@article{14843,
  abstract     = {The coupling between Ca2+ channels and release sensors is a key factor defining the signaling properties of a synapse. However, the coupling nanotopography at many synapses remains unknown, and it is unclear how it changes during development. To address these questions, we examined coupling at the cerebellar inhibitory basket cell (BC)-Purkinje cell (PC) synapse. Biophysical analysis of transmission by paired recording and intracellular pipette perfusion revealed that the effects of exogenous Ca2+ chelators decreased during development, despite constant reliance of release on P/Q-type Ca2+ channels. Structural analysis by freeze-fracture replica labeling (FRL) and transmission electron microscopy (EM) indicated that presynaptic P/Q-type Ca2+ channels formed nanoclusters throughout development, whereas docked vesicles were only clustered at later developmental stages. Modeling suggested a developmental transformation from a more random to a more clustered coupling nanotopography. Thus, presynaptic signaling developmentally approaches a point-to-point configuration, optimizing speed, reliability, and energy efficiency of synaptic transmission.},
  author       = {Chen, JingJing and Kaufmann, Walter and Chen, Chong and Arai, Itaru and Kim, Olena and Shigemoto, Ryuichi and Jonas, Peter M},
  issn         = {1097-4199},
  journal      = {Neuron},
  publisher    = {Elsevier},
  title        = {{Developmental transformation of Ca2+ channel-vesicle nanotopography at a central GABAergic synapse}},
  doi          = {10.1016/j.neuron.2023.12.002},
  year         = {2024},
}

@article{12542,
  abstract     = {In this issue of Neuron, Espinosa-Medina et al.1 present the TEMPO (Temporal Encoding and Manipulation in a Predefined Order) system, which enables the marking and genetic manipulation of sequentially generated cell lineages in vertebrate species in vivo.},
  author       = {Villalba Requena, Ana and Hippenmeyer, Simon},
  issn         = {1097-4199},
  journal      = {Neuron},
  number       = {3},
  pages        = {291--293},
  publisher    = {Elsevier},
  title        = {{Going back in time with TEMPO}},
  doi          = {10.1016/j.neuron.2023.01.006},
  volume       = {111},
  year         = {2023},
}

@article{10753,
  abstract     = {This is a comment on "Meta-learning synaptic plasticity and memory addressing for continual familiarity detection." Neuron. 2022 Feb 2;110(3):544-557.e8.},
  author       = {Confavreux, Basile J and Vogels, Tim P},
  issn         = {1097-4199},
  journal      = {Neuron},
  number       = {3},
  pages        = {361--362},
  publisher    = {Elsevier},
  title        = {{A familiar thought: Machines that replace us?}},
  doi          = {10.1016/j.neuron.2022.01.014},
  volume       = {110},
  year         = {2022},
}

@article{8544,
  abstract     = {The synaptotrophic hypothesis posits that synapse formation stabilizes dendritic branches, yet this hypothesis has not been causally tested in vivo in the mammalian brain. Presynaptic ligand cerebellin-1 (Cbln1) and postsynaptic receptor GluD2 mediate synaptogenesis between granule cells and Purkinje cells in the molecular layer of the cerebellar cortex. Here we show that sparse but not global knockout of GluD2 causes under-elaboration of Purkinje cell dendrites in the deep molecular layer and overelaboration in the superficial molecular layer. Developmental, overexpression, structure-function, and genetic epistasis analyses indicate that dendrite morphogenesis defects result from competitive synaptogenesis in a Cbln1/GluD2-dependent manner. A generative model of dendritic growth based on competitive synaptogenesis largely recapitulates GluD2 sparse and global knockout phenotypes. Our results support the synaptotrophic hypothesis at initial stages of dendrite development, suggest a second mode in which cumulative synapse formation inhibits further dendrite growth, and highlight the importance of competition in dendrite morphogenesis.},
  author       = {Takeo, Yukari H. and Shuster, S. Andrew and Jiang, Linnie and Hu, Miley and Luginbuhl, David J. and Rülicke, Thomas and Contreras, Ximena and Hippenmeyer, Simon and Wagner, Mark J. and Ganguli, Surya and Luo, Liqun},
  issn         = {1097-4199},
  journal      = {Neuron},
  number       = {4},
  pages        = {P629--644.E8},
  publisher    = {Elsevier},
  title        = {{GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells}},
  doi          = {10.1016/j.neuron.2020.11.028},
  volume       = {109},
  year         = {2021},
}

@article{9793,
  abstract     = {Astrocytes extensively infiltrate the neuropil to regulate critical aspects of synaptic development and function. This process is regulated by transcellular interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes coordinate developmental processes among one another to parse out the synaptic neuropil and form non-overlapping territories is unknown. Here we identify a molecular mechanism regulating astrocyte-astrocyte interactions during development to coordinate astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked, astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for territory and morphological complexity in the developing mouse cortex. Furthermore, conditional deletion of Hepacam from developing astrocytes significantly impairs gap junction coupling between astrocytes and disrupts the balance between synaptic excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy with subcortical cysts in humans. Therefore, our findings suggest that disruption of astrocyte self-organization mechanisms could be an underlying cause of neural pathology.},
  author       = {Baldwin, Katherine T. and Tan, Christabel X. and Strader, Samuel T. and Jiang, Changyu and Savage, Justin T. and Elorza-Vidal, Xabier and Contreras, Ximena and Rülicke, Thomas and Hippenmeyer, Simon and Estévez, Raúl and Ji, Ru-Rong and Eroglu, Cagla},
  issn         = {1097-4199},
  journal      = {Neuron},
  number       = {15},
  pages        = {2427--2442.e10},
  publisher    = {Elsevier},
  title        = {{HepaCAM controls astrocyte self-organization and coupling}},
  doi          = {10.1016/j.neuron.2021.05.025},
  volume       = {109},
  year         = {2021},
}

@article{6454,
  abstract     = {Adult neural stem cells and multiciliated ependymalcells are glial cells essential for neurological func-tions. Together, they make up the adult neurogenicniche. Using both high-throughput clonal analysisand single-cell resolution of progenitor division pat-terns and fate, we show that these two componentsof the neurogenic niche are lineally related: adult neu-ral stem cells are sister cells to ependymal cells,whereas most ependymal cells arise from the termi-nal symmetric divisions of the lineage. Unexpectedly,we found that the antagonist regulators of DNA repli-cation, GemC1 and Geminin, can tune the proportionof neural stem cells and ependymal cells. Our find-ings reveal the controlled dynamic of the neurogenicniche ontogeny and identify the Geminin familymembers as key regulators of the initial pool of adultneural stem cells.},
  author       = {Ortiz-Álvarez, G and Daclin, M and Shihavuddin, A and Lansade, P and Fortoul, A and Faucourt, M and Clavreul, S and Lalioti, ME and Taraviras, S and Hippenmeyer, Simon and Livet, J and Meunier, A and Genovesio, A and Spassky, N},
  issn         = {1097-4199},
  journal      = {Neuron},
  number       = {1},
  pages        = {159--172.e7},
  publisher    = {Elsevier},
  title        = {{Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members}},
  doi          = {10.1016/j.neuron.2019.01.051},
  volume       = {102},
  year         = {2019},
}