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[蜗牛(Helix lucorum)中联合性食物厌恶条件反射再巩固的神经元机制]

[Neuronal mechanisms of associative food aversion conditioning reconsolidation in snail Helix lucorum].

作者信息

Kozyrev S A, Nikitin V P

出版信息

Ross Fiziol Zh Im I M Sechenova. 2009 Jun;95(6):652-62.

Abstract

We have previously showed that reactivation of long-term memory during protin synthesis inhibitor application initiated disruption of memory recalling in snails Helix lucorum with food aversion conditioning reflex. In present work cellular mechanisms of memory reactivation were studied in snail LP11 and RP11 command neurons of defense behavior. In first trial experiments mechanisms of amnesia induction were investigated in semiintact preparations 24 hours after aversion conditioning with single type of food. It was found that application of conditioned food stimulus on snail lip during CNS perfusion with cycloheximide (protein synthesis inhibitor) initiated depression of synaptic response evoked by conditioned stimulus 2.5 hours after reminding. In second tria experiments neuronal mechanisms of amnesia development were studied. Snails were conditioned with two types of food. Cycloheximide was injected into mantle cavity and conditioned stimulus of one type of food was presented 24 hours after snail learning. Semiintact preparations were prepared 1,3, 7 and 15 days after cycloheximide injection + reminding procedure. It was found that neural responses evoked by conditioned food stimulus which was used as reminding stimulus gradually decreased during 1, 3 and 7 days. Neural responses evoked by the conditioned stimulus at 7 and 15 days were not significantly differed from control differentiated food stimulus and were significantly weaker then neural responses evoked by second conditioned food stimulus which was not used as a reminding stimulus. It was suggested that specific and protein synthesis-dependent changes in synaptic connections effectiveness in LP11 and RP11 neurons is one of the cellular mechanisms of amnesia obtained after disruption of long-term memory reconsolidation in snail.

摘要

我们之前已经表明,在应用蛋白质合成抑制剂期间长期记忆的重新激活会引发以食物厌恶条件反射训练的光亮大蜗牛的记忆回忆中断。在目前的工作中,我们在防御行为的大蜗牛LP11和RP11指令神经元中研究了记忆重新激活的细胞机制。在首次试验实验中,在用单一类型食物进行厌恶条件反射24小时后的半完整标本中研究了遗忘诱导机制。结果发现,在用环己酰亚胺(蛋白质合成抑制剂)进行中枢神经系统灌注期间,当条件食物刺激施加于蜗牛唇部时,在提醒2.5小时后会引发条件刺激诱发的突触反应抑制。在第二次试验实验中,研究了遗忘发展的神经元机制。用两种类型的食物对蜗牛进行条件反射训练。将环己酰亚胺注入外套腔,并在蜗牛学习24小时后呈现一种类型食物的条件刺激。在环己酰亚胺注射 + 提醒程序后的1、3、7和15天制备半完整标本。结果发现,用作提醒刺激的条件食物刺激诱发的神经反应在1、3和7天期间逐渐降低。在7天和15天时,条件刺激诱发的神经反应与对照的区分食物刺激没有显著差异,并且明显弱于未用作提醒刺激的第二种条件食物刺激诱发的神经反应。有人提出,LP11和RP11神经元中突触连接有效性的特定且依赖蛋白质合成的变化是蜗牛长期记忆再巩固中断后获得遗忘的细胞机制之一。

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