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Receptor selectivity of cholecystokinin effects on mesoaccumbens dopamine neurons
Author(s) -
Kelland Mark D.,
Zhang Jing,
Chiodo Louis A.,
Freeman Arthur S.
Publication year - 1991
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890080207
Subject(s) - quinpirole , chemistry , cholecystokinin , cholecystokinin receptor , agonist , proglumide , medicine , endocrinology , cholecystokinin b receptor , receptor antagonist , antagonist , receptor , dopamine , biology , biochemistry
Extracellular recording techniques were combined with antidromic stimulation to examine the effects of C‐terminal cholecystokinin (CCK) fragments and CCK antagonists on the activity of identified mesoaccumbens dopamine (MADA) neurons in chloral hydrate‐anesthetized rats. These experiments were designed to determine the receptor selectivity of sulfated CCK octapeptide (CCK‐8S) effects on MADA cells. Neither CCK tetrapeptide (CCK‐4) nor unsulfated CCK octapeptide (CCK‐8U) significantly altered MADA cell basal firing rate or responsiveness to the inhibitory effects of the D2 DA agonist quinpirole. As reported previously for ventral tegmental area DA cells, CCK‐8S produced increases or decreases in the firing rate of most MADA cells sampled. CCK‐8S also enhanced the sensitivity of MADA neurons to quinpirole‐induced inhibition. This increase in sensitivity to quinpirole was blocked by pretreatment with the nonselective CCK receptor antagonist proglumide and the preferential CCK‐A receptor antagonist CR 1409 but not by the preferential CCK‐B receptor antagonist L‐365, 260. The inactivity of CCK‐4 and CCK‐8U in these tests and the results with the antagonists suggest that the effects of CCK‐8S on MADA neuronal activity are mediated by CCK‐A receptors.