Somatostatin and CCK-8 modulate release of striatal amino acids: Role of dopamine receptors

Abstract

The effects of somatostatin (SOM) and cholecystokinin octapeptide (CCK-8) on basal and potassium-evoked release of neurotransmitter amino acids were investigated in slices of rat caudate nucleus (CN) and, for comparison, cerebral cortex (CX). Endogenous aspartate (Asp), glutamate (Glu), glycine (Gly), and gamma-aminobutyric acid (GABA) were measured by high performance liquid chromatography. In both CN and CX, potassium (5–55 mM) produced a concentration-dependent increase in the release of Asp, Glu, Gly, and GABA in the presence of extracellular Ca 2+. CCK-8 (1 μM) stimulated in CN the basal and K +-evoked release of Gly to 231% and 160% of control, respectively; this effect was blocked by sulpiride (SULP), a dopamine receptor antagonist. In contrast, SOM (1 μM) inhibited the K +-evoked release of Glu in CN by 26%, an effect that was not blocked by SULP. SOM and CCK-8 did not significantly affect the basal or K + (35 mM)-evoked release of other amino acids in the CN or of any amino acids in CX. The results indicate that: (a) CCK-8 facilitation of Gly release is dependent on dopamine receptor activation, whereas the inhibition by SOM of Glu release is not; and (b) the effects of SOM and CCK-8 are specific with respect to the brain region affected.