Roles of prefrontal cortical GABAergic interneurons in psychosis and cognitive deficits in schizophrenia
© Tanaka; licensee BioMed Central Ltd. 2008
Published: 11 July 2008
Analysis of postmortem brains of patients with schizophrenia from the Stanley Foundation brain collection have shown consistent reduction of reelin, parvalbumin and GAD67, the 67-kilodalton isoform of glutamic acid decarboxylase, in the prefrontal cortex (PFC) and other brain regions . In the PFC, this suggests a decrease in GABAergic inhibition that might be responsible for psychosis. Cognitive deficits are also a core symptom of schizophrenia, which might also be caused by GABAergic dysregulation.
A summary of the variations of the parameter values of the two different types of GABAergic inhibition used in the simulation. The figures in the parentheses indicate the relative strength of the inhibitory action on the pyramidal neurons in the model PFC circuit.
other GABA neurons
Both chandelier neurons and other GABAergic neurons play critical roles in shaping the dopaminergic modulation profile of PFC activity. Chandelier neurons would suppress hyperactivity with hyper-dopaminergic neurotransmission, which is associated with psychotic states. Other GABAergic neurons regulate the inverted-U shaped profile with moderate levels of dopaminergic neurotransmission, which is important for normal cognitive functions.
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