期刊
BRAIN RESEARCH BULLETIN
卷 87, 期 2-3, 页码 244-249出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2011.10.015
关键词
Sodium channel Nav1.6; Diabetes; Neuropathic pain; Dorsal root ganglion
Neuropathic pain is one of the most common chronic complications of diabetes, of which the underlying mechanisms are unclear. Expression changes of voltage-gated sodium channels in dorsal root ganglia (DRG) are involved in the production of ectopic spontaneous activity. In the present study, we examined the changes of DRG Nav1.6 expression in a mouse model of type 2 diabetes (db/db mice). Db/db mice developed significant and persistent mechanical allodynia from postnatal 2 months compared to the heterozygous littermates (db/+) and C57 mice. Immunofluorescent staining showed that Nav1.6 was highly expressed in the normal DRG (approximately 31.3 +/- 5.2% of total DRG neurons), especially in the large-diameter neurons. In postnatal 5 months in db/db mice, percentage of Nav1.6 positive cells (62.9 +/- 5.5%) was significantly higher than that in C57 and db/+ mice. Western blot showed that from 2 to 5 months, Nav1.6 was increased by 1.67 +/- 0.16, 2.12 +/- 0.23, 1.89 +/- 0.32, and 2.01 +/- 0.35 folds of C57 mice, which were significantly higher than that of the C57 and db/+ mice. Real-time PCR showed that in postnatal 1 month of db/db mice, mRNA level of Nav1.6 was increased by 1.72 +/- 0.22 fold, which was significantly higher than that of C57 and db/+ mice. Nav1.6 mRNA was increased thereafter and maintained at high levels throughout the observed period. Our results provide direct evidence that type 2 diabetes induces significant and persistent increase of Nav1.6 expression in the DRG, which may participate in the diabetic neuropathic pain. (C) 2011 Elsevier Inc. All rights reserved.
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