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Normal formation of the postsynaptic elements of GABAergic synapses in the reeler cerebellum

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/17164

Title: Normal formation of the postsynaptic elements of GABAergic synapses in the reeler cerebellum
Authors: Takayama, Chitoshi Browse this author →KAKEN DB
Inoue, Yoshiro Browse this author →KAKEN DB
Keywords: GABAA receptor
Glutamic acid decarboxylase
Purkinje cell
Synaptic glomerulus
Neuronal maturation
Issue Date: 12-Nov-2003
Publisher: Elsevier B.V.
Journal Title: Developmental Brain Research
Volume: 145
Issue: 2
Start Page: 197
End Page: 211
Publisher DOI: 10.1016/j.devbrainres.2003.08.003
PMID: 14604760
Abstract: Synaptic transmission mediated by γ-amino butyric acid (GABA) plays an important role in inhibition of glutamatergic excitatory transmission and expression of higher brain functions, such as memory, learning and anxiety. To elucidate mechanisms underlying formation of the postsynaptic elements for GABAergic transmission, we employed the reeler mutant mice in this study. In the reeler cerebellum, abnormal cytoarchitecture and an aberrant environment affect the formation of neural networks and maturation of neurons. We examined the expression and localization of GABAA receptor α subunits in the reeler cerebellum and determined whether various abnormalities in the reeler mice affected formation of the postsynaptic elements. In situ hybridization analysis revealed that the specific expression of α subunit mRNAs in each neuronal type was preserved. Abnormal expression of α subunits was not detected, although GABAergic networks were altered and neuronal maturation was severely disturbed. Immunohistochemistry for the α1 and α6 subunits, which were expressed abundantly in the reeler cerebellum, revealed that both subunit proteins accumulated at positions adjacent to GABAergic terminals. These results, taken together, suggested that expression of the GABAA receptor subunits in postsynaptic neurons might be genetically determined, but trafficking and accumulation of the subunit proteins at the GABAergic synapse may be induced by GABAergic innervation.
Type: article (author version)
URI: http://hdl.handle.net/2115/17164
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 高山 千利

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