Maudhuit C, Jolas T, Chastanet M, Hamon M, Adrien J
INSERM U288, CHU Pitié-Salpêtrière, Paris, France.
Biol Psychiatry. 1996 Nov 15;40(10):1000-7. doi: 10.1016/0006-3223(95)00583-8.
Previous studies showed that chronic deprivation of rapid eye movement (REM) sleep had the same behavioral effects as antidepressant drugs in helpless rats. Since long-term treatment with antidepressants is known to affect central serotoninergic neurotransmission, we investigated whether REM sleep deprivation also exerts an influence on the activity of serotoninergic neurons within the dorsal raphe nucleus (DRN) in rats. REM sleep deprivation was performed using the platform technique. Recording of serotoninergic neurons in the DRN revealed no difference in the basal firing rate, but a reduced inhibitory response to the selective serotonin (5-HT) reuptake blockers cericlamine and citalopram after repeated but not acute REM sleep deprivation. These observations suggest that REM sleep deprivation renders serotoninergic DRN neurons less sensitive to the inhibitory effect of 5-HT reuptake blockers, probably because of functional desensitization of somatodendritic 5-HT1A autoreceptors, like that previously reported after chronic treatment with several antidepressants. Accordingly, REM sleep deprivation might alleviate depression through neurophysiological mechanisms similar to those induced by antidepressants.
先前的研究表明，快速眼动（REM）睡眠的长期剥夺在无助大鼠中具有与抗抑郁药物相同的行为效应。由于已知长期使用抗抑郁药物会影响中枢5-羟色胺能神经传递，我们研究了REM睡眠剥夺是否也会对大鼠中缝背核（DRN）内5-羟色胺能神经元的活性产生影响。使用平台技术进行REM睡眠剥夺。对DRN中5-羟色胺能神经元的记录显示，基础放电率没有差异，但在反复而非急性REM睡眠剥夺后，对选择性5-羟色胺（5-HT）再摄取阻滞剂西拉敏和西酞普兰的抑制反应降低。这些观察结果表明，REM睡眠剥夺使DRN中5-羟色胺能神经元对5-HT再摄取阻滞剂的抑制作用敏感性降低，这可能是由于躯体树突状5-HT1A自身受体的功能脱敏，类似于先前在几种抗抑郁药物长期治疗后所报道的情况。因此，REM睡眠剥夺可能通过与抗抑郁药物诱导的机制类似的神经生理机制来缓解抑郁。
