Liang K C
Department of Psychology, National Taiwan University, Taipei, ROC.
Eur J Neurosci. 1999 May;11(5):1491-500. doi: 10.1046/j.1460-9568.1999.00561.x.
The present study investigated the effect of buspirone on memory formation in an aversive learning task. Male Wistar rats were trained on the inhibitory avoidance task and tested for retention 1 day after training. They received peripheral or intra-amygdala administration of buspirone or other 5-HT1A drugs either before or after training. Results indicated that pretraining systemic injections of buspirone caused a dose-dependent retention deficit; 5. 0 mg/kg had a marked effect and 1.0 mg/kg had no effect. Post-training injections of the drug caused a time-dependent retention deficit, which was not due to a state-dependent effect on retrieval. When training in the inhibitory avoidance task was divided into a context-training phase and a shock-training phase, buspirone impaired retention only when administered in the shock-training phase, suggesting that the drug influenced memory processing of affective events. Further results indicated that post-training intra-amygdala infusion of buspirone or the 5-HT1A agonist 8-hydroxy-di-n-propylaminotetralin (8-OH-DPAT) caused a time-dependent and dose-dependent retention deficit. Post-training intra-amygdala infusion of the 5-HT1A antagonist WAY100635 (N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)-N-(2-pyridyl) cyclohexane carboxamine maleate) attenuated the memory-impairing effects of buspirone. These findings suggest that buspirone may modulate memory storage processes in the inhibitory avoidance task through an action on amygdaloid 5-HT1A receptors.
本研究调查了丁螺环酮在厌恶学习任务中对记忆形成的影响。雄性Wistar大鼠接受抑制性回避任务训练,并在训练后1天进行记忆保持测试。在训练前或训练后,它们接受丁螺环酮或其他5-HT1A药物的外周给药或杏仁核内给药。结果表明,训练前全身注射丁螺环酮会导致剂量依赖性的记忆保持缺陷;5.0mg/kg有显著作用,1.0mg/kg无作用。训练后注射该药物会导致时间依赖性的记忆保持缺陷,这并非由于对记忆提取的状态依赖性作用。当将抑制性回避任务的训练分为情境训练阶段和电击训练阶段时,丁螺环酮仅在电击训练阶段给药时会损害记忆保持,这表明该药物影响了情感事件的记忆处理。进一步的结果表明,训练后杏仁核内注入丁螺环酮或5-HT1A激动剂8-羟基-二正丙基氨基四氢萘(8-OH-DPAT)会导致时间依赖性和剂量依赖性的记忆保持缺陷。训练后杏仁核内注入5-HT1A拮抗剂WAY100635(N-(2-(4-(2-甲氧基苯基)-1-哌嗪基)-N-(2-吡啶基)环己烷羧酰胺马来酸盐)可减弱丁螺环酮的记忆损害作用。这些发现表明,丁螺环酮可能通过作用于杏仁核5-HT1A受体来调节抑制性回避任务中的记忆存储过程。