Somatostatin and cholecystokinin octapeptide differentially modulate the release of [3H]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 microM), CCK-8 (1 microM) and the dopamine (DA) receptor agonist, apomorphine (APO, 30 microM) 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 microM), 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.
Arnerić
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D000109:Acetylcholine / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002421:Caudate Nucleus / Q000187:drug effects / Q000378:metabolism*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D012844:Sincalide / Q000494:pharmacology*; D013004:Somatostatin / Q000494:pharmacology*; D013997:Time Factors
D011954:Receptors, Dopamine; D013004:Somatostatin; D012844:Sincalide; D001058:Apomorphine; D000109:Acetylcholine; D011188:Potassium