title: Unilateral lesion of the nigrostriatal pathway decreases the response of GABA interneurons in the dorsal raphe nucleus to 5-HT(1A) receptor stimulation in the rat.
abstract: This study examined the firing rate and pattern of electrophysiologically and chemically identified GABA interneurons in the dorsal raphe nucleus (DRN), and role of 5-HT(1A) receptor agonist 8-OH-DPAT and the medial prefrontal cortex (mPFC) in the firing activity in rats with 6-hydroxydopamine lesions of the substantia nigra pars compacta (SNc). The interneurons in rats with lesions of the SNc showed a more burst-firing, while having no change in the firing rate; the mPFC and combined mPFC and SNc lesions in rats decreased the firing rate of the interneurons and firing pattern shifted towards a more burst-firing compared to rats with sham lesions of the SNc, respectively. In rats with sham lesions of the SNc, administration of 8-OH-DPAT (1-243 μg/kg, i.v.) produced excitatory-inhibitory, excitatory and inhibitory effects in the firing rate of individual interneurons. However, when these effects were averaged over the group, 8-OH-DPAT had no significant effect on firing rate. In rats with lesions of the SNc, mPFC and the paired lesions, 8-OH-DPAT, at the same doses, inhibited all interneurons tested, respectively. Cumulative doses producing inhibition in rats with the paired lesions were higher than that of rats with lesions of the mPFC. In contrast to rats with sham lesions of the SNc, SNc lesion reduced expression of 5-HT(1A) receptor on parvalbumin positive neurons in the DRN, a subpopulation of GABA interneurons. Our results indicate that the SNc and mPFC regulate the firing activity of GABA interneurons in the DRN. Furthermore, response of likely GABA interneurons to systemic administration of 8-OH-DPAT is altered by lesion of the SNc and mPFC.
authors.affiliation: Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, China.
authors.forename: C
authors.initials: C
authors.lastname: Hou
authors.forename: L
authors.initials: L
authors.lastname: Xue
authors.forename: J
authors.initials: J
authors.lastname: Feng
authors.forename: L
authors.initials: L
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: T
authors.initials: T
authors.lastname: Wang
authors.forename: Q J
authors.initials: QJ
authors.lastname: Zhang
authors.forename: J
authors.initials: J
authors.lastname: Liu
mesh_terms: D017371:8-Hydroxy-2-(di-n-propylamino)tetralin / Q000494:pharmacology*; D000200:Action Potentials / Q000502:physiology; D000818:Animals; D002452:Cell Count; D003342:Corpus Striatum / Q000293:injuries* / Q000503:physiopathology; D059290:Dopaminergic Neurons / Q000473:pathology; D059330:GABAergic Neurons / Q000737:chemistry / Q000502:physiology*; D007051:Ibotenic Acid / Q000633:toxicity; D007395:Interneurons / Q000502:physiology*; D008297:Male; D009419:Nerve Tissue Proteins / Q000032:analysis; D016627:Oxidopamine / Q000633:toxicity; D020734:Parkinsonian Disorders / Q000503:physiopathology; D010320:Parvalbumins / Q000032:analysis; D017397:Prefrontal Cortex / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D011903:Raphe Nuclei / Q000166:cytology / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044282:Receptor, Serotonin, 5-HT1A / Q000187:drug effects* / Q000502:physiology; D058825:Serotonin 5-HT1 Receptor Agonists / Q000494:pharmacology*; D013378:Substantia Nigra / Q000293:injuries* / Q000503:physiopathology; D017557:Ventral Tegmental Area / Q000473:pathology
chemical_list: D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D058825:Serotonin 5-HT1 Receptor Agonists; D044282:Receptor, Serotonin, 5-HT1A; D007051:Ibotenic Acid; D017371:8-Hydroxy-2-(di-n-propylamino)tetralin; D016627:Oxidopamine