Kameyama T, Ukai M, Miura M
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Meijo University, Nagoya, Japan.
Neuropharmacology. 1994 Oct;33(10):1167-9. doi: 10.1016/s0028-3908(05)80006-1.
The present study examined the effects of intracerebroventricular injection of dynorphin A-(1-13) on memory processes by using the passive avoidance task in mice. Galanin (0.3 microgram) significantly shortened the step-down latency when given 15 min before retention tests. Although dynorphin A-(1-13) (1 or 3 micrograms) did not prolong the step-down latency induced by weaker electroshocks, it inhibited the galanin (0.3 micrograms)-induced shortening of step-down latency. The effects of dynorphin A-(1-13) (3 micrograms) on the galanin-induced shortening of step-down latency were almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms), a kappa-selective opioid antagonist. These results strongly suggest that dynorphin A-(1-13) attenuates galanin-induced impairment of memory processes through the mediation of kappa-opioid receptors.
本研究通过在小鼠中使用被动回避任务，检测了脑室内注射强啡肽A-(1-13)对记忆过程的影响。甘丙肽（0.3微克）在记忆测试前15分钟给予时，显著缩短了跳台潜伏期。尽管强啡肽A-(1-13)（1或3微克）并未延长较弱电击诱导的跳台潜伏期，但它抑制了甘丙肽（0.3微克）诱导的跳台潜伏期缩短。强啡肽A-(1-13)（3微克）对甘丙肽诱导的跳台潜伏期缩短的作用几乎被κ-选择性阿片受体拮抗剂 nor-纳曲酮（4微克）预处理完全逆转。这些结果强烈表明，强啡肽A-(1-13)通过κ-阿片受体的介导减轻了甘丙肽诱导的记忆过程损伤。
