Journal
JOURNAL OF NEURAL TRANSMISSION
Volume 109, Issue 5-6, Pages 881-889Publisher
SPRINGER-VERLAG WIEN
DOI: 10.1007/s007020200072
Keywords
schizophrenia; GABA; calcium binding proteins; cerebral cortex; human brain
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Research aimed at understanding the neurotransmitter pathology of schizophrenia has been underway for half a century, with much emphasis on the dopamine system. Although this approach has advanced our understanding of treatment mechanisms, identification of primary dopaminergic abnormalities in the disease has been elusive. The increasing emphasis on a neuronal pathology of schizophrenia has led to the identification of abnormalities in GABAergic and glutamatergic systems; and we have identified selective deficits in GABAergic interneurons containing the calcium binding proteins parvalbumin and calbindin. Here we report further evidence for a loss of parvalbumin-immunoreactive neurons in both dorsolateral prefrontal and medial temporal cortex, indicating that these deficits are consistent with a subtle neurodevelopmental pathogenesis and hypothesising that they may contribute to a further degenerative process in schizophrenia.
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