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Altered Cortical Glutamate Neurotransmission in Schizophrenia
Author(s) -
LEWIS DAVID A.,
GLANTZ LEISA A.,
PIERRI JOSEPH N.,
SWEET ROBERT A.
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1300.007
Subject(s) - neuroscience , glutamatergic , neurotransmission , glutamate receptor , dorsolateral prefrontal cortex , pyramidal cell , dendritic spine , prefrontal cortex , schizophrenia (object oriented programming) , axon , neuron , excitatory postsynaptic potential , biology , psychology , hippocampus , hippocampal formation , inhibitory postsynaptic potential , psychiatry , receptor , biochemistry , cognition
A bstract : Multiple lines of evidence from pharmacological, neuroimaging, and postmortem studies implicate disturbances in cortical glutamate neurotransmission in the pathophysiology of schizophrenia. Given that pyramidal neurons are the principal source of cortical glutamate neurotransmission, as well as the targets of the majority of cortical glutamate‐containing axon terminals, understanding the nature of altered glutamate neurotransmission in schizophrenia requires an appreciation of both the types of pyramidal cell abnormalities and the specific class(es) of pyramidal cells that are affected in the illness. In this chapter, we review evidence indicating that a subpopulation of pyramidal neurons in the dorsolateral prefrontal cortex exhibits reductions in dendritic spine density, a marker of the number of excitatory inputs, and in somal volume, a measure correlated with a neuron's dendritic and axonal architecture. Specifically, pyramidal neurons located in deep layer 3 of the dorsolateral prefrontal cortex and that lack immunoreactivity for nonphosphorylated neurofilament protein may be particularly involved in the pathophysiology of schizophrenia. The presence of similar changes in pyramidal neurons located in deep layer 3 of auditory association cortex suggests that a shared property, which remains to be determined, confers cell type‐specific vulnerability to a subpopulation of cortical glutamatergic neurons in schizophrenia.