Orexin-A modulates glutamatergic NMDA-dependent spinal reflex potentiation via inhibition of NR2B subunit

doi:10.1152/ajpendo.90243.2008

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/3789

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题名:	Orexin-A modulates glutamatergic NMDA-dependent spinal reflex potentiation via inhibition of NR2B subunit
作者:	Hsien-Yu Peng;Hung-Ming Chang;Sarah Y. Chang;Kwong-Chung Tung;Shin-Da Lee;Dylan Chou;Cheng-Yuan Lai;Chun-Hsien Chiu;Gin-Den Chen;Tzer-Bin Lin
贡献者:	中山醫學大學:醫學系
关键词:	spinal cord;pelvic nerve;urethra;rats
日期:	2008
上传时间:	2011-05-20T08:45:00Z (UTC)
ISSN:	0193-1849
摘要:	Glucose-sensitive neurons in the lateral hypothalamic area produce orexin-A (OxA) as well as orexin-B (OxB) and send their axons to the spinal dorsal horn, which predominantly expresses orexin receptor-1 (OX-1), showing a higher sensitivity to OxA. The purpose of the present study was to assess the effects of OxA on the induction of a novel form of activity-dependent reflex potentiation, spinal reflex potentiation (SRP), in the pelvic-urethral reflex activity. External urethra sphincter electromyogram in response to pelvic afferent nerve test stimulation (TS; 1/30 Hz) or repetitive stimulation (RS; 1 Hz) was recorded in anesthetized rats. TS evoked a baseline reflex activity, whereas RS produced SRP, which was abolished by intrathecal OxA (30 nM, 10 ?l). Intrathecal SB-408124 (10 ?M, 10 ?l), an OX-1 antagonist, reversed the abolition on SRP caused by OxA. Although there is, so far, no NR2A- and NR2B-specific agonist available, N-methyl-D-aspartate (NMDA) reversed the abolition on the RS-induced SRP caused by the co-administration of OxA and Co-101244 (30 nM, 10 ?l; an NMDA NR2B subunit antagonist), but it did not reverse the abolition by the co-administration of OxA and PPPA (300 nM, 10 ?l; an NMDA NR2A subunit antagonist). In conclusion, the activation of descending orexinergic fibers may inhibit the repetitive afferent input-induced central sensitization of pelvic-urethral reflex activity and urethra hyperactivity, indicating that spinal orexinergic neural transmission may be a novel target for the treatment of patients with neuropathetic or postinflammatory pain of pelvic origin.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/3789 http://dx.doi.org/10.1152/ajpendo.90243.2008
關聯:	Am J Physiol Endocrinol Metab, July 1, 2008 295:E117-E129; published ahead of print May 13, 2008
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