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杏仁核、小脑深部核团和红核有助于 C57BL/6 小鼠的延迟性眼动条件反射。

Amygdala, deep cerebellar nuclei and red nucleus contribute to delay eyeblink conditioning in C57BL /6 mice.

机构信息

Laboratory of Behavioral Neuroendocrinology, Graduate School of Comprehensive Human Science, University of Tsukuba, Japan.

出版信息

Eur J Neurosci. 2010 Nov;32(9):1537-51. doi: 10.1111/j.1460-9568.2010.07406.x. Epub 2010 Sep 30.

DOI:10.1111/j.1460-9568.2010.07406.x
PMID:20880362
Abstract

That the cerebellum plays an essential role in delay eyeblink conditioning is well established in the rabbit, but not in the mouse. To elucidate the critical brain structures involved in delay eyeblink conditioning in mice, we examined the roles of the deep cerebellar nuclei (DCN), the amygdala and the red nucleus (RN) through the use of electrolytic lesions and reversible inactivation. All mice received eyeblink training of 50 trials during a daily session in the higher-intensity conditioned stimulus (CS) condition (10 kHz, 70 dB). DCN lesions caused severe ataxia; nonetheless, the mice acquired conditioned responses (CRs). Reversible inactivation of DCN, by muscimol (MSC) injection, led to a severe CR impairment in the early sessions of conditioning; however, in later sessions, the mice acquired CRs. Amygdala lesions impaired the acquisition of CRs, which did not reach the level of sham-operated mice, even after prolonged training sessions. MSC injections into the lateral amygdala severely impaired CRs, which began to recover after the removal of MSC. RN inactivation with MSC completely abolished CRs, and removal of MSC immediately restored CRs to the level of control mice. The results indicate that: (i) the DCN are important, but not essential, at least for the late acquisition in mouse eyeblink conditioning; (ii) the amygdala plays an important role in the acquisition and expression of CRs; and (iii) the RN is essential for the expression of CRs. Our findings reveal the various brain areas critically involved in mouse eyeblink conditioning, which include the cerebellum, amygdala and RN.

摘要

小脑在兔子的延迟性眨眼条件反射中起着至关重要的作用,但在老鼠中并非如此。为了阐明涉及老鼠延迟性眨眼条件反射的关键大脑结构,我们通过使用电解损伤和可逆失活来研究深小脑核(DCN)、杏仁核和红核(RN)的作用。所有小鼠在每日的高强度条件刺激(CS)条件下(10 kHz,70 dB)接受 50 次眨眼训练。DCN 损伤导致严重的共济失调;尽管如此,小鼠还是获得了条件反射(CR)。通过向 DCN 注射 muscimol(MSC)可逆失活,导致 CR 在训练早期严重受损;然而,在后期,小鼠获得了 CR。杏仁核损伤损害了 CR 的获得,即使经过长时间的训练,也未能达到假手术组的水平。向外侧杏仁核注射 MSC 严重损害了 CR,在去除 MSC 后,CR 开始恢复。用 MSC 失活 RN 完全消除了 CR,并且去除 MSC 后立即将 CR 恢复到对照小鼠的水平。结果表明:(i)DCN 很重要,但不是必需的,至少在老鼠眨眼条件反射的后期获得中是这样;(ii)杏仁核在 CR 的获得和表达中起重要作用;(iii)RN 对于 CR 的表达是必需的。我们的发现揭示了涉及老鼠眨眼条件反射的各种关键大脑区域,包括小脑、杏仁核和 RN。

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