Biala Grazyna, Kruk Marta
Chair and Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, 4 Staszica Street, 20-081 Lublin, Poland.
Behav Brain Res. 2008 Oct 10;192(2):198-202. doi: 10.1016/j.bbr.2008.04.004. Epub 2008 Apr 16.
The purpose of the experiments was to examine the memory-related effects of nicotine using the mouse elevated plus maze. It has been shown that the acute doses of nicotine (0.1 and 0.5 mg/kg) significantly decreased the time of transfer latency (TL2) on the retention trial, indicating that nicotine improved memory processes. Similarly, acute doses of the CB1 cannabinoid receptor antagonist AM 251 (0.5, 1, 1.5 and 3 mg/kg) significantly decreased TL2 values. WIN55,212-2, a non-selective CB cannabinoid receptor agonist, at any dose tested (0.25, 0.5 and 1 mg/kg), did not provoke any effect in this model. Moreover, the acute injection of both WIN55,212-2 (0.25 and 0.5 mg/kg) and AM 251 (0.25 mg/kg), prior to injections of nicotine (0.1 and 0.5 mg/kg), significantly prevented nicotine-induced memory improvement. The results of this study provide clear evidence that the endogenous cannabinoid system participates in the responses induced by nicotine on memory-related behaviour in mice.
这些实验的目的是利用小鼠高架十字迷宫来检测尼古丁对记忆的相关影响。研究表明，尼古丁的急性剂量（0.1和0.5毫克/千克）在记忆保持试验中显著缩短了转移潜伏期（TL2）的时间，这表明尼古丁改善了记忆过程。同样，CB1大麻素受体拮抗剂AM 251的急性剂量（0.5、1、1.5和3毫克/千克）也显著降低了TL2值。非选择性CB大麻素受体激动剂WIN55,212-2在任何测试剂量（0.25、0.5和1毫克/千克）下，在该模型中均未产生任何影响。此外，在注射尼古丁（0.1和0.5毫克/千克）之前，急性注射WIN55,212-2（0.25和0.5毫克/千克）和AM 251（0.25毫克/千克）均能显著阻止尼古丁诱导的记忆改善。这项研究的结果提供了明确的证据，表明内源性大麻素系统参与了尼古丁对小鼠记忆相关行为诱导的反应。
