Protocadherin 17 Regulates Presynaptic Assembly in Topographic Corticobasal Ganglia Circuits

被引：63

作者：

Hoshina, Naosuke ^{[1
,9
]}

Tanimura, Asami ^{[3
]}

Yamasaki, Miwako ^{[4
]}

Inoue, Takeshi ^{[1
]}

Fukabori, Ryoji ^{[5
]}

Kuroda, Teiko ^{[6
]}

Yokoyama, Kazumasa ^{[1
]}

Tezuka, Tohru ^{[1
]}

Sagara, Hiroshi ^{[2
]}

Hirano, Shinji ^{[7
]}

Kiyonari, Hiroshi ^{[8
]}

Takada, Masahiko ^{[6
]}

Kobayashi, Kazuto ^{[5
]}

Watanabe, Masahiko ^{[4
]}

Kano, Masanobu ^{[3
]}

Nakazawa, Takanobu ^{[1
,3
]}

Yamamoto, Tadashi ^{[1
,9
]}

机构：

[1] Univ Tokyo, Inst Med Sci, Div Oncol, Tokyo 1088639, Japan

[2] Univ Tokyo, Inst Med Sci, Med Prote Lab, Tokyo 1088639, Japan

[3] Univ Tokyo, Grad Sch Med, Dept Neurophysiol, Tokyo 1130033, Japan

[4] Hokkaido Univ, Grad Sch Med, Dept Anat, Sapporo, Hokkaido 0608638, Japan

[5] Fukushima Med Univ, Sch Med, Inst Biomed Sci, Dept Mol Genet, Fukushima 9601295, Japan

[6] Kyoto Univ, Primate Res Inst, Syst Neurosci Sect, Inuyama, Aichi 4848506, Japan

[7] Kochi Med Sch, Dept Neurobiol & Anat, Nankoku, Kochi 7838505, Japan

[8] RIKEN, Ctr Dev Biol, Lab Anim Resources & Genet Engn, Kobe, Hyogo 6500047, Japan

[9] Okinawa Inst Sci & Technol, Cell Signal Unit, Onna Son 9040495, Japan

来源：

NEURON | 2013年 / 78卷 / 05期

关键词：

BASAL GANGLIA; ANATOMICAL EVIDENCE; TYROSINE PHOSPHORYLATION; MOLECULAR-MECHANISMS; OL-PROTOCADHERIN; N-CADHERIN; RECEPTOR; SPINE; MOUSE; LOCALIZATION;

D O I：

10.1016/j.neuron.2013.03.031

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Highly topographic organization of neural circuits exists for the regulation of various brain functions in corticobasal ganglia circuits. Although neural circuit-specific refinement during synapse development is essential for the execution of particular neural functions, the molecular and cellular mechanisms for synapse refinement are largely unknown. Here, we show that protocadherin 17 (PCDH17), one of the nonclustered delta 2-protocadherin family members, is enriched along corticobasal ganglia synapses in a zone-specific manner during synaptogenesis and regulates presynaptic assembly in these synapses. PCDH17 deficiency in mice causes facilitated presynaptic vesicle accumulation and enhanced synaptic transmission efficacy in corticobasal ganglia circuits. Furthermore, PCDH17(-/-) mice exhibit antidepressant-like phenotypes that are known to be regulated by corticobasal ganglia circuits. Our findings demonstrate a critical role for PCDH17 in the synaptic development of specific corticobasal ganglia circuits and suggest the involvement of PCDH17 in such circuits in depressive behaviors.

引用

页码：839 / 854

页数：16

共 58 条

[1] FUNCTIONAL ARCHITECTURE OF BASAL GANGLIA CIRCUITS - NEURAL SUBSTRATES OF PARALLEL PROCESSING [J].