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Dual Modulation of Dopamine Release from Anterior Nucleus Accumbens Through Cholecystokinin‐B Receptor Subsites
Author(s) -
Léna Isabelle,
Roques Bernard P.,
Durieux Christiane
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68010162.x
Subject(s) - nucleus accumbens , cholecystokinin , chemistry , cholecystokinin b receptor , agonist , dopamine , antagonist , stimulation , cholecystokinin receptor , tetrodotoxin , endocrinology , receptor , medicine , biophysics , biochemistry , biology
Previous binding studies have suggested the existence of two affinity states for cholecystokinin‐B (CCK‐B) receptor. One study, using BC 197 and BC 264, two highly selective CCK‐B agonists, has shown that BC 197 is selective for one subsite, B 1 , and that BC 264 has the same affinity for the two subsites, B 1 and B 2 . Therefore, the possible involvement of CCK‐B subsites in the modulation of endogenous dopamine (DA) release from slices of the anterior part of the nucleus accumbens was investigated with these two agonists in order to associate a functional response with activation of each subsite. The selective B 1 agonist BC 197 produced a dose‐dependent increase of 35 m M K + ‐stimulated DA release. In contrast, at a low concentration (20 n M ), BC 264 inhibited the K + ‐evoked DA release, whereas at a higher concentration (1 µ M ), it stimulated the DA release. These two opposing effects were suppressed by the CCK‐B antagonist PD‐134,308, but not by the CCK‐A antagonist L‐364,718 and were not prevented by tetrodotoxin, a Na + ‐channel blocker. Moreover, BC 264 at 20 n M , in the presence of PD‐134,308 at a concentration that would block the B 2 subsites (0.1 n M ), increased the evoked DA release. All together, these results support further the existence of distinct CCK‐B subsites and suggest that, in the anterior nucleus accumbens, their stimulation mediates opposite effects on K + ‐stimulated DA release via a presynaptic mechanism.