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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >CCKA, but not CCKB, agonists suppress the hyperlocomotion induced by endogenous enkephalins, protected from enzymatic degradation by systemic RB 101.
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CCKA, but not CCKB, agonists suppress the hyperlocomotion induced by endogenous enkephalins, protected from enzymatic degradation by systemic RB 101.

机译：CCKA而非CCKB激动剂可抑制内源性脑啡肽诱导的过度运动，并受到全身性RB 101的酶促降解保护。

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摘要

Interactions between CCKergic and enkephalinergic systems were studied in mice using behavioral responses measured in Animex. The hyperlocomotion induced by 5 mg/kg of RB 101, a mixed inhibitor of enkephalin-degrading enzymes able to cross the blood-brain barrier, was previously shown to be mediated by delta-opioid receptor stimulation. The IP administration of a CCKA agonist, Boc-Tyr-Lys-(CONH-o-tolyl)-Asp-Phe-NH2 (0.1, 1, 10 micrograms/kg), suppressed the hyperlocomotion produced by IV injection of 5 mg/kg of RB 101. The effect of the CCKA agonist was suppressed by a selective CCKA antagonist, devazepide, injected IP at doses of 20 and 200 micrograms/kg and was potentiated by the selective delta-opioid antagonist naltrindole at the doses of 0.03 mg/kg. IP injection of the selective CCKB agonist BC 264 (0.1-1 mg/kg) did not modify the RB 101-induced hyperlocomotor effect. These results reinforce the observed physiological antagonism between the endogenous CCK and opioid systems but are at variance with the responses measured in stressful conditions. It is concluded that CCKA, but not CCKB, receptor activation counteracts the opioid-related hyperlocomotion.
机译：使用Animex中测量的行为反应，在小鼠中研究了CCK能系统和脑啡能系统之间的相互作用。先前显示，由5 mg / kg的RB 101（一种能穿过血脑屏障的脑啡肽降解酶的混合抑制剂）引起的运动过度，是由δ阿片受体刺激介导的。腹腔注射CCKA激动剂Boc-Tyr-Lys-（CONH-o-甲苯基）-Asp-Phe-NH2（0.1，1，10微克/ kg），抑制了静脉注射5 mg / kg产生的运动过度RB 101的作用。CCKA激动剂的作用被选择性CCKA拮抗剂devazepide抑制，以20和200微克/ kg的剂量注射IP，并被0.03 mg / kg的选择性δ-阿片样物质拮抗剂naltrindole增强。 。腹膜内注射选择性CCKB激动剂BC 264（0.1-1 mg / kg）不会改变RB 101诱导的运动过度效应。这些结果加强了内源性CCK与阿片类药物系统之间的生理拮抗作用，但与在压力条件下测得的反应不一致。结论是CCKA而不是CCKB受体激活抵消了与阿片样物质相关的过度运动。

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