Chronic spinal cord injury causes upregulation of serotonin (5-HT)2A and 5-HT2C receptors in lumbosacral cord motoneurons
Chronic spinal cord injury causes upregulation of serotonin (5-HT)2A and 5-HT2C receptors in lumbosacral cord motoneurons
复制标题
慢性脊髓损伤导致腰骶脊髓运动神经元中血清素 (5-HT)2A 和 5-HT2C 受体上调
DOI：
10.1111/bju.13964
复制
发表时间：
2018-01-01
影响因子：
4.5
通讯作者：
Andersson, Karl-Erik
中科院分区：
文献类型：
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作者：
Cao, Nailong;Ni, Jianshu;Andersson, Karl-Erik
目的探讨5-羟色胺（5-HT）（2A/2C）受体激动剂2，5-二甲氧基-4-碘苯基-2-氨基丙烷盐酸盐（DOI）对脊髓损伤（SCI）大鼠排尿功能的影响。并探讨其机制是否与5-HT_（2A）和5-HT_（2C）有关。材料和方法将雌性SD大鼠分为两组（SCI组和正常对照组）。在乌拉坦麻醉下，进行膀胱测压，以检查连续鞘内（i. t.）将不同剂量的DOI施用到腰骶髓中。结果与NC大鼠相比，SCI大鼠膀胱容量和排尿后残余尿量明显增加，排尿效率明显降低。脊髓损伤后，DOI改善排尿效率，可能通过外尿道括约肌（EUS）的活动。结论DOI可提高SCI大鼠排尿效率，其机制可能与上调腰骶部脊髓运动神经元5-HT 2A和2C受体表达有关。
ObjectivesTo investigate whether the voiding dysfunction caused by spinal cord injury (SCI) in rats can be improved by i.v. administration of the serotonin (5-HT)(2A/2C) receptor agonist 2,5-dimethoxy-4-iodophenyl-2-aminopropanehydrochloride (DOI), and to discuss whether the mechanism can be ascribed to 5-HT2A and 5-HT (2C) receptor upregulation in lumbosacral cord motoneurons.Materials and MethodsFemale Sprague-Dawley rats were divided into two groups (SCI group vs normal control [NC] group). Under urethane anaesthesia, cystometry was performed to examine the variation in urodynamic variables before and after successive intrathecal (i.t.) administration of various doses of DOI into the lumbosacral cord. Changes in 5-HT2A and -(2C) receptors in the lumbosacral cord were also investigated using immunohistochemical staining and Western blot analysis.ResultsCompared with NC rats, the SCI rats had higher bladder capacity and post-void residual urine volume, and lower voiding efficiency. After SCI, DOI improved voiding efficiency, probably via external urethral sphincter (EUS) activity. Immunohistochemical staining and Western blot analysis showed that 5-HT2A and -(2C) receptors were upregulated in lumbosacral cord motoneurons.ConclusionIn rats with SCI, DOI can improve voiding efficiency; this may be attributable to 5-HT2A and -(2C) receptor upregulation in lumbosacral cord motoneurons controlling EUS activity.