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Effect of BCH 325 (Pro-D-Phe-Pro-Gly) on Central Dopaminergic Functions

, : Effect of BCH 325 (Pro-D-Phe-Pro-Gly) on Central Dopaminergic Functions. Peptides (Tarrytown) 16(4): 635-640

Three behavioral models were used to characterize the pharmacological action of BCH 325 on central dopaminergic transmission. The effect of acute SC treatment with BCH 325 upon dopaminergic mechanisms affecting motor activity was studied on the climbing behavior of mice. It was shown that the beta-casomorphin analogue evoked a dose-dependent increase in apomorphine (APO)-induced hypoactivity that was reversed by sulpiride (SULP). In in vitro studies on slices of nucleus accumbens of mice it could be demonstrated that 10-6 M APO caused a reduction of K+-stimulated (14C)dopamine (DA) release that was potentiated following simultaneous incubation with 10-6 M BCH 325. To prove a postsynaptic influence in D-1 receptor-mediated behavior pattern, the action of BCH 325 was studied on bromocriptine (BROMO)-evoked yawning behavior of rats after pretreatment with reserpine (RES) or saline. The peptide could not influence the BROMO yawning after saline administration, but it was able to normalize the number of yawns, which were reduced after RES. To investigate the effect of BCH 325 on postsynaptic D-2 receptors, jerking behavior on RES-pretreated rats after a high dose of BROMO was used. Following RES pretreatment only, the number of BROMO-induced jerks was decreased by treatment of rats with 0.5 mu-mol/kg BCH 325. In contrast, the jerking behavior was enhanced by 0.5 mu-mol/kg BCH 325 in rats that were additionally treated with alpha-methyl-p-tyrosine (MPT). In biochemical studies on slices of the nucleus accumbens of mice, the in vivo pretreatment with RES caused a reduction of K+-stimulated (14C)DA release that was blocked by the SC administration of 0.5 mu-mol/kg BCH 325. The results indicate that BCH 325 was not able to influence the action of DA agonists on postsynaptic localized D-1 receptors. BCH 325 potentiated the pharmacological action of dopaminergic agonists on presynaptic DA autoreceptors and on D-2 receptors on the postsynaptic site of dopaminergic transmission by an alteration of the efficacy of D-2 receptor-coupled processes. The tetrapeptide normalizes the reduced K+-stimulated DA release after RES pretreatment.


PMID: 7479296

DOI: 10.1016/0196-9781(95)00015-c

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