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Dexmedetomidine enhances cerebral cortex GIRK1 protein expression and attenuates Acute Postoperative Pain in rats
Author(s) -
Wang Lingzhi,
Wu Zhikun,
Liu Shiming,
Li Haobo,
Xia Zhengyuan,
Huang Huansen
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb503
Subject(s) - dexmedetomidine , medicine , anesthesia , agonist , pharmacology , opioid , nociception , stimulation , receptor , sedation
Dexmedetomidine (DEX), a highly selective α 2 ‐adrenoceptor agonist, produces both sedative and antinociceptive action. However, the mechanism for DEX analgesia remains unclear. Opening of G protein‐activated inwardly rectifying K+ (GIRK) channels at spinal sites are involved in antinociception induced by opioid and no‐opioid receptor agonists (Pain. 2013;154(12):2853‐9). We investigated the antihyperalgesic effects induced by intravenous administration of DEX in acute incisional pain model in rats and its potential effect on the expression of GIRK1 at the supraspinal sites. The hyperalgesic effects induced by the plantar incision were verified by a significant and transient decrease in the mechanical paw withdrawal threshold for 24 hours (h) after hindpaw incision. The decreases of paw withdrawal threshold at 0.5h, 1h, 2h, 4h after incision were significantly suppressed by intravenous pre‐administration of 5 or 10 ug/kg of DEX. Furthermore, pretreatment with DEX increased the expression of GIRK1 in the cerebral cortex at 2h and 4h after plantar incision as assessed by immunofluorescence and western blotting. It is concluded that administration of DEX before surgery induces antihyperalgesic effects in rats suffering from acute incision pain and that stimulation of GIRK1 expression in the cerebral cortex may represent a mechanism whereby DEX confers antinociception in acute postoperative pain.