KMID : 0811720170210010065
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Korean Journal of Physiology & Pharmacology 2017 Volume.21 No. 1 p.65 ~ p.74
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Participation of central GABAA receptors in the trigeminal processing of mechanical allodynia in rats
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Kim Min-Ji
Park Young-Hong Yang Kui-Ye Ju Jin-Sook Bae Yong-Chul Han Seong-Kyu Ahn Dong-Kuk
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Abstract
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Here we investigated the central processing mechanisms of mechanical allodynia and found a direct excitatory link with low-threshold input to nociceptive neurons. Experiments were performed on male Sprague-Dawley rats weighing 230-280 g. Subcutaneous injection of interleukin 1 beta (IL-1¥â) (1 ng/10 ¥ìL) was used to produce mechanical allodynia and thermal hyperalgesia. Intracisternal administration of bicuculline, a gamma aminobutyric acid A (GABAA) receptor antagonist, produced mechanical allodynia in the orofacial area under normal conditions. However, intracisternal administration of bicuculline (50 ng) produced a paradoxical anti-allodynic effect under inflammatory pain conditions. Pretreatment with resiniferatoxin (RTX), which depletes capsaicin receptor protein in primary afferent fibers, did not alter the paradoxical anti-allodynic effects produced by the intracisternal injection of bicuculline. Intracisternal injection of bumetanide, an Na-K-Cl cotransporter (NKCC 1) inhibitor, reversed the IL-1¥â-induced mechanical allodynia. In the control group, application of GABA (100 ¥ìM) or muscimol (3 ¥ìM) led to membrane hyperpolarization in gramicidin perforated current clamp mode. However, in some neurons, application of GABA or muscimol led to membrane depolarization in the IL-1¥â-treated rats. These results suggest that some large myelinated A¥â fibers gain access to the nociceptive system and elicit pain sensation via GABAA receptors under inflammatory pain conditions.
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KEYWORD
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GABAA receptor, IL-1¥â, Mechanical allodynia, NKCC1, Paradoxical anti-allodynic effect
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