Cataplexy-related neurons in the amygdala of the narcoleptic dog
Cataplexy-related neurons in the amygdala of the narcoleptic dog
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DOI：
10.1016/s0306-4522(02)00089-1
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发表时间：
2002-01-01
期刊：
影响因子：
3.3
通讯作者：
Siegel, JM
中科院分区：
文献类型：
--
作者：
Gulyani, S;Wu, MF;Siegel, JM
杏仁核在解释情绪上重要的刺激方面起着重要的作用，并对脑干区域有很强的投射，调节肌肉张力和睡眠。发作性睡病的一种症状是肌肉张力的丧失，通常由突然强烈的情绪引发。在发作性睡病狗的杏仁核中进行了细胞外单单位记录，以检验杏仁核神经元亚群的异常活动与cataemosis有关的假设。在记录的218个细胞中，31个是睡眠活跃的，78个在清醒和快速眼动睡眠中都活跃，88个在清醒时最活跃，21个是状态独立的。两个群体的细胞显示出显着的变化，在活性与catabetamine。位于中央和基底核的一群睡眠活跃细胞在cataebralization之前和期间增加放电。一个人口的唤醒活跃的细胞定位于皮质核减少活动之前和过程中cataabolism。我们假设这些细胞群通过与控制肌张力的脑桥中间区域的相互作用在调解或调节紧张症中发挥作用。抗胆碱酯酶毒扁豆碱，在剂量增加cataplexy，并没有改变cataplexy相关的细胞或其他杏仁核细胞的活性，这表明其对cataplexy的影响是介导的杏仁核的“下游”。α-1受体阻滞剂哌唑嗪，在剂量增加的cataelasticity，增加放电的cataelasticity活性细胞的一个亚组，并在一些其他杏仁核细胞，表明哌唑嗪可能调制cataelasticity通过其对杏仁核细胞或其传入的作用。由Elsevier Science Ltd代表IBRO发布。
The amygdala plays an important role in the interpretation of emotionally significant stimuli and has strong projections to brainstem regions regulating muscle tone and sleep. Cataplexy, a symptom of narcolepsy, is a loss of muscle tone usually triggered by sudden, strong emotions. Extracellular single-unit recordings were carried out in the amygdala of narcoleptic dogs to test the hypothesis that abnormal activity of a subpopulation of amygdala neurons is linked to cataplexy.Of the 218 cells recorded, 31 were sleep active, 78 were active in both waking and rapid-eye-movement sleep, 88 were maximally active during waking, and 21 were state independent. Two populations of cells showed a significant change in activity with cataplexy. A population of sleep active cells localized to central and basal nucleus increased discharges prior to and during cataplexy. A population of wake active cells localized to the cortical nucleus decreased activity prior to and during cataplexy. We hypothesize that these cell populations have a role in mediation or modulation of cataplexy through interactions with meso-pontine regions controlling atonia. The anticholinesterase physostigmine, at doses which increased cataplexy, did not alter the activity of the cataplexy-related cells or of other amygdala cells, suggesting that its effect on cataplexy is mediated 'downstream' of the amygdala. The alpha-1 blocker prazosin, at doses which increased cataplexy, increased discharge in a subgroup of the cataplexy active cells and in a number of other amygdala cells, indicating that prazosin may modulate cataplexy by its action on amygdala cells or their afferents. Published by Elsevier Science Ltd on behalf of IBRO.