Understanding the neurotransmitter pathology of schizophrenia: selective deficits of subtypes of cortical GABAergic neurons.
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 hypothesizing that they may contribute to a further degenerative process in schizophrenia.
Department of Biomedical Science, University of Sheffield, Sheffield, United Kingdom. g.p.reynolds@sheffield.ac.uk
G P
GP
Reynolds
C L
CL
Beasley
Z J
ZJ
Zhang
D001714:Bipolar Disorder / Q000378:metabolism; D064032:Calbindin 2; D064026:Calbindins; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D003863:Depression / Q000378:metabolism; D006801:Humans; D009474:Neurons / Q000145:classification / Q000378:metabolism / Q000473:pathology; D018377:Neurotransmitter Agents / Q000378:metabolism*; D010320:Parvalbumins / Q000378:metabolism; D012016:Reference Values; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D012559:Schizophrenia / Q000378:metabolism* / Q000473:pathology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D064032:Calbindin 2; D064026:Calbindins; D018377:Neurotransmitter Agents; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; D005680:gamma-Aminobutyric Acid