Inhibition of sympathetic activity by stimulating in the raphe nuclei and the role of XXXX in this effect.

@entity3858 @entity7201 @entity7782 @entity750 @entity468 @entity10105
The possibility that the putative transmitter @entity750 ( @entity750 ) is involved in the mediation of long latency to onset raphe-spinal inhibition of sympathetic preganglionic neurones was investigated in anaesthetized @entity468 by stimulating sites located in nucleus raphe pallidus and obscurus and recording sympathetic discharge in T3 or T10 white rami evoked either reflexively or by intraspinal stimulation at cervical level. Several putative @entity750 antagonists were administered intravenously (i.v.) or topically to the spinal cord. In 7 @entity468 @entity10105 (LSD) in a dose range 25-50 microgram/kg i.v. or 0.6 microgram topically, reversibly reduced the raphe spinal inhibition by 40-100%. Topical application was more effective than i.v. administration. In 5 @entity468 stimulating within the ventromedial reticular formation at sites unlikely to involved @entity750 neurones produced a short latency to onset inhibition which was unaffected by LSD. @entity3858 , @entity7201 and @entity7782 depressed sympathetic discharge in the absence of brain stimulation in @entity468 with CNS intact and in unanaesthetized decerebrate spinal @entity468 . The results are discussed in the light of the known actions of the putative @entity750 antagonists.
