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NMDA-receptor hypofunction versus excessive synaptic elimination as models of schizophrenia

Published online by Cambridge University Press:  03 September 2003

Ralph E. Hoffman  and
Thomas H. McGlashan
Ralph E. Hoffman
Affiliation:
ralph.hoffman@yale.eduthomas.mcglashan@yale.edu
Thomas H. McGlashan
Affiliation:
ralph.hoffman@yale.eduthomas.mcglashan@yale.edu
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Abstract

We propose that the primary cause of schizophrenia is a pathological extension of synaptic pruning involving local connectivity that unfolds ordinarily during adolescence. Computer simulations suggest that this pathology provides reasonable accounts of a range of symptoms in schizophrenia, and is consistent with recent postmortem and genetic studies. NMDA-receptors play a regulatory role in maintaining and/or eliminating cortical synapses, and therefore may play a pathophysiological role.

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Article Commentary
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Behavioral and Brain Sciences , Volume 26 , Issue 1 , February 2003 , pp. 92
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Copyright © Cambridge University Press 2003

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