modifiers of NAD-ICDH (NADH, ADP, ATP, Ca2+ etc), potentially giving rise to large changes in the net flux from iso-citrate to α-ketoglutarate. Furthermore, changes in the level of Δp resulting from changes in the demand for ATP would, via H+-Thase, shift the redox state of the NADP pool and this, in turn, would lead to a change in the rate of the reaction catalysed by NADP-ICDH and hence to an additional and complementary effect on the net metabolic flux from isocitrate to α-ketoglutarate. Other consequences of this substrate cycle are, (i) the production of heat at the expense of Δp, which may contribute to thermoregulation in the animal, and (ii) an increased rate of dissipation of Δp (leak)."}],"oa":1},{"article_type":"original","date_published":"1994-11-28T00:00:00Z","month":"11","date_updated":"2022-06-09T12:58:57Z","publist_id":"5133","publisher":"Elsevier","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","main_file_link":[{"open_access":"1","url":"https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2894%2901109-5"}],"day":"28","status":"public","volume":355,"title":"Inhibition of the respiratory burst in mouse macrophages by ultra-low doses of an opioid peptide is consistent with a possible adaptation mechanism","publication":"FEBS Letters","_id":"1953","type":"journal_article","article_processing_charge":"No","issue":"2","oa_version":"Published Version","date_created":"2018-12-11T11:54:53Z","author":[{"full_name":"Efanov, Alexander","first_name":"Alexander","last_name":"Efanov"},{"first_name":"Aleksei","last_name":"Koshkin","full_name":"Koshkin, Aleksei"},{"first_name":"Leonid A","id":"338D39FE-F248-11E8-B48F-1D18A9856A87","last_name":"Sazanov","orcid":"0000-0002-0977-7989","full_name":"Sazanov, Leonid A"},{"first_name":"O I","last_name":"Borodulina","full_name":"Borodulina, O I"},{"full_name":"Varfolomeev, Sergei","first_name":"Sergei","last_name":"Varfolomeev"},{"last_name":"Zaǐtsev","first_name":"Sergei","full_name":"Zaǐtsev, Sergei"}],"abstract":[{"text":"The respiratory burst induced by phorbol myristate acetate in mouse macrophages was inhibited by ultra-low doses (10-15 -10-13 M) of an opioid peptide [d-Ala2] methionine enkephalinamide. The effect disappeared at concentrations above and below this range. The inhibition approached 50% and was statistically significant (P &lt; 0.001). Increasing the time of the opioid incubation with cells brought about a shift in the maximal effect to lower concentrations of the opioid (from 10-13 to 5 · 10-15 M) and led to a decrease in the value of the effect, fully in accord with the previously proposed adaptation mechanism of the action of ultra-low doses.","lang":"eng"}],"oa":1,"external_id":{"pmid":["7982481"]},"page":"114 - 116","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0014-5793"]},"year":"1994","intvolume":"       355","pmid":1,"extern":"1","quality_controlled":"1","doi":"10.1016/0014-5793(94)01109-5","citation":{"ama":"Efanov A, Koshkin A, Sazanov LA, Borodulina OI, Varfolomeev S, Zaǐtsev S. Inhibition of the respiratory burst in mouse macrophages by ultra-low doses of an opioid peptide is consistent with a possible adaptation mechanism. <i>FEBS Letters</i>. 1994;355(2):114-116. doi:<a href=\"https://doi.org/10.1016/0014-5793(94)01109-5\">10.1016/0014-5793(94)01109-5</a>","apa":"Efanov, A., Koshkin, A., Sazanov, L. A., Borodulina, O. I., Varfolomeev, S., &#38; Zaǐtsev, S. (1994). Inhibition of the respiratory burst in mouse macrophages by ultra-low doses of an opioid peptide is consistent with a possible adaptation mechanism. <i>FEBS Letters</i>. Elsevier. <a href=\"https://doi.org/10.1016/0014-5793(94)01109-5\">https://doi.org/10.1016/0014-5793(94)01109-5</a>","short":"A. Efanov, A. Koshkin, L.A. Sazanov, O.I. Borodulina, S. Varfolomeev, S. Zaǐtsev, FEBS Letters 355 (1994) 114–116.","chicago":"Efanov, Alexander, Aleksei Koshkin, Leonid A Sazanov, O I Borodulina, Sergei Varfolomeev, and Sergei Zaǐtsev. “Inhibition of the Respiratory Burst in Mouse Macrophages by Ultra-Low Doses of an Opioid Peptide Is Consistent with a Possible Adaptation Mechanism.” <i>FEBS Letters</i>. Elsevier, 1994. <a href=\"https://doi.org/10.1016/0014-5793(94)01109-5\">https://doi.org/10.1016/0014-5793(94)01109-5</a>.","ieee":"A. Efanov, A. Koshkin, L. A. Sazanov, O. I. Borodulina, S. Varfolomeev, and S. Zaǐtsev, “Inhibition of the respiratory burst in mouse macrophages by ultra-low doses of an opioid peptide is consistent with a possible adaptation mechanism,” <i>FEBS Letters</i>, vol. 355, no. 2. Elsevier, pp. 114–116, 1994.","ista":"Efanov A, Koshkin A, Sazanov LA, Borodulina OI, Varfolomeev S, Zaǐtsev S. 1994. Inhibition of the respiratory burst in mouse macrophages by ultra-low doses of an opioid peptide is consistent with a possible adaptation mechanism. FEBS Letters. 355(2), 114–116.","mla":"Efanov, Alexander, et al. “Inhibition of the Respiratory Burst in Mouse Macrophages by Ultra-Low Doses of an Opioid Peptide Is Consistent with a Possible Adaptation Mechanism.” <i>FEBS Letters</i>, vol. 355, no. 2, Elsevier, 1994, pp. 114–16, doi:<a href=\"https://doi.org/10.1016/0014-5793(94)01109-5\">10.1016/0014-5793(94)01109-5</a>."}},{"day":"01","volume":479,"title":"Na+-activated K+ channels localized in the nodal region of myelinated axons of Xenopus","status":"public","oa_version":"Published Version","date_created":"2018-12-11T12:03:31Z","article_processing_charge":"No","_id":"3475","type":"journal_article","publication":"Journal of Physiology","author":[{"full_name":"Koh, Duk","first_name":"Duk","last_name":"Koh"},{"orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","last_name":"Jonas"},{"last_name":"Vogel","first_name":"Werner","full_name":"Vogel, Werner"}],"month":"01","date_published":"1994-01-01T00:00:00Z","article_type":"original","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","publisher":"Wiley-Blackwell","date_updated":"2022-06-03T11:09:21Z","publist_id":"2912","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1155738/","open_access":"1"}],"year":"1994","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0022-3751"]},"pmid":1,"intvolume":"       479","citation":{"ama":"Koh D, Jonas PM, Vogel W. Na+-activated K+ channels localized in the nodal region of myelinated axons of Xenopus. <i>Journal of Physiology</i>. 1994;479:183-197. doi:<a href=\"https://doi.org/10.1113/jphysiol.1994.sp020287\">10.1113/jphysiol.1994.sp020287</a>","apa":"Koh, D., Jonas, P. M., &#38; Vogel, W. (1994). Na+-activated K+ channels localized in the nodal region of myelinated axons of Xenopus. <i>Journal of Physiology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1113/jphysiol.1994.sp020287\">https://doi.org/10.1113/jphysiol.1994.sp020287</a>","short":"D. Koh, P.M. Jonas, W. Vogel, Journal of Physiology 479 (1994) 183–197.","chicago":"Koh, Duk, Peter M Jonas, and Werner Vogel. “Na+-Activated K+ Channels Localized in the Nodal Region of Myelinated Axons of Xenopus.” <i>Journal of Physiology</i>. Wiley-Blackwell, 1994. <a href=\"https://doi.org/10.1113/jphysiol.1994.sp020287\">https://doi.org/10.1113/jphysiol.1994.sp020287</a>.","ista":"Koh D, Jonas PM, Vogel W. 1994. Na+-activated K+ channels localized in the nodal region of myelinated axons of Xenopus. Journal of Physiology. 479, 183–197.","ieee":"D. Koh, P. M. Jonas, and W. Vogel, “Na+-activated K+ channels localized in the nodal region of myelinated axons of Xenopus,” <i>Journal of Physiology</i>, vol. 479. Wiley-Blackwell, pp. 183–197, 1994.","mla":"Koh, Duk, et al. “Na+-Activated K+ Channels Localized in the Nodal Region of Myelinated Axons of Xenopus.” <i>Journal of Physiology</i>, vol. 479, Wiley-Blackwell, 1994, pp. 183–97, doi:<a href=\"https://doi.org/10.1113/jphysiol.1994.sp020287\">10.1113/jphysiol.1994.sp020287</a>."},"doi":"10.1113/jphysiol.1994.sp020287","quality_controlled":"1","extern":"1","acknowledgement":"We thank Drs M.Häusser and A. Villarroel for critically reading the manuscript, Dr E. v. Kitzing and A. Roth for many helpful discussions. This work was supported by the Deutsche Forschungsgemeinschaft (Vo188/13-2). ","oa":1,"abstract":[{"lang":"eng","text":"1. A potassium channel activated by internal Na+ ions (K+Na channel) was identified in peripheral myelinated axons of Xenopus laevis using the cell-attached and excised configurations of the patch clamp technique. 2. The single-channel conductance for the main open state was 88 pS with [K+]o = 105 mM and pS with [K+]o = 2.5 mM ([K+]i = 105 mM). The channel was selectively permeable to K+ over Na+ ions. A characteristic feature of the K+Na channel was the frequent occurrence of subconductance states. 3. The open probability of the channel was strongly dependent on the concentration of Na+ ions at the inner side of the membrane. The half-maximal activating Na+ concentration and the Hill coefficient were 33 mM and 2.9, respectively. The open probability of the channel showed only weak potential dependence. 