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Vol. 285, Issue 1, 350-357, April 1998
-Aminobutyric Acid
Levels in the Prefrontal Cortex of the Rat1
Departments of Pharmacology and Psychiatry, Yale University School
of Medicine, New Haven, Connecticut and Psychiatry Service, Department
of Veterans Affairs Medical Center, West Haven, Connecticut
Dopaminergic axons in the prefrontal cortex synapse with interneurons
as well as pyramidal cells. Electrophysiological data suggest that
dopamine depolarizes certain 
-aminobutyric acid (GABA)-containing
interneurons in the cortex. We investigated the dopaminergic regulation
of extracellular GABA levels in the prefrontal cortex using in
vivo microdialysis. Systemic administration of the mixed
D1/D2 dopamine receptor agonist apomorphine
increased extracellular GABA levels in the prefrontal cortex, but did
not increase levels of glycine; the apomorphine-elicited increase in
GABA levels was blocked by tetrodotoxin infusion into the prefrontal cortex. Local administration of the D2 agonist quinpirole
into the cortex via the dialysis probe resulted in a
dose-dependent increase in extracellular GABA levels. In contrast,
administration of the D1 agonist SKF 38393 did not alter
GABA levels. The ability of systemic apomorphine to increase
extracellular GABA levels in the prefrontal cortex was blocked by local
administration of the D2-like antagonist sulpiride to the
cortex, but was not attenuated significantly by local perfusion of the
D1 antagonist SCH 23390. Similarly, the ability of local
infusion of the D2 agonist quinpirole to enhance
extracellular GABA levels was blocked by sulpiride but not by SCH
23390. These data suggest that dopamine agonists increase the release
of GABA in the prefrontal cortex through a D2-like
receptor. In view of posited changes in prefrontal cortical dopamine
and GABA systems in schizophrenia, it is possible that changes in
GABAergic function in the cortex in schizophrenia are secondary to
changes in cortical dopamine function.
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