Several lines of evidence indicate that anesthetic doses of the non-competitive N-methyl-D-aspartate receptor antagonist ketamine disrupt memory functions in rodents. The mechanism by which anesthetic ketamine produces its adverse behavioural effects is not yet clarified. The implication of nicotinic acetylcholine receptor as a potential site of action of anesthetic ketamine adverse effects on memory is proposed. We investigated the ability of α4β2 nicotinic receptor agonist ABT-418 (0.01, 0.03, 0.1 mg/kg, i.p.) and α7 nicotinic receptor agonist GTS-21 (0.3, 1, 3 mg/kg, i.p.) to counteract recognition memory deficits produced by acute post-training administration of anesthetic ketamine (100 mg/kg, i.p.) in rats. For this purpose, the novel object recognition test, a behavioural paradigm assessing recognition memory abilities in rodents was used. Post-training acute administration of GTS-21 (3 mg/kg) counteracted anesthetic ketamine-induced performance deficits in the novel object recognition memory task. By contrast, ABT-418 failed to reverse the recognition memory deficits caused by anesthetic ketamine. The present findings propose that an α7 nicotinic receptor component might modulate anesthetic ketamine’s adverse effects on recognition memory.

一些证据表明，非竞争性N-甲基-D-天冬氨酸受体拮抗剂氯胺酮的麻醉剂量会破坏啮齿动物的记忆功能。麻醉剂氯胺酮产生不良行为影响的机制尚不清楚。提出了烟碱型乙酰胆碱受体作为麻醉剂氯胺酮对记忆的不利影响的潜在作用部位的含义。我们研究了α4β2烟碱受体激动剂 ABT-418 (0.01, 0.03, 0.1 mg/kg, ip) 和α7 的能力烟碱样受体激动剂 GTS-21 (0.3, 1, 3 mg/kg, ip) 可抵消大鼠训练后急性注射麻醉剂氯胺酮 (100 mg/kg, ip) 产生的识别记忆缺陷。为此，使用了新的物体识别测试，这是一种评估啮齿动物识别记忆能力的行为范式。GTS-21 (3 mg/kg) 的训练后急性给药抵消了麻醉剂氯胺酮引起的新型物体识别记忆任务中的性能缺陷。相比之下，ABT-418 未能逆转麻醉氯胺酮引起的识别记忆缺陷。目前的研究结果表明，α7烟碱受体成分可能会调节麻醉剂氯胺酮对识别记忆的不利影响。