GABA Neuron Alterations, Cortical Circuit Dysfunction and Cognitive Deficits in Schizophrenia
Year: 2011
Type: article
Abstract: Schizophrenia is a brain disorder associated with cognitive deficits that severely affect the patients' capacity for daily functioning. Whereas our understanding of its pathophysiology is limited, postmortem studies suggest that schizophrenia is associated with deficits of GABA-mediated synaptic transmission. A major role of GABA-mediated transmission may be producing synchronized network oscillations which are currently hypothesized to be essential for normal cognitive function. Therefore, cognitive deficits in schizophrenia may result from a GABA synapse dysfunction that disturbs neural synchrony. Here, we highlight recent studies further suggesting alterations of GABA transmission and network oscillations in schizophrenia. We also review current models for the mechanisms of GABA-mediated synchronization of neural activity, focusing on parvalbumin-positive GABA neurons, which are altered in schizophrenia and whose function has been strongly linked to the production of neural synchrony. Alterations of GABA signaling that impair gamma oscillations and, as a result, cognitive function suggest paths for novel therapeutic interventions.
Source: Neural Plasticity
DOI: 10.1155/2011/723184
Institution: University of Pittsburgh
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,830
Awards: G1023197008, G1301299755, Differential Terminal Expression of GAD67/GAD65 ? Relevance to Schizophrenia, G1516920479, G2369869669, G2467451836, Chandelier cell inputs to pyramidal neurons in schizophrenia and development, G4510370855, Schizophrenia and synaptic pruning: Circuit specificity and functional consequences, G817915945, G9000055903, G9000094857, G9000218885
OpenAlex ID: W1978104463