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1 Department of Biotechnology, Ming-Chuan University, Taiwan - Republic of China
2 Physiology, Chung-Shan Medical University, Taichug, Taiwan - Republic of China; Veterinary Medicine, National Chung-Hsing University, Taichug, Taiwan - Republic of China
3 Surgery and Medical Department, St. Paul's Hospital, Taiwan - Republic of China
4 Department of Medical Engineering, Ming-Chuan University, United States
5 School of Physical Therapy, China Medical University, Taichung, Taiwan - Republic of China
6 Division of Urology, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan - Republic of China
7 Physiology, Chung-Shan Medical University, Taichug, Taiwan - Republic of China
8 Department of Physiology, College of Medicine, Chung-Shan Medical University, Taichung, United States
9 Department of Obstetrics and Gynecology, Chung Shan Medical University, Taiwan - Republic of China
10 Department of Physiology, College of Medicine, Chung-Shan Medical University, Tai-Chung, United States
* To whom correspondence should be addressed. E-mail: tblin{at}csmu.edu.tw.
This study was conducted to investigate the possible neurotransmitter, which 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 63 anesthetized rats were recorded with or without microinjection of nicotinic cholinergic receptor (nAChR) agonists, acetylcholine 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 APV (1.60±0.89 spikes/stimulation, N=40) and was attenuated by NBQX (7.10±0.84 spikes/stimulation, N=40). Acetylcholine 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 resulted 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 activating of nAChR at DPT may modulate NMDA-dependent reflex potentiation via descending serotonergic neurotransmission. This descending modulation may have physiological/pathological relevance in the neural controls of urethral closure.
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  H.-Y. Peng, H.-M. Chang, S. Y. Chang, K.-C. Tung, S.-D. Lee, D. Chou, C.-Y. Lai, C.-H. Chiu, G.-D. Chen, and T.-B. Lin Orexin-A modulates glutamatergic NMDA-dependent spinal reflex potentiation via inhibition of NR2B subunit Am J Physiol Endocrinol Metab, July 1, 2008; 295(1): E117 - E129. [Abstract] [Full Text] [PDF]
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