title: Nicotine-activated descending facilitation on spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats.
abstract: This study was conducted to investigate the possible neurotransmitter that activates the descending pathways coming from the dorsolateral pontine tegmentum (DPT) to modulate spinal pelvic-urethra reflex potentiation. External urethra sphincter electromyogram (EUSE) activity in response to test stimulation (TS, 1/30 Hz) and repetitive stimulation (RS, 1 Hz) on the pelvic afferent nerve of 63 anesthetized rats were recorded with or without microinjection of nicotinic cholinergic receptor (nAChR) agonists, ACh and nicotine, to the DPT. TS evoked a baseline reflex activity with a single action potential (1.00 +/- 0.00 spikes/stimulation, n = 40), whereas RS produced a long-lasting reflex potentiation (16.14 +/- 0.96 spikes/stimulation, n = 40) that was abolished by d-2-amino-5-phosphonovaleric acid (1.60 +/- 0.89 spikes/stimulation, n = 40) and was attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline (7.10 +/- 0.84 spikes/stimulation, n = 40). ACh and nicotine microinjections to DPT both produced facilitation on the RS-induced reflex potentiation (23.57 +/- 2.23 and 28.29 +/- 2.36 spikes/stimulation, P < 0.01, n = 10 and 20, respectively). Pretreatment of selective nicotinic receptor antagonist, chlorisondamine, reversed the facilitation on RS-induced reflex potentiation caused by nicotine (19.41 +/- 1.21 spikes/stimulation, P < 0.01, n = 10) Intrathecal WAY-100635 and spinal transection at the T(1) level both abolished the facilitation on reflex potentiation resulting from the DPT nicotine injection (12.86 +/- 3.13 and 15.57 +/- 1.72 spikes/stimulation, P < 0.01, n = 10 each). Our findings suggest that activation of nAChR at DPT may modulate N-methyl-d-aspartic acid-dependent reflex potentiation via descending serotonergic neurotransmission. This descending modulation may have physiological/pathological relevance in the neural controls of urethral closure.
authors.affiliation: Department of Biotechnology, Ming-Chuan University, Taoyuan, Taiwan.
authors.forename: Shwu-Fen
authors.initials: SF
authors.lastname: Pan
authors.forename: Hsien-Yu
authors.initials: HY
authors.lastname: Peng
authors.forename: Chi-Chung
authors.initials: CC
authors.lastname: Chen
authors.forename: Mei-Jung
authors.initials: MJ
authors.lastname: Chen
authors.forename: Shin-Da
authors.initials: SD
authors.lastname: Lee
authors.forename: Chen-Li
authors.initials: CL
authors.lastname: Cheng
authors.forename: Jyh-Cherng
authors.initials: JC
authors.lastname: Shyu
authors.forename: Jiuan-Miaw
authors.initials: JM
authors.lastname: Liao
authors.forename: Gin-Den
authors.initials: GD
authors.lastname: Chen
authors.forename: Tzer-Bin
authors.initials: TB
authors.lastname: Lin
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002404:Catheterization; D004558:Electric Stimulation; D005260:Female; D007278:Injections, Spinal; D008845:Microinjections; D016202:N-Methylaspartate / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000502:physiology; D009538:Nicotine / Q000008:administration & dosage / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000008:administration & dosage / Q000494:pharmacology*; D010879:Piperazines / Q000494:pharmacology; D011149:Pons / Q000187:drug effects*; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011978:Receptors, Nicotinic / Q000187:drug effects; D012018:Reflex / Q000187:drug effects*; D012701:Serotonin / Q000494:pharmacology; D012702:Serotonin Antagonists / Q000494:pharmacology; D013116:Spinal Cord / Q000187:drug effects / Q000378:metabolism*
chemical_list: D018377:Neurotransmitter Agents; D018722:Nicotinic Agonists; D010879:Piperazines; D011725:Pyridines; D011978:Receptors, Nicotinic; D012702:Serotonin Antagonists; D012701:Serotonin; D016202:N-Methylaspartate; D009538:Nicotine; C090413:N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide