title: Effects of intrathecal monoamine antagonists on the nociceptive c-Fos expression in a lesioned rat spinal cord.
abstract: Effects of intrathecal (i.t.) administration of monoamine antagonists on formalin-induced neuronal c-Fos expression in two sides of the lumbar dorsal horn were observed in rats with unilateral transection of the dorsolateral funiculus at T11-12 level. The results showed that: 1) pretreated with i.t. normal saline (control) and then an equal volume of formalin was injected into the two hindpaws, the number of Fos-like immunoreactive neurons were 44% lower on the side of lumbar dorsal horn with intact dorsolateral funiculus (57 +/- 3.1 vs. 103 +/- 3.8). 2) Pretreatment with i.t. phentolamine (a non-selective alpha-adrenoceptor antagonist) caused an increase of Fos-like immunoreactive neurons on the intact side so showing only a reduction rate of 23% to the lesioned side (p < .01); 3) pretreatment with i.t. cyproheptadine (a 5-HT-receptor antagonist) caused a similar reduction rate of 21% (p < .01) of Fos-like immunoreactive neurons on the intact side; and 4) combined i.t. pretreatment with phentolamine and cyproheptadine caused a reduction of Fos-like immunoreactive neurons of only 4% on the intact side, namely, the differences in the number of Fos-like immunoreactive neurons on two sides of the lumbar spinal cord owing to the unilateral dorsolateral funiculus lesion were nearly abolished by i.t. coinjection of phentolamine and cyproheptadine. The results indicate that 1) peripheral noxious inputs can provoke a spinally-descending inhibitory effect on the spinal nociceptive transmission via the dorsolateral funiculus and 2) the descending fibers in dorsolateral funiculus exert their action mainly through the release of either norepinephrine or 5-HT at the spinal level.
authors.affiliation: Department of Neurobiology, Shanxi Medical College, Taiyuan, P.R. China.
authors.forename: R J
authors.initials: RJ
authors.lastname: Liu
authors.forename: R
authors.initials: R
authors.lastname: Wang
authors.forename: H
authors.initials: H
authors.lastname: Nie
authors.forename: R X
authors.initials: RX
authors.lastname: Zhang
authors.forename: J T
authors.initials: JT
authors.lastname: Qiao
authors.forename: N
authors.initials: N
authors.lastname: Dafny
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D003533:Cyproheptadine / Q000494:pharmacology; D004347:Drug Interactions; D005260:Female; D007150:Immunohistochemistry; D007278:Injections, Spinal; D008297:Male; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000378:metabolism; D009638:Norepinephrine / Q000037:antagonists & inhibitors*; D010146:Pain / Q000378:metabolism* / Q000503:physiopathology; D010646:Phentolamine / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D012701:Serotonin / Q000378:metabolism*; D012702:Serotonin Antagonists / Q000494:pharmacology; D013116:Spinal Cord / Q000378:metabolism* / Q000601:surgery; D009435:Synaptic Transmission / Q000502:physiology
chemical_list: D000317:Adrenergic alpha-Antagonists; D016760:Proto-Oncogene Proteins c-fos; D012702:Serotonin Antagonists; D003533:Cyproheptadine; D012701:Serotonin; D009638:Norepinephrine; D010646:Phentolamine