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GABA Transporters GAT-1 and GAT-3 in the Human Dorsolateral Prefrontal Cortex in Schizophrenia
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This study aimed to investigate the binding affinity of [<sup>3</sup>H]GABA and [<sup>3</sup>H]β-alanine to GABA transporters GAT-1 and GAT-3 in the human dorsolateral prefrontal cortex (Brodmanns’ area 9) in schizophrenia. Using post mortem tissue from individuals diagnosed with schizophrenia (n = 6) and control subjects (n = 6), the density of GAT-1 was established by displacing [<sup>3</sup>H]GABA with muscimol, and for GAT-3 [<sup>3</sup>H]β-alanine was used. Data analysis showed a significant decrease of GAT-1 levels (45%), and a significant increase of GAT-3 density (23%) within the dorsolateral prefrontal cortex of individuals diagnosed with schizophrenia when compared to age- and sex-matched controls. The observed decrease of GAT-1 could be explained as a consequence of the GABA hypo-function or the result of volumetric shrinkage of the cerebral cortex previously reported in this disease. The observed elevation of GAT-3 levels could be due to a compensatory effect for any functional loss of GABA re-uptake by the decreased GAT-1 levels.
Title: GABA Transporters GAT-1 and GAT-3 in the Human Dorsolateral Prefrontal Cortex in Schizophrenia
Description:
This study aimed to investigate the binding affinity of [<sup>3</sup>H]GABA and [<sup>3</sup>H]β-alanine to GABA transporters GAT-1 and GAT-3 in the human dorsolateral prefrontal cortex (Brodmanns’ area 9) in schizophrenia.
Using post mortem tissue from individuals diagnosed with schizophrenia (n = 6) and control subjects (n = 6), the density of GAT-1 was established by displacing [<sup>3</sup>H]GABA with muscimol, and for GAT-3 [<sup>3</sup>H]β-alanine was used.
Data analysis showed a significant decrease of GAT-1 levels (45%), and a significant increase of GAT-3 density (23%) within the dorsolateral prefrontal cortex of individuals diagnosed with schizophrenia when compared to age- and sex-matched controls.
The observed decrease of GAT-1 could be explained as a consequence of the GABA hypo-function or the result of volumetric shrinkage of the cerebral cortex previously reported in this disease.
The observed elevation of GAT-3 levels could be due to a compensatory effect for any functional loss of GABA re-uptake by the decreased GAT-1 levels.
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