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

187 Citations (Scopus)


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
Issue number3
Publication statusPublished - 2001
Externally publishedYes


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