4. The K+Na channel was relatively insensitive to external tetraethylammonium (TEA+) in comparison with voltage-dependent axonal K+ channels; the half-maximal inhibitory concentration (IC50) was 21.3 mM (at -90 mV). In contrast, the channel was blocked by low concentrations of external Ba2+ and Cs+ ions, with IC50 values of 0.7 and 1.1 mM, respectively (at -90 mV). The block by Ba2+ and Cs+ was more pronounced at negative than at positive membrane potentials. 5. A comparison of the number of K+Na channels in nodal and paranodal patches from the same axon revealed that the channel density was about 10-fold higher at the node of Ranvier than at the paranode. Moreover, a correlation between the number of K+Na channels and voltage-dependent Na+ channels in the same patches was found, suggesting co-localization of both channel types. 6. As weakly potential-dependent ('leakage') channels, axonal K+Na channels may be involved in setting the resting potential of vertebrate axons. Simulations of Na+ ion diffusion suggest two possible mechanisms of activation of K+Na channels: the local increase of Na+ concentration in a cluster of Na+ channels during a single action potential or the accumulation in the intracellular axonal compartment during a train of action potentials."}],"page":"183 - 197","external_id":{"pmid":["7799220 "]}},{"publisher":"Society for Neuroscience","publist_id":"2911","date_updated":"2022-06-03T09:36:43Z","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","date_published":"1994-08-01T00:00:00Z","month":"08","article_type":"original","scopus_import":"1","main_file_link":[{"url":"https://europepmc.org/article/med/8046439","open_access":"1"}],"status":"public","title":"Detailed passive cable models of whole-cell recorded CA3 pyramidal neurons in rat hippocampal slices","volume":14,"day":"01","author":[{"full_name":"Major, Guy","first_name":"Guy","last_name":"Major"},{"last_name":"Larkman","first_name":"Alan","full_name":"Larkman, Alan"},{"full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","last_name":"Jonas"},{"full_name":"Sakmann, Bert","last_name":"Sakmann","first_name":"Bert"},{"last_name":"Jack","first_name":"Julian","full_name":"Jack, Julian"}],"_id":"3476","type":"journal_article","issue":"8","article_processing_charge":"No","publication":"Journal of Neuroscience","oa_version":"Published Version","date_created":"2018-12-11T12:03:32Z","oa":1,"abstract":[{"lang":"eng","text":"Tight-seal whole-cell recordings were made from cleaned somata of CA3 pyramidal cells deep in hippocampal slices from 19–21-d-old rats. The cells were filled with biocytin, and their voltage responses to short current pulses were recorded. After washout of initial sag, responses scaled linearly with injected current and were stable over time. The dendritic and axonal arbors of four cells were reconstructed and measured using light microscopy. Dendritic spines and axonal boutons were counted and the additional membrane area was incorporated into the relevant segments. The morphology of each neuron was converted into a detailed branching cable model by assuming values for specific membrane capacitance Cm and resistance Rm, and cytoplasmic resistivity Ri. These parameters were optimized for each cell by directly matching the model's response to that of the real cell by means of a modified weighted least-squares fitting procedure. By comparing the deviations between model and experimental responses to control noise recordings, approximate 95% confidence intervals were established for each parameter. If a somatic shunt was allowed, a wide range of possible Rm values produced acceptable fits. With zero shunt, Cm was 0.7–0.8 microFcm-2, Ri was 170–340 omega cm, and Rm ranged between 120 and 200 k omega cm2. The electrotonic lengths of the basal and oblique dendrites were 0.2–0.3 space constants, and those of the apical tufts were 0.4–0.7 space constants. The steady-state electrical geometry of these cells was therefore compact; average dendritic tip/soma relative synaptic efficacies were &gt; 93% for the basal and oblique dendrites, and &gt; 81% for the tufts. With fast transient synaptic inputs, however, the models produced a wide range of postsynaptic potential shapes and marked filtering of voltage-clamp currents."}],"external_id":{"pmid":["8046439 "]},"page":"4613 - 4638","pmid":1,"intvolume":"        14","publication_identifier":{"issn":["0270-6474"]},"language":[{"iso":"eng"}],"year":"1994","acknowledgement":"logy Training Fellowship. A.L. was supported by a Royal Society Fellowship. The Oxford part of the collaboration was funded by a Wellcome Trust Programme Grant, the Heidelberg part by the Max-Planck Gesellschaft. We are grateful to Sir David Cox for his comments on the statistics, to K. Stratford, M. Hausser, D. Flitney, M. O’Neill, S. Gough, G. Stuart, N. Spruston, P. Stem, and K. Bauer for their help and useful discussions, and to M. Kaiser for technical assistance. ","extern":"1","doi":"10.1523/JNEUROSCI.14-08-04613.1994","citation":{"mla":"Major, Guy, et al. “Detailed Passive Cable Models of Whole-Cell Recorded CA3 Pyramidal Neurons in Rat Hippocampal Slices.” <i>Journal of Neuroscience</i>, vol. 14, no. 8, Society for Neuroscience, 1994, pp. 4613–38, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.14-08-04613.1994\">10.1523/JNEUROSCI.14-08-04613.1994</a>.","ista":"Major G, Larkman A, Jonas PM, Sakmann B, Jack J. 1994. Detailed passive cable models of whole-cell recorded CA3 pyramidal neurons in rat hippocampal slices. Journal of Neuroscience. 14(8), 4613–4638.","ieee":"G. Major, A. Larkman, P. M. Jonas, B. Sakmann, and J. Jack, “Detailed passive cable models of whole-cell recorded CA3 pyramidal neurons in rat hippocampal slices,” <i>Journal of Neuroscience</i>, vol. 14, no. 8. Society for Neuroscience, pp. 4613–4638, 1994.","short":"G. Major, A. Larkman, P.M. Jonas, B. Sakmann, J. Jack, Journal of Neuroscience 14 (1994) 4613–4638.","chicago":"Major, Guy, Alan Larkman, Peter M Jonas, Bert Sakmann, and Julian Jack. “Detailed Passive Cable Models of Whole-Cell Recorded CA3 Pyramidal Neurons in Rat Hippocampal Slices.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 1994. <a href=\"https://doi.org/10.1523/JNEUROSCI.14-08-04613.1994\">https://doi.org/10.1523/JNEUROSCI.14-08-04613.1994</a>.","apa":"Major, G., Larkman, A., Jonas, P. M., Sakmann, B., &#38; Jack, J. (1994). Detailed passive cable models of whole-cell recorded CA3 pyramidal neurons in rat hippocampal slices. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.14-08-04613.1994\">https://doi.org/10.1523/JNEUROSCI.14-08-04613.1994</a>","ama":"Major G, Larkman A, Jonas PM, Sakmann B, Jack J. Detailed passive cable models of whole-cell recorded CA3 pyramidal neurons in rat hippocampal slices. <i>Journal of Neuroscience</i>. 1994;14(8):4613-4638. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.14-08-04613.1994\">10.1523/JNEUROSCI.14-08-04613.1994</a>"},"quality_controlled":"1"},{"author":[{"last_name":"Turelli","first_name":"Michael","full_name":"Turelli, Michael"},{"full_name":"Barton, Nicholas H","orcid":"0000-0002-8548-5240","last_name":"Barton","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","first_name":"Nicholas H"}],"publication":"Genetics","type":"journal_article","_id":"3642","issue":"3","article_processing_charge":"No","date_created":"2018-12-11T12:04:24Z","oa_version":"Published Version","status":"public","volume":138,"title":"Genetic and statistical analyses of strong selection on polygenic traits: What, me normal?","day":"01","main_file_link":[{"url":"https://pubmed.ncbi.nlm.nih.gov/7851785/","open_access":"1"}],"date_updated":"2022-06-03T08:18:54Z","publist_id":"2741","publisher":"Genetics Society of America","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_type":"original","date_published":"1994-11-01T00:00:00Z","month":"11","extern":"1","quality_controlled":"1","citation":{"apa":"Turelli, M., &#38; Barton, N. H. (1994). Genetic and statistical analyses of strong selection on polygenic traits: What, me normal? <i>Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1093/genetics/138.3.913\">https://doi.org/10.1093/genetics/138.3.913</a>","short":"M. Turelli, N.H. Barton, Genetics 138 (1994) 913–941.","chicago":"Turelli, Michael, and Nicholas H Barton. “Genetic and Statistical Analyses of Strong Selection on Polygenic Traits: What, Me Normal?” <i>Genetics</i>. Genetics Society of America, 1994. <a href=\"https://doi.org/10.1093/genetics/138.3.913\">https://doi.org/10.1093/genetics/138.3.913</a>.","ieee":"M. Turelli and N. H. Barton, “Genetic and statistical analyses of strong selection on polygenic traits: What, me normal?,” <i>Genetics</i>, vol. 138, no. 3. Genetics Society of America, pp. 913–941, 1994.","ista":"Turelli M, Barton NH. 1994. Genetic and statistical analyses of strong selection on polygenic traits: What, me normal? Genetics. 