Nicotine-activated descending facilitation on spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats

doi:10.1152/ajprenal.00539.2007

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/3616

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題名:	Nicotine-activated descending facilitation on spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats
作者:	Shwu-Fen Pan;Hsien-Yu Peng;Chi-Chung Chen;Mei-Jung Chen;Shin-Da Lee;Chen-Li Cheng;Jyh-Cherng Shyu;Jiuan-Miaw Liao;Gin-Den Chen;Tzer-Bin Lin
貢獻者:	中山醫學大學:醫學系
關鍵詞:	acetylcholine;serotonin;WAY;100635;intrathecal;rats;N;methyl;D;aspartic acid;spinal reflex potentiation
日期:	2008
上傳時間:	2011-03-14T03:51:51Z (UTC)
ISSN:	0363-6127
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-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 T1 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:	https://ir.csmu.edu.tw:8080/handle/310902500/3616 http://dx.doi.org/10.1152/ajprenal.00539.2007
關聯:	Am J Physiol Renal Physiol. 294(5), 1195-1204.
顯示於類別:	[醫學系] 期刊論文

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