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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*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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
Pages (from-to)282-288
Number of pages7
JournalNature Neuroscience
Volume4
Issue number3
DOIs
Publication statusPublished - 2001
Externally publishedYes

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