Somatostatin and cholecystokinin octapeptide differentially modulate the release of [H]acetylcholine from caudate nucleus but not cerebral cortex: Role of dopamine receptor activation

The effects of somatostatin (SOM) and cholecystokinin octapeptide (CCK-8) on basal and potassium-induced release of acetylcholine (ACh) were investigated in slices of rat caudate nucleus (CN) and, for comparison, cerebral cortex (CX). Potassium (5–55 mM) produced a concentration-dependent increase in the release of [³H]ACh in the presence of extracellular Ca²⁺. SOM (1 μ), CCK-8 (1 μM) and the dopamine (DA) receptor agonist, apomorphine (APO, 30 μM) inhibited the K⁺-induced (35 mM) release of [³H]ACh by 26–32% from CN, but did not affect ACh release from CX. Other peptides (1 μM), such as Met-enkephalin, vasoactive intestinal peptide, thyrotropin-releasing hormone and substance P, had no effect on release of [³H]ACh in CN or CX. Sulpiride (SULP), a dopamine receptor antagonist, prevented the effects of APO and SOM, but not CCK-8, to inhibit [³H]ACh release. The results indicate that: (1) SOM and CCK-8 inhibit the release of [³H]ACh in CN, but not CX; and (2) the inhibitory effect of SOM, but not CCK-8, on [³H]ACh release is mediated by dopaminergic mechanisms.