138(3), 913–941.","mla":"Turelli, Michael, and Nicholas H. Barton. “Genetic and Statistical Analyses of Strong Selection on Polygenic Traits: What, Me Normal?” <i>Genetics</i>, vol. 138, no. 3, Genetics Society of America, 1994, pp. 913–41, doi:<a href=\"https://doi.org/10.1093/genetics/138.3.913\">10.1093/genetics/138.3.913</a>.","ama":"Turelli M, Barton NH. Genetic and statistical analyses of strong selection on polygenic traits: What, me normal? <i>Genetics</i>. 1994;138(3):913-941. doi:<a href=\"https://doi.org/10.1093/genetics/138.3.913\">10.1093/genetics/138.3.913</a>"},"doi":"10.1093/genetics/138.3.913","intvolume":"       138","pmid":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0016-6731"]},"year":"1994","external_id":{"pmid":["7851785"]},"page":"913 - 941","abstract":[{"text":"We develop a general population genetic framework for analyzing selection on many loci, and apply it to strong truncation and disruptive selection on an additive polygenic trait. We first present statistical methods for analyzing the infinitesimal model, in which offspring breeding values are normally distributed around the mean of the parents, with fixed variance. These show that the usual assumption of a Gaussian distribution of breeding values in the population gives remarkably accurate predictions for the mean and the variance, even when disruptive selection generates substantial deviations from normality. We then set out a general genetic analysis of selection and recombination. The population is represented by multilocus cumulants describing the distribution of haploid genotypes, and selection is described by the relation between mean fitness and these cumulants. We provide exact recursions in terms of generating functions for the effects of selection on non-central moments. The effects of recombination are simply calculated as a weighted sum over all the permutations produced by meiosis. Finally, the new cumulants that describe the next generation are computed from the non-central moments. Although this scheme is applied here in detail only to selection on an additive trait, it is quite general. For arbitrary epistasis and linkage, we describe a consistent infinitesimal limit in which the short-term selection response is dominated by infinitesimal allele frequency changes and linkage disequilibria. Numerical multilocus results show that the standard Gaussian approximation gives accurate predictions for the dynamics of the mean and genetic variance in this limit. Even with intense truncation selection, linkage disequilibria of order three and higher never cause much deviation from normality. Thus, the empirical deviations frequently found between predicted and observed responses to artificial selection are not caused by linkage-disequilibrium-induced departures from normality. Disruptive selection can generate substantial four-way disequilibria, and hence kurtosis; but even then, the Gaussian assumption predicts the variance accurately. In contrast to the apparent simplicity of the infinitesimal limit, data suggest that changes in genetic variance after 10 or more generations of selection are likely to be dominated by allele frequency dynamics that depend on genetic details.","lang":"eng"}],"oa":1},{"main_file_link":[{"open_access":"1","url":"https://dl.acm.org/doi/10.1145/174462.156635"}],"scopus_import":"1","date_published":"1994-01-01T00:00:00Z","month":"01","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","publisher":"ACM","publist_id":"2088","date_updated":"2022-06-02T12:00:42Z","date_created":"2018-12-11T12:06:34Z","oa_version":"None","_id":"4037","article_processing_charge":"No","type":"journal_article","issue":"1","publication":"ACM Transactions on Graphics","author":[{"last_name":"Edelsbrunner","id":"3FB178DA-F248-11E8-B48F-1D18A9856A87","first_name":"Herbert","full_name":"Edelsbrunner, Herbert","orcid":"0000-0002-9823-6833"},{"last_name":"Mücke","first_name":"Ernst","full_name":"Mücke, Ernst"}],"day":"01","volume":13,"title":"Three-dimensional alpha shapes","status":"public","page":"43 - 72","oa":1,"abstract":[{"text":"Frequently, data in scientific computing is in its abstract form a finite point set in space, and it is sometimes useful or required to compute what one might call the `'shape” of the set. For that purpose, this article introduces the formal notion of the family of alpha-shapes of a finite point set in R3. Each shape is a well-defined polytope, derived from the Delaunay triangulation of the point set, with a parameter alpha is-an-element-of R controlling the desired level of detail. An algorithm is presented that constructs the entire family of shapes for a given set of size n in time O(n2), worst case. A robust implementation of the algorithm is discussed, and several applications in the area of scientific computing are mentioned.","lang":"eng"}],"citation":{"ama":"Edelsbrunner H, Mücke E. Three-dimensional alpha shapes. <i>ACM Transactions on Graphics</i>. 1994;13(1):43-72. doi:<a href=\"https://doi.org/10.1145/174462.156635\">10.1145/174462.156635</a>","mla":"Edelsbrunner, Herbert, and Ernst Mücke. “Three-Dimensional Alpha Shapes.” <i>ACM Transactions on Graphics</i>, vol. 13, no. 1, ACM, 1994, pp. 43–72, doi:<a href=\"https://doi.org/10.1145/174462.156635\">10.1145/174462.156635</a>.","ista":"Edelsbrunner H, Mücke E. 1994. Three-dimensional alpha shapes. ACM Transactions on Graphics. 13(1), 43–72.","ieee":"H. Edelsbrunner and E. Mücke, “Three-dimensional alpha shapes,” <i>ACM Transactions on Graphics</i>, vol. 13, no. 1. ACM, pp. 43–72, 1994.","chicago":"Edelsbrunner, Herbert, and Ernst Mücke. “Three-Dimensional Alpha Shapes.” <i>ACM Transactions on Graphics</i>. ACM, 1994. <a href=\"https://doi.org/10.1145/174462.156635\">https://doi.org/10.1145/174462.156635</a>.","short":"H. Edelsbrunner, E. Mücke, ACM Transactions on Graphics 13 (1994) 43–72.","apa":"Edelsbrunner, H., &#38; Mücke, E. (1994). Three-dimensional alpha shapes. <i>ACM Transactions on Graphics</i>. ACM. <a href=\"https://doi.org/10.1145/174462.156635\">https://doi.org/10.1145/174462.156635</a>"},"doi":"10.1145/174462.156635","quality_controlled":"1","extern":"1","acknowledgement":"National Science Foundation under grant CCR-8921421 and  Alan T. Waterman award, grant CCR-9118874.","year":"1994","language":[{"iso":"eng"}],"intvolume":"        13"},{"month":"01","date_published":"1994-01-14T00:00:00Z","article_type":"original","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","publisher":"American Society for Biochemistry and Molecular Biology","date_updated":"2022-06-02T10:23:48Z","publist_id":"1941","main_file_link":[{"open_access":"1","url":"https://www.sciencedirect.com/science/article/pii/S0021925817421867?via%3Dihub"}],"scopus_import":"1","day":"14","volume":269,"title":"Brain-derived neurotrophic factor increases neurotrophin-3 expression in cerebellar granule neurons","status":"public","oa_version":"None","date_created":"2018-12-11T12:07:25Z","type":"journal_article","_id":"4179","issue":"2","article_processing_charge":"No","publication":"Journal of Biological Chemistry","author":[{"full_name":"Leingärtner, Axel","first_name":"Axel","last_name":"Leingärtner"},{"first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J"},{"last_name":"Kolbeck","first_name":"Roland","full_name":"Kolbeck, Roland"},{"last_name":"Thoenen","first_name":"Hans","full_name":"Thoenen, Hans"},{"last_name":"Lindholm","first_name":"Dan","full_name":"Lindholm, Dan"}],"oa":1,"abstract":[{"text":"Neurotrophin-3 (NT-3) is a member of the neurotrophin gene family and is highly expressed in the developing rat cerebellum. Here we show that brain-derived neurotrophic factor (BDNF) increased by approximately 10-fold the NT-3 mRNA levels in cultured cerebellar granule neurons isolated from postnatal rats, whereas nerve growth factor (NGF) and NT-3 itself had no effect. The effect of BDNF was additive to that of triiodothyronine (T3), which also increased NT-3 mRNA in these neurons. The drug K252a inhibited the BDNF-mediated stimulation of NT-3 expression, suggesting an involvement of trkB receptors. Nuclear run-on experiments showed that BDNF enhanced NT-3 transcription, whereas the stability of NT-3 mRNA remained unchanged. The data presented are the first demonstration that one neurotrophin regulates the expression of another and provide evidence that NT-3 production in granule neurons is regulated by both BDNF and T3.","lang":"eng"}],"page":"828 - 830","year":"1994","language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1083-351X"],"issn":["0021-9258"]},"intvolume":"       269","doi":"10.1016/s0021-9258(17)42186-7","citation":{"ama":"Leingärtner A, Heisenberg C-PJ, Kolbeck R, Thoenen H, Lindholm D. Brain-derived neurotrophic factor increases neurotrophin-3 expression in cerebellar granule neurons. <i>Journal of Biological Chemistry</i>. 