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

Anthony J. Hannan, Colin Blakemore, Alla Katsnelson, Tania Vitalis, Kimberly M. Huber, Mark Bear, John Roder, Daesoo Kim, Hee Sup Shin, Peter C. Kind

Research output: Contribution to journalArticle

171 Scopus citations

Abstract

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-β1 (PLC-β1) by metabotropic glutamate receptors (mGluRs). Homozygous null mutation of either PLC-β1 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-β1-/- mice during barrel development. Our data indicate that PLC-β1 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.

Original languageEnglish (US)
Pages (from-to)282-288
Number of pages7
JournalNature neuroscience
Volume4
Issue number3
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Neuroscience(all)

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