Haefely W, Ruch-Monachon M A, Jalfre M, Schaffner R
Arzneimittelforschung. 1976;26(6):1036-9.
One of the phasic phenomena of REM (rapid eye movement) sleep, the ponto-geniculo-occipital (PGO) waves, are induced in cats by either depleting brain monoamines with the benzoquinolizine derivative Ro 4-1284 or inhibiting the synthesis of 5-hydroxy-tryptamine (5-HT) by p-chlorophenylalanine (PCPA). The effects of the most important psychotropic agents on PGO1284 and PGOPCPA are reported and explained by their interaction with one or more of the 4 neurotransmitters known so far to be involved in the regulation of the PGO wave generation in the pontine reticular formation. Tricyclic antidepressants depress PGO waves by inhibiting the neuronal uptake of norepinephrine (NE) and/or 5-HT. Some neuroleptics increase the density of GO waves by blocking 5-HT and/or NE receptors. Various indole hallucinogens depress PGO waves by stimulating 5-HT receptors. Benzoldiazepines appear to enhance a (gamma-aminobutyric acid)-ergic (GABA)-ergic inhibitory influence on NE neurons and increase the density of PGO waves in the presence of functionally intact NE neurons.
快速眼动(REM)睡眠的阶段性现象之一,即脑桥-膝状体-枕叶(PGO)波,可通过用苯并喹嗪衍生物Ro 4-1284耗尽脑单胺或用对氯苯丙氨酸(PCPA)抑制5-羟色胺(5-HT)的合成在猫中诱导产生。报告了最重要的精神药物对PGO1284和PGOPCPA的影响,并通过它们与迄今为止已知参与脑桥网状结构中PGO波产生调节的4种神经递质中的一种或多种的相互作用来解释。三环类抗抑郁药通过抑制去甲肾上腺素(NE)和/或5-HT的神经元摄取来抑制PGO波。一些抗精神病药物通过阻断5-HT和/或NE受体增加PGO波的密度。各种吲哚类致幻剂通过刺激5-HT受体抑制PGO波。苯二氮䓬类药物似乎增强了对NE神经元的γ-氨基丁酸(GABA)能抑制作用,并在功能完整的NE神经元存在的情况下增加PGO波的密度。