1994;269(2):828-830. doi:<a href=\"https://doi.org/10.1016/s0021-9258(17)42186-7\">10.1016/s0021-9258(17)42186-7</a>","ieee":"A. Leingärtner, C.-P. J. Heisenberg, R. Kolbeck, H. Thoenen, and D. Lindholm, “Brain-derived neurotrophic factor increases neurotrophin-3 expression in cerebellar granule neurons,” <i>Journal of Biological Chemistry</i>, vol. 269, no. 2. American Society for Biochemistry and Molecular Biology, pp. 828–830, 1994.","ista":"Leingärtner A, Heisenberg C-PJ, Kolbeck R, Thoenen H, Lindholm D. 1994. Brain-derived neurotrophic factor increases neurotrophin-3 expression in cerebellar granule neurons. Journal of Biological Chemistry. 269(2), 828–830.","mla":"Leingärtner, Axel, et al. “Brain-Derived Neurotrophic Factor Increases Neurotrophin-3 Expression in Cerebellar Granule Neurons.” <i>Journal of Biological Chemistry</i>, vol. 269, no. 2, American Society for Biochemistry and Molecular Biology, 1994, pp. 828–30, doi:<a href=\"https://doi.org/10.1016/s0021-9258(17)42186-7\">10.1016/s0021-9258(17)42186-7</a>.","apa":"Leingärtner, A., Heisenberg, C.-P. J., Kolbeck, R., Thoenen, H., &#38; Lindholm, D. (1994). Brain-derived neurotrophic factor increases neurotrophin-3 expression in cerebellar granule neurons. <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology. <a href=\"https://doi.org/10.1016/s0021-9258(17)42186-7\">https://doi.org/10.1016/s0021-9258(17)42186-7</a>","short":"A. Leingärtner, C.-P.J. Heisenberg, R. Kolbeck, H. Thoenen, D. Lindholm, Journal of Biological Chemistry 269 (1994) 828–830.","chicago":"Leingärtner, Axel, Carl-Philipp J Heisenberg, Roland Kolbeck, Hans Thoenen, and Dan Lindholm. “Brain-Derived Neurotrophic Factor Increases Neurotrophin-3 Expression in Cerebellar Granule Neurons.” <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology, 1994. <a href=\"https://doi.org/10.1016/s0021-9258(17)42186-7\">https://doi.org/10.1016/s0021-9258(17)42186-7</a>."},"quality_controlled":"1","extern":"1","acknowledgement":"We thank Dorothea Stratmann and Karin Angermayer for skillful technical assistance."},{"scopus_import":"1","main_file_link":[{"url":"https://www.sciencedirect.com/science/article/pii/S0890540184710601?via%3Dihub","open_access":"1"}],"publisher":"Elsevier","date_updated":"2022-06-02T09:24:58Z","publist_id":"227","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","month":"08","date_published":"1994-08-01T00:00:00Z","article_type":"original","author":[{"last_name":"Henzinger","first_name":"Thomas A","id":"40876CD8-F248-11E8-B48F-1D18A9856A87","orcid":"0000−0002−2985−7724","full_name":"Henzinger, Thomas A"},{"last_name":"Manna","first_name":"Zohar","full_name":"Manna, Zohar"},{"full_name":"Pnueli, Amir","first_name":"Amir","last_name":"Pnueli"}],"type":"journal_article","_id":"4501","article_processing_charge":"No","issue":"2","publication":"Information and Computation","oa_version":"None","date_created":"2018-12-11T12:09:10Z","status":"public","title":"Temporal proof methodologies for timed transition systems","volume":112,"day":"01","page":"273 - 337","oa":1,"abstract":[{"lang":"eng","text":"We extend the specification language of temporal logic, the corresponding verification framework, and the underlying computational model to deal with real-;time properties of reactive systems. The abstract notion of timed transition systems generalizes traditional transition systems conservatively: qualitative fairness requirements are replaced (and superseded) by quantitative lower-bound and upper-bound timing constraints on transitions. This framework can model real-time systems that communicate either through shared variables or by message passing and real-time issues such as timeouts, process priorities (interrupts), and process scheduling. We exhibit two styles for the specification of real-time systems. While the first approach uses time-bounded versions of the temporal operators, the second approach allows explicit references to time through a special clock variable. Corresponding to the two styles of specification, we present and compare two different proof methodologies for the verification of timing requirements that are expressed in these styles. For the bounded-operator style, we provide a set of proof rules for establishing bounded-invariance and bounded-responce properties of timed transition systems. This approach generalizes the standard temporal proof rules for verifying invariance and response properties conservatively. For the explicit-clock style, we exploit the observation that every time-bounded property is a safety property and use the standard temporal proof rules for establishing safety properties."}],"acknowledgement":"This research was supported in part by an IBM graduate fellowship, by the National Science Foundation under Grants CCR-9223226 and CCR-9200794. by the Defense Advanced Research Projects Agency under Contract N00039-84-C-0211. by the United States Air Force OMee of Scientific Research under Contracts F49620-93-141139 and F4962043-1-0056. and by the European Community ESPRIT Basic Research Action Project 6021 (REACT). A preliminary version of Part 1 of this paper appeared in the proceedings of the 1991 REX Workshop on Real Time Theory In Prate [HMP92a I a preliminary version of Part II appeared in the proceedings of the 1991 ACM Symposium on Principles of Programming Languages RIMP911. ","extern":"1","doi":"10.1006/inco.1994.1060","citation":{"ama":"Henzinger TA, Manna Z, Pnueli A. Temporal proof methodologies for timed transition systems. <i>Information and Computation</i>. 1994;112(2):273-337. doi:<a href=\"https://doi.org/10.1006/inco.1994.1060\">10.1006/inco.1994.1060</a>","ieee":"T. A. Henzinger, Z. Manna, and A. Pnueli, “Temporal proof methodologies for timed transition systems,” <i>Information and Computation</i>, vol. 112, no. 2. Elsevier, pp. 273–337, 1994.","ista":"Henzinger TA, Manna Z, Pnueli A. 1994. Temporal proof methodologies for timed transition systems. Information and Computation. 112(2), 273–337.","mla":"Henzinger, Thomas A., et al. “Temporal Proof Methodologies for Timed Transition Systems.” <i>Information and Computation</i>, vol. 112, no. 2, Elsevier, 1994, pp. 273–337, doi:<a href=\"https://doi.org/10.1006/inco.1994.1060\">10.1006/inco.1994.1060</a>.","apa":"Henzinger, T. A., Manna, Z., &#38; Pnueli, A. (1994). Temporal proof methodologies for timed transition systems. <i>Information and Computation</i>. Elsevier. <a href=\"https://doi.org/10.1006/inco.1994.1060\">https://doi.org/10.1006/inco.1994.1060</a>","chicago":"Henzinger, Thomas A, Zohar Manna, and Amir Pnueli. “Temporal Proof Methodologies for Timed Transition Systems.” <i>Information and Computation</i>. Elsevier, 1994. <a href=\"https://doi.org/10.1006/inco.1994.1060\">https://doi.org/10.1006/inco.1994.1060</a>.","short":"T.A. Henzinger, Z. Manna, A. Pnueli, Information and Computation 112 (1994) 273–337."},"quality_controlled":"1","intvolume":"       112","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0890-5401"]},"year":"1994"},{"abstract":[{"lang":"eng","text":"A cDNA clone for a new rat metabotropic glutamate receptor termed mGluR7 was isolated through polymerase chain reaction-mediated DNA amplification by using primer sequences conserved among the metabotropic receptor (mGluR) family and by the subsequent screening of a rat forebrain cDNA library. The cloned mGluR7 subtype consists of 915 amino acid residues and exhibits a structural architecture common to the mGluR family with a large extracellular domain preceding the seven putative membrane-spanning domains. mGluR7 shows the highest sequence similarity to mGluR4 and mGluR6 among the members of the mGluR family. Similar to mGluR4 and mGluR6, mGluR7 inhibits forskolin- stimulated cyclic AMP accumulation in response to agonist interaction and potently reacts with L-2-amino-4-phosphonobutyrate and L-serine-O-phosphate in Chinese hamster ovary cells transfected with the cloned cDNA. RNA blot and in situ hybridization analyses of mGluR7 mRNA indicated that it is widely expressed in many neuronal cells of the central nervous system and is thus different from the more limitedly expressed mGluR4 or mGluR6 mRNA. mGluR7 together with mGluR4 thus corresponds to the putative L-2-amino-4- phosphonobutyrate receptor which plays an important role in modulation of glutamate transmission in the central nervous system."