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α ‐Lipoic acid normalizes nociceptive neuronal activity at the spinal cord of diabetic rats
Author(s) -
Morgado C.,
PereiraTerra P.,
Tavares I.
Publication year - 2011
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2011.01399.x
Subject(s) - spinal cord , microglia , hyperalgesia , nociception , medicine , streptozotocin , oxidative stress , lipoic acid , intraperitoneal injection , endocrinology , pharmacology , chemistry , antioxidant , inflammation , diabetes mellitus , biochemistry , receptor , psychiatry
Aim: To evaluate the effects of antioxidant treatment of streptozotocin (STZ)‐diabetic rats with α ‐lipoic acid ( α ‐LA) in neuronal and microglial activation at the spinal cord, an important relay station of nociceptive transmission. Because of the role of the potassium chloride co‐transporter 2 (KCC2) in neuronal activation at the spinal cord and the influence of microglia in KCC2 expression, we also evaluated the effects of α ‐LA in KCC2 expression at the spinal cord. Methods: Four weeks after STZ injection, the rats received daily intraperitoneal injections of α ‐LA (100 mg/kg), during 2 weeks. Mechanical nociception was evaluated before and after α ‐LA treatment. Spinal cords were immunoreacted against 8‐OH‐dG (marker of oxidative stress damage), Fos (marker of neuronal activation) and CD11b (marker of microglia). KCC2 expression was evaluated by immunohistochemistry and western blotting. Results: Treatment with α ‐LA decreased the 8‐OH‐dG and Fos expressions to controls' levels, but did not affect CD11b. Treatment with α ‐LA alleviated mechanical hyperalgesia and partially corrected KCC2 expression. Conclusions: This study shows that neuronal hyperactivity at the spinal cord of STZ‐diabetic rats can be corrected by α ‐LA, which may account for alleviation of mechanical hyperalgesia. These effects are probably partially mediated by KCC2, but are independent from microglia.