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This Article Full Text Full Text (PDF) All Versions of this Article: 294/5/F1195    most recent 00539.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Pan, S.-F. Articles by Lin, T.-B. PubMed PubMed Citation Articles by Pan, S.-F. Articles by Lin, T.-B.

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

¹Department of Biotechnology, ⁵Department of Medical Engineering, Ming-Chuan University, Taoyuan; ²Department of Physiology, College of Medicine and ⁸Department of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Chung Shan Medical University, Taichung; ³Department of Veterinary Medicine, National Chung-Hsing University, Taichung; ⁴Division of Urology, Department of Surgery and ⁹Medical Department, St. Paul's Hospital, Taoyuan; ⁶School of Physical Therapy, College of Medicine, China Medical University, Taichung; ⁷Division of Urology, Department of Surgery, Taichung Veterans General Hospital, Taichung; and ¹⁰Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan

Submitted 15 November 2007 ; accepted in final form 18 February 2008

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.

acetylcholine; serotonin; WAY-100635; intrathecal; rats; N-methyl-D-aspartic acid; spinal reflex potentiation