Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/67867
標題: Nicotine-activated descending facilitation on spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats
作者: Pan, S.F.
Peng, H.Y.
Chen, C.
Chen, M.J.
Lee, S.D.
Cheng, C.L.
Shyu, J.C.
Liao, J.M.
Chen, G.D.
Lin, T.B.
關鍵字: acetylcholine;serotonin;WAY-100635;intrathecal;rats;N-methyl-D-aspartic acid;spinal reflex potentiation;long-term potentiation;external urethral sphincter;excitatory;synaptic-transmission;serotonin receptor agonists;micturition-reflex;anesthetized rats;dorsal-horn;binding-sites;nerve injury;cord-injury
Project: American Journal of Physiology-Renal Physiology
期刊/報告no:: American Journal of Physiology-Renal Physiology, Volume 294, Issue 5, Page(s) F1195-F1204.
摘要: 
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-7sulfamoyl-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.
URI: http://hdl.handle.net/11455/67867
ISSN: 1931-857X
DOI: 10.1152/ajprenal.00539.2007
Appears in Collections:期刊論文

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