Naylor J C, Simson P E, Gibson B, Schneider A M, Wilkins E, Firestone A, Choy M
Department of Psychology, Miami University, Oxford, Ohio, USA.
Alcohol Clin Exp Res. 2001 Nov;25(11):1683-8.
Behavioral studies using pharmacological manipulations that increase neuronal activity of the central nucleus of the amygdala (CeA) have implicated the CeA in enhancement of memory modulation. To date, however, there has been a dearth of studies investigating the effect of a drug that decreases CeA activity on memory modulation-a drug that inhibits the neuronal activity of the CeA might be expected to impair memory modulation. To determine whether ethanol inhibits CeA activity and, if so, whether decreased CeA activity is associated with impairment of memory modulation, this study investigated the effect of ethanol on spontaneous single-unit activity of CeA neurons and retention in the passive-avoidance task.
The effect of ethanol (0.35, 0.75, 1.5, 2.5 g/kg) was determined on spontaneously firing neurons in the CeA in urethane-anesthetized rats by use of standard in vivo single-unit electrophysiological recording techniques. Additionally, the effect of ethanol when administered immediately after training in a standard passive-avoidance task was determined on retention the following day.
Ethanol profoundly inhibited spontaneous CeA firing rates in urethane-anesthetized rats at all doses tested. Maximal inhibition was related to dose. Each dose of ethanol significantly inhibited CeA activity within 15 min of administration; within 35 min of administration, 0.75 g/kg of ethanol inhibited CeA activity by 65.2%, and the highest dose (2.5 g/kg) produced nearly complete suppression of CeA activity (81.3%). Although ethanol markedly inhibited CeA activity, these same doses of ethanol failed to impair retention in the passive-avoidance task: 0.35, 0.75, 1.5, and 2.5 g/kg of ethanol, administered immediately after training, failed to alter latency to step-through the following day.
These results show that ethanol profoundly inhibits spontaneous CeA activity and suggest that inhibition of the CeA is not sufficient to impair retention in the passive-avoidance task.
使用药理学操作增加杏仁核中央核（CeA）神经元活动的行为学研究表明，CeA参与记忆调节的增强。然而，迄今为止，缺乏研究探讨降低CeA活性的药物对记忆调节的影响——一种抑制CeA神经元活动的药物可能会损害记忆调节。为了确定乙醇是否抑制CeA活性，如果是，CeA活性降低是否与记忆调节受损有关，本研究调查了乙醇对CeA神经元自发单单位活动的影响以及在被动回避任务中的记忆保持情况。
采用标准的体内单单位电生理记录技术，测定乙醇（0.35、0.75、1.5、2.5 g/kg）对氨基甲酸乙酯麻醉大鼠CeA中自发放电神经元的影响。此外，还测定了在标准被动回避任务训练后立即给予乙醇对次日记忆保持的影响。
在所有测试剂量下，乙醇都能显著抑制氨基甲酸乙酯麻醉大鼠的CeA自发放电率。最大抑制作用与剂量有关。各剂量的乙醇在给药后15分钟内均能显著抑制CeA活性；给药后35分钟内，0.75 g/kg的乙醇使CeA活性降低65.2%，最高剂量（2.5 g/kg）几乎完全抑制了CeA活性（81.3%）。尽管乙醇显著抑制了CeA活性，但相同剂量的乙醇并未损害被动回避任务中的记忆保持：训练后立即给予0.35、0.75、1.5和2.5 g/kg的乙醇，并未改变次日的步过潜伏期。
这些结果表明，乙醇能显著抑制CeA的自发活性，并提示抑制CeA不足以损害被动回避任务中的记忆保持。
