title: Dorsal raphe stimulation modulates responses of substantia nigra, pars reticulata neurons to painful stimulation.
abstract: There are but few data that substantia nigra neurons are involved in the pain-processing mechanisms in the CNS. In contrast, a great deal of evidence suggests a participation of the dorsal raphe nucleus (RD) in these processes. The purpose of the present study was to examine the effects of painful stimulation (suprathreshold electrical stimulation of the peroneal nerve--NP) on the extracellular activity of neurons of substantia nigra, pars reticulata (SNR) in cats, and to determine if a train of stimuli applied to RD could affect the responses of SNR neurons to this type of painful stimulation. The majority of SNR neurons (83.3%) responded to NP-stimulation either with an increase or with a decrease in the firing rate. The RD-stimulation when applied simultaneously or just before the NP-stimulation reduced or even eliminated the increase in the firing rate caused by pain irrespective of the ability of RD-stimulation applied proviously alone to reduce or not the spontaneous activity of the SNR neurons. In cells which responded with inhibition to NP- and RD-stimulations when applied alone, RD-stimulation applied just before NP-stimulation slightly prolonged the NP-induced inhibition. The results indicate that in addition to the descending pain modulation pathway from the dorsal raphe nucleus to the spinal cord, which pathway is well established, there may be an ascending one to some supraspinal structures, the substantia nigra being one of them.
authors.affiliation: Institute of Physiology, Bulgarian Academy of Sciences.
authors.forename: S
authors.initials: S
authors.lastname: Moyanova
authors.forename: L
authors.initials: L
authors.lastname: Ta
mesh_terms: D000818:Animals; D002415:Cats; D004558:Electric Stimulation; D008297:Male; D009474:Neurons / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D011903:Raphe Nuclei / Q000502:physiology*; D013378:Substantia Nigra / Q000503:physiopathology*