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Cerebral Cortex Advance Access originally published online on August 5, 2004
Cerebral Cortex 2005 15(4):385-393; doi:10.1093/cercor/bhh141
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Cerebral Cortex V 15 N 4 © Oxford University Press 2004; all rights reserved

Activity-dependent Regulation of Synapse and Dendritic Spine Morphology in Developing Barrel Cortex Requires Phospholipase C-ß1 Signalling

Tara L. Spires1,2, Zoltán Molnár3, Peter C. Kind4, Patricia M. Cordery1, A. Louise Upton1, Colin Blakemore1 and Anthony J. Hannan1,5

1 University Laboratory of Physiology, University of Oxford, Parks Road, Oxford, UK, 3 Department of Human Anatomy and Genetics, University of Oxford, South Parks Road, Oxford, UK and 4 Biomedical Sciences, Edinburgh University, Hugh Robson Building, George Square, Edinburgh, UK, 2 Present address: MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Department of Neurology, Charlestown, MA, USA, 5 Present address: Howard Florey Institute, University of Melbourne, Melbourne, Australia

Address correspondence to Tara Spires, Massachusetts General Hospital, Department of Neurology, Alzheimer's Disease Research Laboratory, 114 16th Street, Room 2021, Charlestown, MA 02129, USA. Email: tara.spires{at}physiol.ox.ac.uk.

The phospholipase C-ß1 (PLC-ß1) signalling pathway, activated via metabotropic glutamate receptors (mGluRs), is implicated in activity-dependent development of the cerebral cortex, as both PLC-ß1 and mGluR5 knockout mice exhibit disrupted barrel formation in somatosensory cortex. To characterize the effects of this signalling system on development of synaptic circuitry in barrel cortex, we have examined neuronal ultrastructure, synapse formation and dendritic spine morphology in PLC-ß1 knockout mice. Qualitative ultrastructure of neurons and synapse density in layers 2–4 of barrel cortex were unchanged in PLC-ß1 knockout mice during development [postnatal day (P) 5] and in mature cortex (P19–21). We found a decrease in the proportion of synapses with symmetric morphology at P5 that was gone by P19–21, indicating a transient imbalance in excitatory and inhibitory circuitry. We also investigated dendritic spines by back-labelling layer 5 pyramidal neurons with carbocyanine. We observed normal dendritic spine densities on apical dendrites as they passed through layer 4 of barrel cortex, but spine morphology was altered in PLC-ß1 knockout mice at P9. These observations indicate that the PLC-ß1 signalling pathway plays a role in the development of normal cortical circuitry. Interrupting this regulation leads to changes in synapse and dendritic spine morphology, possibly altering post-synaptic integration of signal.

Key Words: cortical development • mGluR5 • PLC-ß1 • stereology • synapse morphology • synaptogenesis


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