کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6281327 1615111 2015 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Ca2+ influx mediates the TRPV4-NO pathway in neuropathic hyperalgesia following chronic compression of the dorsal root ganglion
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
Ca2+ influx mediates the TRPV4-NO pathway in neuropathic hyperalgesia following chronic compression of the dorsal root ganglion
چکیده انگلیسی
Chronic compression of the dorsal root ganglion (DRG) (CCD) in rats is a typical model of neuropathic pain. TRPV4 contributed to mechanical allodynia induced by the CCD model. Our previous study demonstrated that TRPV4 enhances neuropathic hyperalgesia through a NO-cGMP-PKG cascade. However, the underlying mechanism(s) is still largely unknown. Therefore, the aim of the present study was to test whether TRPV4-mediated Ca2+ influx is involved in the TRPV4-NO pathway. Regulation of intracellular calcium concentration by intrathecal injection of TRPV4-targeted siRNA significantly decreased the behavioural hyperalgesia, NF-κB activity, and NO content in CCD rats. Intraperitoneal (i.p.) injection of mibefradil significantly induced dose-dependent increases in the paw withdrawal latency (PWL) and mechanical withdrawal thresholds (MWT), as well as decreases in NF-κB activity and NO content in DRG of CCD rats. Moreover, pre-treatment with 4α-PDD attenuated the suppressive effects of mibefradil on CCD-induced neuropathic hyperalgesia, NF-κB activity, and NO production. The data showed that TRPV4-mediated Ca2+ influx might be engaged in the TRPV4-NO pathway in neuropathic hyperalgesia in the CCD model.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 588, 19 February 2015, Pages 159-165
نویسندگان
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