首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Antagonism by CPP (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, of beta-phenylethylamine (PEA)-induced hypermotility in mice of different strains.
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Antagonism by CPP (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, of beta-phenylethylamine (PEA)-induced hypermotility in mice of different strains.

机译:CPP(+/-)-3-(2-羧基哌嗪-4-基)-丙基-1-膦酸对不同品系小鼠的β-苯乙胺(PEA)诱导的过度运动的拮抗作用。

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摘要

In male C57BL/6, BALB/c, and SHR (bred from Swiss) mice, pretreatment with (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), a competitive antagonist of N-methyl-D-aspartate (NMDA) receptor, attenuated the hyperlocomotion induced by beta-phenylethylamine (PEA). This effect of CPP was blocked by intracerebroventricularly (ICV) administered NMDA (0.2 nM). CPP did not alter the hyperlocomotion induced by d-amphetamine. PEA rarely inhibited spontaneous motor activity in those strains. Two other competitive antagonists of NMDA, 2-amino-5-phosphonopentanoic acid (AP-5) and 2-amino-7-phosphonoheptanoic acid (AP-7), ICV at doses of 0.01-0.1 microgram, were ineffective. The noncompetitive antagonists of NMDA, dizocilpine (MK-801) and phencyclidine, at subthreshold doses of 0.1-0.5 mg/kg, potentiated the stimulant effect of PEA. In earlier studies we also observed antagonism between CPP and PEA in NIH-Swiss mice, a strain in which PEA inhibits locomotion. Relationships between the stimulant and the anxiogenic effects of PEA are discussed.
机译:在雄性C57BL / 6,BALB / c和SHR(从瑞士繁殖)小鼠中,用(+/-)-3-(2-羧基哌嗪-4-基)-丙基-1-膦酸(CPP)进行预处理N-甲基-D-天冬氨酸(NMDA)受体的竞争性拮抗剂,减弱了由β-苯乙胺(PEA)引起的运动过度。 CPP的这种作用被脑室内(ICV)施用的NMDA(0.2 nM)阻断。 CPP不会改变d-苯异丙胺所引起的运动过度。 PEA在这些菌株中很少抑制自发运动活动。 NMDA的另外两种竞争性拮抗剂,ICV,剂量为0.01-0.1微克的2-氨基-5-膦基戊酸(AP-5)和2-氨基-7-膦基庚酸(AP-7)无效。亚阈值剂量为0.1-0.5 mg / kg的NMDA,地佐西平(MK-801)和苯环利定的非竞争性拮抗剂增强了PEA的刺激作用。在较早的研究中,我们还观察到NIH-Swiss小鼠中CPP与PEA之间的拮抗作用,其中PEA抑制了运动。讨论了兴奋剂与PEA的抗焦虑作用之间的关系。

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