}],"oa":1,"external_id":{"pmid":["8288585"]},"page":"1231 - 1236","language":[{"iso":"eng"}],"year":"1994","intvolume":"       269","pmid":1,"extern":"1","quality_controlled":"1","doi":"10.1016/S0021-9258(17)42247-2","citation":{"ama":"Okamoto N, Hori S, Akazawa C, et al. Molecular characterization of a new metabotropic glutamate receptor mGluR7 coupled to inhibitory cyclic AMP signal transduction. <i>Journal of Biological Chemistry</i>. 1994;269(2):1231-1236. doi:<a href=\"https://doi.org/10.1016/S0021-9258(17)42247-2\">10.1016/S0021-9258(17)42247-2</a>","apa":"Okamoto, N., Hori, S., Akazawa, C., Hayashi, Y., Shigemoto, R., Mizuno, N., &#38; Nakanishi, S. (1994). Molecular characterization of a new metabotropic glutamate receptor mGluR7 coupled to inhibitory cyclic AMP signal transduction. <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology. <a href=\"https://doi.org/10.1016/S0021-9258(17)42247-2\">https://doi.org/10.1016/S0021-9258(17)42247-2</a>","chicago":"Okamoto, Naoyuki, Seiji Hori, Chihiro Akazawa, Yasunori Hayashi, Ryuichi Shigemoto, Noboru Mizuno, and Shigetada Nakanishi. “Molecular Characterization of a New Metabotropic Glutamate Receptor MGluR7 Coupled to Inhibitory Cyclic AMP Signal Transduction.” <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology, 1994. <a href=\"https://doi.org/10.1016/S0021-9258(17)42247-2\">https://doi.org/10.1016/S0021-9258(17)42247-2</a>.","short":"N. Okamoto, S. Hori, C. Akazawa, Y. Hayashi, R. Shigemoto, N. Mizuno, S. Nakanishi, Journal of Biological Chemistry 269 (1994) 1231–1236.","ista":"Okamoto N, Hori S, Akazawa C, Hayashi Y, Shigemoto R, Mizuno N, Nakanishi S. 1994. Molecular characterization of a new metabotropic glutamate receptor mGluR7 coupled to inhibitory cyclic AMP signal transduction. Journal of Biological Chemistry. 269(2), 1231–1236.","ieee":"N. Okamoto <i>et al.</i>, “Molecular characterization of a new metabotropic glutamate receptor mGluR7 coupled to inhibitory cyclic AMP signal transduction,” <i>Journal of Biological Chemistry</i>, vol. 269, no. 2. American Society for Biochemistry and Molecular Biology, pp. 1231–1236, 1994.","mla":"Okamoto, Naoyuki, et al. “Molecular Characterization of a New Metabotropic Glutamate Receptor MGluR7 Coupled to Inhibitory Cyclic AMP Signal Transduction.” <i>Journal of Biological Chemistry</i>, vol. 269, no. 2, American Society for Biochemistry and Molecular Biology, 1994, pp. 1231–36, doi:<a href=\"https://doi.org/10.1016/S0021-9258(17)42247-2\">10.1016/S0021-9258(17)42247-2</a>."},"acknowledgement":"We are grateful to Akira Uesugi for photographic assistance.","date_published":"1994-01-14T00:00:00Z","month":"01","publist_id":"4348","date_updated":"2022-06-08T15:11:44Z","publisher":"American Society for Biochemistry and Molecular Biology","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","main_file_link":[{"open_access":"1","url":"https://www.sciencedirect.com/science/article/pii/S0021925817422472?via%3Dihub"}],"scopus_import":"1","day":"14","status":"public","title":"Molecular characterization of a new metabotropic glutamate receptor mGluR7 coupled to inhibitory cyclic AMP signal transduction","volume":269,"publication":"Journal of Biological Chemistry","issue":"2","_id":"2550","type":"journal_article","article_processing_charge":"No","oa_version":"None","date_created":"2018-12-11T11:58:20Z","author":[{"full_name":"Okamoto, Naoyuki","first_name":"Naoyuki","last_name":"Okamoto"},{"full_name":"Hori, Seiji","last_name":"Hori","first_name":"Seiji"},{"full_name":"Akazawa, Chihiro","first_name":"Chihiro","last_name":"Akazawa"},{"full_name":"Hayashi, Yasunori","last_name":"Hayashi","first_name":"Yasunori"},{"last_name":"Shigemoto","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444"},{"last_name":"Mizuno","first_name":"Noboru","full_name":"Mizuno, Noboru"},{"last_name":"Nakanishi","first_name":"Shigetada","full_name":"Nakanishi, Shigetada"}]},{"intvolume":"       472","pmid":1,"publication_identifier":{"issn":["0022-3751"]},"language":[{"iso":"eng"}],"year":"1993","acknowledgement":"We are indebted to Professor B. Katz for critically reading the manuscript and for helpful suggestions. We especially thank Professor D. Colquhoun for several discussions, for generously providing the source codes of programs for maximum-likelihood fit with sums of Gaussian functions, a routine for calculating the error function and for critically reading the manuscript. We also thank Drs A. Larkman, P. Ruppersberg, N. Spuston and G. Stuart for critically reading the manuscript, P. Andersen, B. Betz, J. Evans, K. Harris, E. v. Kitzing, R. Rahamimov and K. Stratford for helpful discussions, and J. J. B. Jack for much-needed advice and guidance to G.M. We thank K. Bauer, F. Helmchen, M. Huke, B. Manz and especially A. Roth for computer programming, B. Werner for typing the manuscript, and M. Kaiser for excellent technical assistance. Part of the project was supported by the Deutsche Forschungsgemeinschaft (SFB-317)\r\nand the Wellcome Trust.","extern":"1","quality_controlled":"1","citation":{"mla":"Jonas, Peter M., et al. “Quantal Components of Unitary EPSCs at the Mossy Fibre Synapse on CA3 Pyramidal Cells of Rat Hippocampus.” <i>Journal of Physiology</i>, vol. 472, Wiley-Blackwell, 1993, pp. 615–63, doi:<a href=\"https://doi.org/10.1113/jphysiol.1993.sp019965\">10.1113/jphysiol.1993.sp019965</a>.","ista":"Jonas PM, Major G, Sakmann B. 1993. Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus. Journal of Physiology. 472, 615–663.","ieee":"P. M. Jonas, G. Major, and B. Sakmann, “Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus,” <i>Journal of Physiology</i>, vol. 472. Wiley-Blackwell, pp. 615–663, 1993.","chicago":"Jonas, Peter M, Guy Major, and Bert Sakmann. “Quantal Components of Unitary EPSCs at the Mossy Fibre Synapse on CA3 Pyramidal Cells of Rat Hippocampus.” <i>Journal of Physiology</i>. Wiley-Blackwell, 1993. <a href=\"https://doi.org/10.1113/jphysiol.1993.sp019965\">https://doi.org/10.1113/jphysiol.1993.sp019965</a>.","short":"P.M. Jonas, G. Major, B. Sakmann, Journal of Physiology 472 (1993) 615–663.","apa":"Jonas, P. M., Major, G., &#38; Sakmann, B. (1993). Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus. <i>Journal of Physiology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1113/jphysiol.1993.sp019965\">https://doi.org/10.1113/jphysiol.1993.sp019965</a>","ama":"Jonas PM, Major G, Sakmann B. Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus. <i>Journal of Physiology</i>. 1993;472:615-663. doi:<a href=\"https://doi.org/10.1113/jphysiol.1993.sp019965\">10.1113/jphysiol.1993.sp019965</a>"},"doi":"10.1113/jphysiol.1993.sp019965","abstract":[{"text":"1. Excitatory postsynaptic currents (EPSCs) were recorded in CA3 pyramidal cells of hippocampal slices of 15- to 24-day-old rats (22 degrees C) using the whole-cell configuration of the patch clamp technique. 2. Composite EPSCs were evoked by extracellular stimulation of the mossy fibre tract. Using the selective blockers 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D-2-amino-5-phosphonopentanoic acid (APV), a major alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor-mediated component and a minor NMDA receptor-mediated component with slower time course were distinguished. For the AMPA/kainate receptor-mediated component, the peak current-voltage (I-V) relation was linear, with a reversal potential close to 0 mV. The half-maximal blocking concentration of CNQX was 353 nM. 3. Unitary EPSCs of the mossy fibre terminal (MF)-CA3 pyramidal cell synapse were evoked at membrane potentials of -70 to -90 mV by low-intensity extracellular stimulation of granule cell somata using fine-tipped pipettes. The EPSC peak amplitude as a function of stimulus intensity showed all-or-none behaviour. The region of low threshold was restricted to a few micrometres. This suggests that extracellular stimulation was focal, and that the stimulus-evoked EPSCs were unitary. 4. Latency and rise time histograms of EPSCs evoked by granule cell stimulation showed narrow unimodal distributions within each experiment. The mean latency was 4.2 +/- 1.0 ms, and the mean 20-80% rise time was 0.6 +/- 0.1 ms (23 cells). When fitted within the range 0.7 ms to 20 ms after the peak, the decay of the EPSCs with the fastest rise (rise time 0.5 ms or less) could be described by a single exponential function; the mean time constant was in the range 3.0-6.6 ms with a mean of 4.8 ms (8 cells). 5. Peak amplitudes of the EPSCs evoked by suprathreshold granule cell stimulation fluctuated between trials. The apparent EPSC peak conductance in normal extracellular solution (2 mM Ca2+, 1 mM Mg2+), excluding failures, was 1 nS. Reducing the Ca2+ concentration and increasing the Mg2+ concentration reduced the mean peak amplitude in a concentration-dependent manner. 