Abstract
Here we have explored whether dopamine is able to modulate the release of gamma-aminobutyric acid (GABA) from striatal terminals to substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and caudate-putamen. The type of dopamine receptors involved was assessed by the blocking effect of either SCH 23390 (D1 antagonist) or (-)-sulpiride (D2 antagonist) of the dopamine effect. Dopamine stimulated (EC50 3.2 microM) the depolarization-induced release of [3H]GABA from slices isolated from all of the above mentioned nuclei. SCH 23390 dose-dependently blocked the dopamine stimulation, but (-)-sulpiride did not show any blocking effect. The results suggest that dopamine via D1 receptors modulates the release of GABA from striatal GABAergic terminals.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Basal Ganglia / drug effects
-
Basal Ganglia / physiology*
-
Benzazepines / pharmacology
-
Caudate Nucleus / drug effects
-
Caudate Nucleus / physiology
-
Corpus Striatum / drug effects
-
Corpus Striatum / physiology
-
Dopamine / pharmacology*
-
Globus Pallidus / drug effects
-
Globus Pallidus / physiology
-
Hydroxydopamines
-
In Vitro Techniques
-
Male
-
Oxidopamine
-
Putamen / drug effects
-
Putamen / physiology
-
Rats
-
Rats, Inbred Strains
-
Receptors, Dopamine / drug effects
-
Receptors, Dopamine / physiology*
-
Receptors, Dopamine D1
-
Substantia Nigra / drug effects
-
Substantia Nigra / physiology*
-
Sulpiride / pharmacology
-
gamma-Aminobutyric Acid / metabolism*
Substances
-
Benzazepines
-
Hydroxydopamines
-
Receptors, Dopamine
-
Receptors, Dopamine D1
-
gamma-Aminobutyric Acid
-
Sulpiride
-
Oxidopamine
-
Dopamine