Kubin L, Tojima H, Reignier C, Pack A I, Davies R O
Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA.
Sleep. 1996 Apr;19(3):187-95.
The facilitatory effect of serotonin (5HT) on hypoglossal (XII) motoneurons is likely to be reduced during rapid eye movement (REM) sleep, when the activity of the brainstem serotonergic system reaches its nadir. Therefore, we assessed the hypothesis that application of exogenous 5HT will attenuate the REM sleep-like suppression of XII motoneurons produced in decerebrate cats by pontine microinjections of a cholinergic agonist, carbachol. Microinjections of 5HT or 5-carboxamidotryptamine into the XII nucleus increased XII nerve activity to 182 +/- 53% (standard deviation; SD) of control. Subsequent pontine microinjections of carbachol reduced XII nerve activity by 55 +/- 21% of the pre-5HT level (n = 12). Microinjections of methysergide (a 5HT antagonist) into the XII nucleus reduced XII nerve activity to 54 +/- 17% of the pre-methysergide control (n = 6). Pontine carbachol injections after methysergide further reduced XII nerve activity by 49 +/- 20% of the pre-methysergide level. Treatments with both agonists and the antagonist attenuated the carbachol-induced decrease when compared to two previous studies using the same model: 1) In experiments with no injections of serotonergic agents, pontine carbachol injections decreased XII nerve activity by 90 +/- 6% of control. 2) After enhancement of XII nerve activity by inhibitory amino acid antagonists (to 135 +/- 60%), the subsequent carbachol-induced decrease was even larger, 112 +/- 62% of control. We propose that serotonergic excitation can significantly attenuate the REM sleep-like suppression of XII nerve activity, and that this is achieved, in part, by substituting for the decreased endogenous 5HT in the XII nucleus. The study also demonstrates that other, non-serotonergic, mechanisms also contribute to the carbachol-induced suppression.
在快速眼动（REM）睡眠期间，当脑干血清素能系统的活动达到最低点时，血清素（5HT）对舌下（XII）运动神经元的促进作用可能会减弱。因此，我们评估了以下假设：通过脑桥微量注射胆碱能激动剂卡巴胆碱在去大脑猫中产生的XII运动神经元的REM睡眠样抑制，外源性5HT的应用将减弱这种抑制。向XII核微量注射5HT或5-羧酰胺色胺可使XII神经活动增加至对照的182±53%（标准差；SD）。随后脑桥微量注射卡巴胆碱使XII神经活动降低至5HT注射前水平的55±21%（n = 12）。向XII核微量注射麦角新碱（一种5HT拮抗剂）使XII神经活动降低至麦角新碱注射前对照的54±17%（n = 6）。麦角新碱注射后进行脑桥卡巴胆碱注射，使XII神经活动进一步降低至麦角新碱注射前水平下的49±20%。与之前使用相同模型的两项研究相比，激动剂和拮抗剂治疗均减弱了卡巴胆碱诱导的降低：1）在未注射血清素能药物的实验中，脑桥卡巴胆碱注射使XII神经活动降低至对照的90±6%。2）在通过抑制性氨基酸拮抗剂增强XII神经活动（至135±60%）后，随后卡巴胆碱诱导的降低甚至更大，为对照的112±62%。我们提出，血清素能兴奋可显著减弱XII神经活动的REM睡眠样抑制，并且这部分是通过替代XII核中减少的内源性5HT来实现的。该研究还表明，其他非血清素能机制也有助于卡巴胆碱诱导的抑制。