6. Peaks in EPSC peak amplitude distributions were apparent in low Ca2+ and high Mg2+. Using the criteria of equidistance and the presence of peaks and dips in the autocorrelation function, five of nine EPSC peak amplitude distributions were judged to be quantal.","lang":"eng"}],"oa":1,"external_id":{"pmid":["7908327"]},"page":"615 - 663","status":"public","title":"Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampus","volume":472,"day":"01","author":[{"full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Guy","last_name":"Major","full_name":"Major, Guy"},{"full_name":"Sakmann, Bert","last_name":"Sakmann","first_name":"Bert"}],"publication":"Journal of Physiology","article_processing_charge":"No","_id":"3474","type":"journal_article","date_created":"2018-12-11T12:03:31Z","oa_version":"Published Version","publist_id":"2913","date_updated":"2022-03-30T09:33:19Z","publisher":"Wiley-Blackwell","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_type":"original","month":"12","date_published":"1993-12-01T00:00:00Z","scopus_import":"1","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1160505"}]},{"intvolume":"       122","pmid":1,"year":"1993","publication_identifier":{"issn":["0021-9525"]},"language":[{"iso":"eng"}],"acknowledgement":"E. Castrtn is an Alexander von Humboldt fellow. M. Berzaghi is supported by a scholarship from CNPQ, Brasil. L. F. Parada, P. Tsoulfas, and L. Tesarollo were supported by a National Institutes of Health grant. We thank D. Stratmann and K. Angermeyer for skillful technical assistance; I. Hajjar for secretarial work and Dr. R. G~rtner for help with\r\ninducing hypothyroidism; Dr. W. Hunzieker for the calbindin-28 kD eDNA; Dr. M. Fishman for the GAP-43 eDNA; and Dr. Y.-A. Barde for critical comments.","quality_controlled":"1","citation":{"ista":"Lindholm D, Castrén E, Tsoulfas P, Kolbeck R, Berzaghi M, Leingärtner A, Heisenberg C-PJ, Tesarollo L, Parada L, Thoenen H. 1993. Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes Purkinje cell differentiation. Journal of Cell Biology. 122(2), 443–450.","ieee":"D. Lindholm <i>et al.</i>, “Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes Purkinje cell differentiation,” <i>Journal of Cell Biology</i>, vol. 122, no. 2. Rockefeller University Press, pp. 443–450, 1993.","mla":"Lindholm, Dan, et al. “Neurotrophin-3 Induced by Tri-Iodothyronine in Cerebellar Granule Cells Promotes Purkinje Cell Differentiation.” <i>Journal of Cell Biology</i>, vol. 122, no. 2, Rockefeller University Press, 1993, pp. 443–50, doi:<a href=\"https://doi.org/10.1083/jcb.122.2.443\">10.1083/jcb.122.2.443</a>.","apa":"Lindholm, D., Castrén, E., Tsoulfas, P., Kolbeck, R., Berzaghi, M., Leingärtner, A., … Thoenen, H. (1993). Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes Purkinje cell differentiation. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.122.2.443\">https://doi.org/10.1083/jcb.122.2.443</a>","chicago":"Lindholm, Dan, Eero Castrén, Pantelis Tsoulfas, Roland Kolbeck, Maria Berzaghi, Axel Leingärtner, Carl-Philipp J Heisenberg, Lino Tesarollo, Luis Parada, and Hans Thoenen. “Neurotrophin-3 Induced by Tri-Iodothyronine in Cerebellar Granule Cells Promotes Purkinje Cell Differentiation.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 1993. <a href=\"https://doi.org/10.1083/jcb.122.2.443\">https://doi.org/10.1083/jcb.122.2.443</a>.","short":"D. Lindholm, E. Castrén, P. Tsoulfas, R. Kolbeck, M. Berzaghi, A. Leingärtner, C.-P.J. Heisenberg, L. Tesarollo, L. Parada, H. Thoenen, Journal of Cell Biology 122 (1993) 443–450.","ama":"Lindholm D, Castrén E, Tsoulfas P, et al. Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes Purkinje cell differentiation. <i>Journal of Cell Biology</i>. 1993;122(2):443-450. doi:<a href=\"https://doi.org/10.1083/jcb.122.2.443\">10.1083/jcb.122.2.443</a>"},"doi":"10.1083/jcb.122.2.443","extern":"1","abstract":[{"lang":"eng","text":"Thyroid hormones play an important role in brain development, but the mechanism(s) by which triiodothyronine (T3) mediates neuronal differentiation is poorly understood. Here we demonstrate that T3 regulates the neurotrophic factor, neurotrophin-3 (NT-3), in developing rat cerebellar granule cells both in cell culture and in vivo. In situ hybridization experiments showed that developing Purkinje cells do not express NT-3 mRNA but do express trkC, the putative neuronal receptor for NT-3. Addition of recombinant NT-3 to cerebellar cultures from embryonic rat brain induces hypertrophy and neurite sprouting of Purkinje cells, and upregulates the mRNA encoding the calcium-binding protein, calbindin-28 kD. The present study demonstrates a novel interaction between cerebellar granule neurons and developing Purkinje cells in which NT-3 induced by T3 in the granule cells promotes Purkinje cell differentiation."}],"oa":1,"page":"443 - 450","external_id":{"pmid":["8320266"]},"volume":122,"title":"Neurotrophin-3 induced by tri-iodothyronine in cerebellar granule cells promotes Purkinje cell differentiation","status":"public","day":"15","author":[{"first_name":"Dan","last_name":"Lindholm","full_name":"Lindholm, Dan"},{"full_name":"Castrén, Eero","first_name":"Eero","last_name":"Castrén"},{"last_name":"Tsoulfas","first_name":"Pantelis","full_name":"Tsoulfas, Pantelis"},{"full_name":"Kolbeck, Roland","last_name":"Kolbeck","first_name":"Roland"},{"last_name":"Berzaghi","first_name":"Maria","full_name":"Berzaghi, Maria"},{"last_name":"Leingärtner","first_name":"Axel","full_name":"Leingärtner, Axel"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Tesarollo, Lino","first_name":"Lino","last_name":"Tesarollo"},{"first_name":"Luis","last_name":"Parada","full_name":"Parada, Luis"},{"full_name":"Thoenen, Hans","last_name":"Thoenen","first_name":"Hans"}],"oa_version":"None","date_created":"2018-12-11T12:07:25Z","publication":"Journal of Cell Biology","_id":"4177","issue":"2","type":"journal_article","article_processing_charge":"No","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","date_updated":"2022-03-24T12:59:20Z","publist_id":"1942","publisher":"Rockefeller University Press","article_type":"original","month":"07","date_published":"1993-07-15T00:00:00Z","scopus_import":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119654/","open_access":"1"}]},{"oa":1,"abstract":[{"text":"In a stably subdivided population with symmetric migration, the chance that a favoured allele will be fixed is independent of population structure. However, random extinction introduces an extra component of sampling drift, and reduces the probability of fixation. In this paper, the fixation probability is calculated using the diffusion approximation; comparison with exact solution of the discrete model shows this to be accurate. The key parameters are the rates of selection, migration and extinction, scaled relative to population size (S = 4Ns, M = 4Nm, Λ = 4Nλ); results apply to a haploid model, or to diploids with additive selection. If new colonies derive from many demes, the fixation probability cannot be reduced by more than half. However, if colonies are initially homogeneous, fixation probability can be much reduced. In the limit of low migration and extinction rates (M, Λ 1), it is 2s/{1 + (Λ/MS)(1 −exp(−S))}, whilst in the opposite limit (S  1), it is 4sM/{Λ(Λ + M)}. In the limit of weak selection (M, Λ  1), it is 4sM/{Λ(Λ + M)}. These factors are not the same as the reduction in effective population size (Ne/N), showing that the effects of population structure on selected alleles cannot be understood from the behaviour of neutral markers.","lang":"eng"}],"page":"149 - 158","intvolume":"        62","year":"1993","publication_identifier":{"issn":["0016-6723"]},"language":[{"iso":"eng"}],"acknowledgement":"This work was supported by grants from the SERC (GR/H/09928) and NERC (GR/3/8002), and by the Darwin Trust of Edinburgh. Thanks are due to B. Nürnberger for convincing me that population structure does reduce fixation probability, to M. Whitlock for discussions on calculations of effective population size, and to W. G. Hill, P. Keightley and the anonymous referees for their comments.","doi":"10.1017/S0016672300031748","citation":{"ieee":"N. H. Barton, “The probability of fixation of a favoured allele in a subdivided population,” <i>Genetics Research</i>, vol. 62, no. 2. Cambridge University Press, pp. 149–158, 1993.","ista":"Barton NH. 1993. The probability of fixation of a favoured allele in a subdivided population. Genetics Research. 