Nishino S, Honda K, Riehl J, Okura M, Mignot E
Center for Narcolepsy, Department of Psychiatry and Behavioral Science, Stanford University School of Medicine, Palo Alto, CA 94304, USA.
Neuroreport. 1998 Nov 16;9(16):3653-61. doi: 10.1097/00001756-199811160-00017.
Cholinergic stimulation in the basal forebrain (BF) triggers cataplexy in canine narcolepsy. Extracellular single unit recordings in the BF were carried out in freely moving narcoleptic dogs to study the neuronal mechanisms mediating cataplexy induction in the BF. Among the 64 recorded neurons, 12 were wake-active, three were slow wave sleep (SWS)-active, 17 were wake-/REM-active, 11 were REM sleep-active, three were cataplexy-active, and the other 18 were state-independent. Systemic administration of physostigmine, a cholinesterase inhibitor, induces status cataplecticus, decreases SWS and increases acetylcholine levels in the BF. Firing of most of the state-dependent neurons in the BF was significantly modified by physostigmine. Some of these neurons may thus mediate sleep stage changes or the effect on cataplexy observed after cholinergic stimulation in the BF.
基底前脑（BF）中的胆碱能刺激会引发犬发作性睡病中的猝倒。在自由活动的发作性睡病犬中对BF进行细胞外单单位记录，以研究介导BF中猝倒诱导的神经元机制。在记录的64个神经元中，12个在清醒时活跃，3个在慢波睡眠（SWS）时活跃，17个在清醒/快速眼动（REM）时活跃，11个在REM睡眠时活跃，3个在猝倒时活跃，另外18个与状态无关。全身给予胆碱酯酶抑制剂毒扁豆碱可诱发全身猝倒状态，减少SWS并增加BF中的乙酰胆碱水平。BF中大多数与状态相关的神经元的放电受到毒扁豆碱的显著影响。因此，其中一些神经元可能介导睡眠阶段变化或BF中胆碱能刺激后观察到的对猝倒的影响。
