Bjørkum A A, Bjorvatn B, Neckelmann D, Ursin R
Department of Physiology, University of Bergen, Norway.
Brain Res. 1995 Sep 18;692(1-2):251-8. doi: 10.1016/0006-8993(95)00689-n.
The modulating effect of an intrathecally (i.t.) administered 5-HT1A agonist and an NMDA antagonist on sleep, waking and EEG power spectra was investigated in rats. The 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (38 nmol) increased total slow wave sleep (TSWS) and decreased waking over the 8 h recording period. The TSWS increase was mostly due to an increase in SWS1. Sleep latency to SWS1 was also reduced. The NMDA antagonist dl-2-amino 5-phosphonovaleric acid (AP-5) (31.5 nmol) reduced waking. SWS1 was increased, but TSWS was not changed. An increase in REM sleep was seen during the last part of the recording. Combined treatment with 8-OH-DPAT and AP-5 reduced waking and increased TSWS. No change in REM sleep was seen. There were no systematic changes in either waking, TSWS or REM fronto-frontal or fronto-parietal EEG power spectrum after any of the treatments. The results suggest that in the spinal cord stimulation of 5-HT1A receptors have a dampening effect on transmission of sensory information, leading to deactivation and thereby increased possibilities for sleep induction. Blockade of the NMDA receptors may also lead to a small dampening of sensory transmission with similar consequences.
研究了鞘内注射5-羟色胺1A（5-HT1A）激动剂和N-甲基-D-天冬氨酸（NMDA）拮抗剂对大鼠睡眠、觉醒及脑电图功率谱的调节作用。5-HT1A激动剂8-羟基-2-（二正丙基氨基）四氢萘（8-OH-DPAT）（38纳摩尔）在8小时记录期内增加了总慢波睡眠（TSWS）并减少了觉醒。TSWS的增加主要是由于慢波睡眠1期（SWS1）的增加。进入SWS1的睡眠潜伏期也缩短了。NMDA拮抗剂dl-2-氨基-5-磷酸戊酸（AP-5）（31.5纳摩尔）减少了觉醒。SWS1增加，但TSWS未改变。在记录的最后阶段观察到快速眼动睡眠（REM）增加。8-OH-DPAT和AP-5联合治疗减少了觉醒并增加了TSWS。REM睡眠未见变化。任何一种治疗后，觉醒、TSWS或REM的额-额或额-顶脑电图功率谱均无系统性变化。结果表明，在脊髓中，5-HT1A受体的刺激对感觉信息传递有抑制作用，导致失活，从而增加了诱导睡眠的可能性。NMDA受体的阻断也可能导致感觉传递的轻微抑制，产生类似的结果。