62(2), 149–158.","mla":"Barton, Nicholas H. “The Probability of Fixation of a Favoured Allele in a Subdivided Population.” <i>Genetics Research</i>, vol. 62, no. 2, Cambridge University Press, 1993, pp. 149–58, doi:<a href=\"https://doi.org/10.1017/S0016672300031748\">10.1017/S0016672300031748</a>.","apa":"Barton, N. H. (1993). The probability of fixation of a favoured allele in a subdivided population. <i>Genetics Research</i>. Cambridge University Press. <a href=\"https://doi.org/10.1017/S0016672300031748\">https://doi.org/10.1017/S0016672300031748</a>","short":"N.H. Barton, Genetics Research 62 (1993) 149–158.","chicago":"Barton, Nicholas H. “The Probability of Fixation of a Favoured Allele in a Subdivided Population.” <i>Genetics Research</i>. Cambridge University Press, 1993. <a href=\"https://doi.org/10.1017/S0016672300031748\">https://doi.org/10.1017/S0016672300031748</a>.","ama":"Barton NH. The probability of fixation of a favoured allele in a subdivided population. <i>Genetics Research</i>. 1993;62(2):149-158. doi:<a href=\"https://doi.org/10.1017/S0016672300031748\">10.1017/S0016672300031748</a>"},"quality_controlled":"1","extern":"1","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","publisher":"Cambridge University Press","publist_id":"1762","date_updated":"2022-03-23T15:41:32Z","date_published":"1993-10-01T00:00:00Z","month":"10","article_type":"original","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://www.cambridge.org/core/journals/genetics-research/article/probability-of-fixation-of-a-favoured-allele-in-a-subdivided-population/3257B4AEC7044AFE40436C2DC15FBC4C#article"}],"title":"The probability of fixation of a favoured allele in a subdivided population","volume":62,"status":"public","day":"01","author":[{"orcid":"0000-0002-8548-5240","full_name":"Barton, Nicholas H","first_name":"Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","last_name":"Barton"}],"oa_version":"None","date_created":"2018-12-11T12:08:09Z","issue":"2","_id":"4303","type":"journal_article","article_processing_charge":"No","publication":"Genetics Research"},{"page":"35 - 77","oa":1,"abstract":[{"lang":"eng","text":"The theory of the natural numbers with linear order and monadic predicates underlies propositional linear temporal logic. To study temporal logics that are suitable for reasoning about real-time systems, we combine this classical theory of infinite state sequences with a theory of discrete time, via a monotonic function that maps every state to its time. The resulting theory of timed state sequences is shown to be decidable, albeit nonelementary, and its expressive power is characterized by ω-regular sets. Several more expressive variants are proved to be highly undecidable. This framework allows us to classify a wide variety of real-time logics according to their complexity and expressiveness. Indeed, it follows that most formalisms proposed in the literature cannot be decided. We are, however, able to identify two elementary real-time temporal logics as expressively complete fragments of the theory of timed state sequences, and we present tableau-based decision procedures for checking validity. Consequently, these two formalisms are well-suited for the specification and verification of real-time systems.\r\n\r\nCopyright © 1993 Academic Press. All rights reserved."}],"acknowledgement":"We thank David Dill, Zohar Manna, and Amir Pnueli for helpful discussion.","doi":"10.1006/inco.1993.1025","citation":{"ista":"Alur R, Henzinger TA. 1993. Real-time logics: Complexity and expressiveness. Information and Computation. 104(1), 35–77.","ieee":"R. Alur and T. A. Henzinger, “Real-time logics: Complexity and expressiveness,” <i>Information and Computation</i>, vol. 104, no. 1. Elsevier, pp. 35–77, 1993.","mla":"Alur, Rajeev, and Thomas A. Henzinger. “Real-Time Logics: Complexity and Expressiveness.” <i>Information and Computation</i>, vol. 104, no. 1, Elsevier, 1993, pp. 35–77, doi:<a href=\"https://doi.org/10.1006/inco.1993.1025\">10.1006/inco.1993.1025</a>.","apa":"Alur, R., &#38; Henzinger, T. A. (1993). Real-time logics: Complexity and expressiveness. <i>Information and Computation</i>. Elsevier. <a href=\"https://doi.org/10.1006/inco.1993.1025\">https://doi.org/10.1006/inco.1993.1025</a>","short":"R. Alur, T.A. Henzinger, Information and Computation 104 (1993) 35–77.","chicago":"Alur, Rajeev, and Thomas A Henzinger. “Real-Time Logics: Complexity and Expressiveness.” <i>Information and Computation</i>. Elsevier, 1993. <a href=\"https://doi.org/10.1006/inco.1993.1025\">https://doi.org/10.1006/inco.1993.1025</a>.","ama":"Alur R, Henzinger TA. Real-time logics: Complexity and expressiveness. <i>Information and Computation</i>. 1993;104(1):35-77. doi:<a href=\"https://doi.org/10.1006/inco.1993.1025\">10.1006/inco.1993.1025</a>"},"quality_controlled":"1","extern":"1","intvolume":"       104","year":"1993","publication_identifier":{"eissn":["0890-5401"]},"language":[{"iso":"eng"}],"scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://www.sciencedirect.com/science/article/pii/S0890540183710254?via%3Dihub"}],"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","publication_status":"published","publisher":"Elsevier","date_updated":"2022-03-23T13:08:27Z","publist_id":"116","date_published":"1993-05-01T00:00:00Z","month":"05","article_type":"original","author":[{"first_name":"Rajeev","last_name":"Alur","full_name":"Alur, Rajeev"},{"id":"40876CD8-F248-11E8-B48F-1D18A9856A87","first_name":"Thomas A","last_name":"Henzinger","full_name":"Henzinger, Thomas A","orcid":"0000−0002−2985−7724"}],"oa_version":"Published Version","date_created":"2018-12-11T12:09:38Z","type":"journal_article","_id":"4589","issue":"1","article_processing_charge":"No","publication":"Information and Computation","title":"Real-time logics: Complexity and expressiveness","volume":104,"status":"public","day":"01"},{"acknowledgement":"This work was supported in part by research grants from the Ministry of Education, Science and Culture of Japan, the Ministry of Health and Welfare, the Yamanouchi Foundation for Research on Metabolic Disorders, the Uehara Memorial Foundation, and the Inamori Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. \r\n\r\nWe are grateful to Akira Uesugi for photographic assistance.","extern":"1","quality_controlled":"1","citation":{"ama":"Nakajima Y, Iwakabe H, Akazawa C, et al. Molecular characterization of a novel retinal metabotropic glutamate receptor mGluR6 with a high agonist selectivity for L-2-amino-4- phosphonobutyrate. <i>Journal of Biological Chemistry</i>. 1993;268(16):11868-11873. doi:<a href=\"https://doi.org/10.1016/S0021-9258(19)50280-0\">10.1016/S0021-9258(19)50280-0</a>","apa":"Nakajima, Y., Iwakabe, H., Akazawa, C., Nawa, H., Shigemoto, R., Mizuno, N., &#38; Nakanishi, S. (1993). Molecular characterization of a novel retinal metabotropic glutamate receptor mGluR6 with a high agonist selectivity for L-2-amino-4- phosphonobutyrate. <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology. <a href=\"https://doi.org/10.1016/S0021-9258(19)50280-0\">https://doi.org/10.1016/S0021-9258(19)50280-0</a>","short":"Y. Nakajima, H. Iwakabe, C. Akazawa, H. Nawa, R. Shigemoto, N. Mizuno, S. Nakanishi, Journal of Biological Chemistry 268 (1993) 11868–11873.","chicago":"Nakajima, Yoshiaki, Hideki Iwakabe, Chihiro Akazawa, Hiroyuki Nawa, Ryuichi Shigemoto, Noboru Mizuno, and Shigetada Nakanishi. “Molecular Characterization of a Novel Retinal Metabotropic Glutamate Receptor MGluR6 with a High Agonist Selectivity for L-2-Amino-4- Phosphonobutyrate.” <i>Journal of Biological Chemistry</i>. American Society for Biochemistry and Molecular Biology, 1993. <a href=\"https://doi.org/10.1016/S0021-9258(19)50280-0\">https://doi.org/10.1016/S0021-9258(19)50280-0</a>.","ista":"Nakajima Y, Iwakabe H, Akazawa C, Nawa H, Shigemoto R, Mizuno N, Nakanishi S. 1993. Molecular characterization of a novel retinal metabotropic glutamate receptor mGluR6 with a high agonist selectivity for L-2-amino-4- phosphonobutyrate. Journal of Biological Chemistry. 268(16), 11868–11873.","ieee":"Y. Nakajima <i>et al.</i>, “Molecular characterization of a novel retinal metabotropic glutamate receptor mGluR6 with a high agonist selectivity for L-2-amino-4- phosphonobutyrate,” <i>Journal of Biological Chemistry</i>, vol. 268, no. 16. American Society for Biochemistry and Molecular Biology, pp. 11868–11873, 1993.","mla":"Nakajima, Yoshiaki, et al. “Molecular Characterization of a Novel Retinal Metabotropic Glutamate Receptor MGluR6 with a High Agonist Selectivity for L-2-Amino-4- Phosphonobutyrate.” <i>Journal of Biological Chemistry</i>, vol. 268, no. 16, American Society for Biochemistry and Molecular Biology, 1993, pp. 11868–73, doi:<a href=\"https://doi.org/10.1016/S0021-9258(19)50280-0\">10.1016/S0021-9258(19)50280-0</a>."