@article{9955,
  abstract     = {Neurons can change their classical neurotransmitters during ontogeny, sometimes going through stages of dual release. Here, we explored the development of the neurotransmitter identity of neurons of the avian nucleus isthmi parvocellularis (Ipc), whose axon terminals are retinotopically arranged in the optic tectum (TeO) and exert a focal gating effect upon the ascending transmission of retinal inputs. Although cholinergic and glutamatergic markers are both found in Ipc neurons and terminals of adult pigeons and chicks, the mRNA expression of the vesicular acetylcholine transporter, VAChT, is weak or absent. To explore how the Ipc neurotransmitter identity is established during ontogeny, we analyzed the expression of mRNAs coding for cholinergic (ChAT, VAChT, and CHT) and glutamatergic (VGluT2 and VGluT3) markers in chick embryos at different developmental stages. We found that between E12 and E18, Ipc neurons expressed all cholinergic mRNAs and also VGluT2 mRNA; however, from E16 through posthatch stages, VAChT mRNA expression was specifically diminished. Our ex vivo deposits of tracer crystals and intracellular filling experiments revealed that Ipc axons exhibit a mature paintbrush morphology late in development, experiencing marked morphological transformations during the period of presumptive dual vesicular transmitter release. Additionally, although ChAT protein immunoassays increasingly label the growing Ipc axon, this labeling was consistently restricted to sparse portions of the terminal branches. Combined, these results suggest that the synthesis of glutamate and acetylcholine, and their vesicular release, is complexly linked to the developmental processes of branching, growing and remodeling of these unique axons.},
  author       = {Reyes‐Pinto, Rosana and Ferrán, José L. and Vega Zuniga, Tomas A and González‐Cabrera, Cristian and Luksch, Harald and Mpodozis, Jorge and Puelles, Luis and Marín, Gonzalo J.},
  issn         = {1096-9861},
  journal      = {Journal of Comparative Neurology},
  number       = {2},
  pages        = {553--573},
  publisher    = {Wiley},
  title        = {{Change in the neurochemical signature and morphological development of the parvocellular isthmic projection to the avian tectum}},
  doi          = {10.1002/cne.25229},
  volume       = {530},
  year         = {2022},
}

@article{7148,
  abstract     = {In the cerebellum, GluD2 is exclusively expressed in Purkinje cells, where it regulates synapse formation and regeneration, synaptic plasticity, and motor learning. Delayed cognitive development in humans with GluD2 gene mutations suggests extracerebellar functions of GluD2. However, extracerebellar expression of GluD2 and its relationship with that of GluD1 are poorly understood. GluD2 mRNA and protein were widely detected, with relatively high levels observed in the olfactory glomerular layer, medial prefrontal cortex, cingulate cortex, retrosplenial granular cortex, olfactory tubercle, subiculum, striatum, lateral septum, anterodorsal thalamic nucleus, and arcuate hypothalamic nucleus. These regions were also enriched for GluD1, and many individual neurons coexpressed the two GluDs. In the retrosplenial granular cortex, GluD1 and GluD2 were selectively expressed at PSD‐95‐expressing glutamatergic synapses, and their coexpression on the same synapses was shown by SDS‐digested freeze‐fracture replica labeling. Biochemically, GluD1 and GluD2 formed coimmunoprecipitable complex formation in HEK293T cells and in the cerebral cortex and hippocampus. We further estimated the relative protein amount by quantitative immunoblotting using GluA2/GluD2 and GluA2/GluD1 chimeric proteins as standards for titration of GluD1 and GluD2 antibodies. Intriguingly, the relative amount of GluD2 was almost comparable to that of GluD1 in the postsynaptic density fraction prepared from the cerebral cortex and hippocampus. In contrast, GluD2 was overwhelmingly predominant in the cerebellum. Thus, we have determined the relative extracerebellar expression of GluD1 and GluD2 at regional, neuronal, and synaptic levels. These data provide a molecular–anatomical basis for possible competitive and cooperative interactions of GluD family members at synapses in various brain regions.},
  author       = {Nakamoto, Chihiro and Konno, Kohtarou and Miyazaki, Taisuke and Nakatsukasa, Ena and Natsume, Rie and Abe, Manabu and Kawamura, Meiko and Fukazawa, Yugo and Shigemoto, Ryuichi and Yamasaki, Miwako and Sakimura, Kenji and Watanabe, Masahiko},
  issn         = {1096-9861},
  journal      = {Journal of Comparative Neurology},
  number       = {6},
  pages        = {1003--1027},
  publisher    = {Wiley},
  title        = {{Expression mapping, quantification, and complex formation of GluD1 and GluD2 glutamate receptors in adult mouse brain}},
  doi          = {10.1002/cne.24792},
  volume       = {528},
  year         = {2020},
}