PLC-β1, activated via mGluRs, mediates activity-dependent differentiation in cerebral cortex

被引：175

作者：

Hannan, AJ

Blakemore, C

Katsnelson, A

Vitalis, T

Huber, KM

Bear, M

Roder, J

Kim, D

Shin, HS

Kind, PC

机构：

[1] Univ Oxford, Physiol Lab, Oxford OX1 3PT, England

[2] Univ Edinburgh, Dept Biomed Sci, Edinburgh EH8 9XD, Midlothian, Scotland

[3] Brown Univ, Dept Neurosci, Providence, RI 02912 USA

[4] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada

[5] Pohang Univ Sci & Technol, Dept Life Sci, Natl CRI Ctr Calcium & Learning, Pohang 790784, South Korea

来源：

NATURE NEUROSCIENCE | 2001年 / 4卷 / 03期

基金：

英国医学研究理事会; 英国惠康基金;

关键词：

D O I：

10.1038/85132

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

During development of the cerebral cortex, the invasion of thalamic axons and subsequent differentiation of cortical neurons are tightly coordinated. Here we provide evidence that glutamate neurotransmission triggers a critical signaling mechanism involving the activation of phospholipase C-beta1 (PLC-beta1) by metabotropic glutamate receptors (mGluRs). Homozygous null mutation of either PLC-beta1 or mGluR5 dramatically disrupts the cytoarchitectural differentiation of 'barrels' in the mouse somatosensory cortex, despite segregation in the pattern of thalamic innervation. Furthermore, group 1 mGluR-stimulated phosphoinositide hydrolysis is dramatically reduced in PLC-beta1(-/-) mice during barrel development. Our data indicate that PLC-beta1 activation via mGluR5 is critical for the coordinated development of the neocortex, and that presynaptic and postsynaptic components of cortical differentiation can be genetically dissociated.

引用

页码：282 / 288

页数：7