},"doi":"10.1016/S0021-9258(19)50280-0","intvolume":"       268","pmid":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0021-9258"]},"year":"1993","external_id":{"pmid":["8389366"]},"page":"11868 - 11873","abstract":[{"lang":"eng","text":"A cDNA clone for a new metabotropic glutamate receptor, termed mGluR6, was isolated from a rat retinal cDNA library by cross-hybridization with the previously isolated cDNA clone for a metabotropic glutamate receptor. The cloned mGluR6 subtype consists of 871 amino acid residues and exhibits a structural architecture common to the metabotropic receptor family, possessing a large extracellular domain preceding the seven putative membrane-spanning domains. mGluR6 shows the highest sequence similarity to mGluR4 among the metabotropic receptor subtypes and inhibits the forskolin- stimulated cyclic AMP accumulation in Chinese hamster ovary cells transfected with the cloned cDNA. mGluR6 potently reacts with L-2-amino-4- phosphonobutyrate (L-AP4) and L-serine-O-phosphate, and the potencies of these compounds are one order of magnitude greater than that of L-glutamate. Blot and in situ hybridization analyses indicated that mGluR6 mRNA is restrictedly expressed in the inner nuclear layer of the retina where ON- bipolar cells are distributed. The metabotropic receptor that responds strongly to L-AP4 and L-serine-O-phosphate in ON-bipolar cells is known to mediate glutamate synaptic transmission between photoreceptor cells and ON- bipolar cells. On the basis of the agonist selectivity of mGluR6 and its specific expression in retinal cells, the physiological role of this receptor subtype in the visual system is discussed."}],"oa":1,"author":[{"first_name":"Yoshiaki","last_name":"Nakajima","full_name":"Nakajima, Yoshiaki"},{"full_name":"Iwakabe, Hideki","last_name":"Iwakabe","first_name":"Hideki"},{"full_name":"Akazawa, Chihiro","last_name":"Akazawa","first_name":"Chihiro"},{"full_name":"Nawa, Hiroyuki","last_name":"Nawa","first_name":"Hiroyuki"},{"last_name":"Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444"},{"first_name":"Noboru","last_name":"Mizuno","full_name":"Mizuno, Noboru"},{"last_name":"Nakanishi","first_name":"Shigetada","full_name":"Nakanishi, Shigetada"}],"publication":"Journal of Biological Chemistry","_id":"2536","issue":"16","type":"journal_article","article_processing_charge":"No","date_created":"2018-12-11T11:58:15Z","oa_version":"Published Version","status":"public","volume":268,"title":"Molecular characterization of a novel retinal metabotropic glutamate receptor mGluR6 with a high agonist selectivity for L-2-amino-4- phosphonobutyrate","day":"05","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/S0021-9258(19)50280-0"}],"publist_id":"4362","date_updated":"2022-04-26T06:56:15Z","publisher":"American Society for Biochemistry and Molecular Biology","publication_status":"published","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_type":"original","month":"06","date_published":"1993-06-05T00:00:00Z"},{"author":[{"last_name":"Tanabe","first_name":"Yasuto","full_name":"Tanabe, Yasuto"},{"last_name":"Nomura","first_name":"Akinori","full_name":"Nomura, Akinori"},{"full_name":"Masu, Masayuki","last_name":"Masu","first_name":"Masayuki"},{"orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Noboru","last_name":"Mizuno","full_name":"Mizuno, Noboru"},{"full_name":"Nakanishi, Shigetada","last_name":"Nakanishi","first_name":"Shigetada"}],"publication":"Journal of Neuroscience","_id":"2537","issue":"4","article_processing_charge":"No","type":"journal_article","oa_version":"Published Version","date_created":"2018-12-11T11:58:15Z","status":"public","title":"Signal transduction, pharmacological properties, and expression patterns of two rat metabotropic glutamate receptors, mGluR3 and mGluR4","volume":13,"day":"01","scopus_import":"1","main_file_link":[{"url":"https://pubmed.ncbi.nlm.nih.gov/8463825/","open_access":"1"}],"publist_id":"4361","date_updated":"2022-03-31T14:49:42Z","publisher":"Society for Neuroscience","publication_status":"published","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_type":"original","month":"04","date_published":"1993-04-01T00:00:00Z","acknowledgement":"We are grateful to Mr. Akira Uesugi for photographic assistance. This work was  supported in part by research grants from the Ministry of Education, Science and Culture of Japan, the Ministry of Health and Welfare of Japan, the Uehara Memorial Foundation, and the Semi Life Science Foundation. ","extern":"1","quality_controlled":"1","citation":{"short":"Y. Tanabe, A. Nomura, M. Masu, R. Shigemoto, N. Mizuno, S. Nakanishi, Journal of Neuroscience 13 (1993) 1372–1378.","chicago":"Tanabe, Yasuto, Akinori Nomura, Masayuki Masu, Ryuichi Shigemoto, Noboru Mizuno, and Shigetada Nakanishi. “Signal Transduction, Pharmacological Properties, and Expression Patterns of Two Rat Metabotropic Glutamate Receptors, MGluR3 and MGluR4.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 1993. <a href=\"https://doi.org/10.1523/JNEUROSCI.13-04-01372.1993\">https://doi.org/10.1523/JNEUROSCI.13-04-01372.1993</a>.","apa":"Tanabe, Y., Nomura, A., Masu, M., Shigemoto, R., Mizuno, N., &#38; Nakanishi, S. (1993). Signal transduction, pharmacological properties, and expression patterns of two rat metabotropic glutamate receptors, mGluR3 and mGluR4. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.13-04-01372.1993\">https://doi.org/10.1523/JNEUROSCI.13-04-01372.1993</a>","mla":"Tanabe, Yasuto, et al. “Signal Transduction, Pharmacological Properties, and Expression Patterns of Two Rat Metabotropic Glutamate Receptors, MGluR3 and MGluR4.” <i>Journal of Neuroscience</i>, vol. 13, no. 4, Society for Neuroscience, 1993, pp. 1372–78, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.13-04-01372.1993\">10.1523/JNEUROSCI.13-04-01372.1993</a>.","ieee":"Y. Tanabe, A. Nomura, M. Masu, R. Shigemoto, N. Mizuno, and S. Nakanishi, “Signal transduction, pharmacological properties, and expression patterns of two rat metabotropic glutamate receptors, mGluR3 and mGluR4,” <i>Journal of Neuroscience</i>, vol. 13, no. 4. Society for Neuroscience, pp. 1372–1378, 1993.","ista":"Tanabe Y, Nomura A, Masu M, Shigemoto R, Mizuno N, Nakanishi S. 1993. Signal transduction, pharmacological properties, and expression patterns of two rat metabotropic glutamate receptors, mGluR3 and mGluR4. Journal of Neuroscience. 13(4), 1372–1378.","ama":"Tanabe Y, Nomura A, Masu M, Shigemoto R, Mizuno N, Nakanishi S. Signal transduction, pharmacological properties, and expression patterns of two rat metabotropic glutamate receptors, mGluR3 and mGluR4. <i>Journal of Neuroscience</i>. 1993;13(4):1372-1378. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.13-04-01372.1993\">10.1523/JNEUROSCI.13-04-01372.1993</a>"},"doi":"10.1523/JNEUROSCI.13-04-01372.1993","intvolume":"        13","pmid":1,"publication_identifier":{"issn":["0270-6474"]},"language":[{"iso":"eng"}],"year":"1993","external_id":{"pmid":["8463825"]},"page":"1372 - 1378","abstract":[{"lang":"eng","text":"The metabotropic glutamate receptors are coupled to intracellular signal transduction via G-proteins and consist of a family of at least five different subtypes, termed mGluR1-mGluR5. We studied the signal transduction mechanism and pharmacological characteristics of the rat mGluR3 and mGluR4 subtypes in Chinese hamster ovary cells permanently expressing the cloned receptors. Both mGluR3 and mGluR4 inhibit the forskolin-stimulated accumulation of intracellular cAMP formation in response to agonist interaction. Consistent with the high degree of sequence similarity to mGluR2, mGluR3 closely resembles mGluR2 in its agonist selectivity; the potency rank order of agonists is L-glutamate &gt; trans-1-aminocyclopentane- 1,3-dicarboxylate &gt; ibotenate &gt; quisqualate. mGluR4 is totally different in its agonist specificity from any other member of the metabotropic receptors. This receptor potently reacts with L-2-amino-4-phosphonobutyrate(L-AP4) in a stereo-selective manner and moderately responds to L-serine-O-phosphate. mGluR4 thus corresponds well to the putative L-AP4 receptor characterized from brain preparations. Blot and in situ hybridization analyses indicated that both mRNAs are widely distributed in the rat brain. mGluR3 mRNA is highly expressed in neuronal cells of the cerebral cortex and the caudate- putamen, and in granule cells of the hippocampal dentate gyrus. The expression pattern of mGluR4 mRNA is more restricted, and this expression is prominent in the cerebellum, olfactory bulb, and thalamus. Furthermore, the mGluR3 mRNA, unlike the other mRNAs for the metabotropic receptors, is highly expressed in glial cells throughout the brain regions. The metabotropic glutamate receptor subtypes can thus be classified into three subgroups according to the similarity in their amino acid sequences, signal transduction, and agonist selectivity: mGluR1/mGluR5, mGluR2/mGluR3, and mGluR4. The mRNAs for the individual receptor subtypes, however, show overlapping but distinct patterns of expression in the rat CNS."}],"oa":1}]