- 作者: Jen-Kun Cheng; Sun-Zhi Lee; Jja-Rung Yang; Chien-Hua Wang; Yan-Yu Liao; Chien-Chuan Chen; Lih-Chu Chiou
- 作者服務機構: Department of Pharmacology, College of Medicine, National Taiwan University, Department of Anesthesiology, Mackay Memorial Hospital, Department of Anesthesiology, Taipei Medical University, Taipei, Taiwan, ROC
- 中文摘要: --
- 英文摘要: Gabapentin, a novel anticonvulsant and analgesic, is ay-aminobutyric acid (GABA) analogue but was showninitially to have little affinity at GABA or GABA recep-tors. It was recently reported to be a selective agonist atGABA receptors containing GABA -GABA hetero-dimers, although several subsequent studies disprovedthat conclusion. In the present study, we examinedwhether gabapentin is an agonist at native GABA recep-tors using a rat model of postoperative pain in vivo andperiaqueductal gray (PAG) slices in vitro; PAG containsGABA receptors, and their activation results in antinoci-ception. An intrathecal injection of gabapentin or baclo-fen, a GABA receptor agonist, induced antiallodynia inthis postoperative pain model. Intrathecal injection ofGABA receptor antagonists CGP 35348 and CGP 55845antagonized baclofen- but not gabapentin-induced an-tiallodynia. In ventrolateral PAG neurons, baclofen acti-vated G-protein-coupled inwardly rectifying K (GIRK)channels in a manner blocked by CGP 35348 or CGP55845. However, gabapentin displayed no effect on themembrane current. In neurons unaffected by gabapen-tin; baclofen activated GIRK channels through GABA receptors. It is concluded that gabapentin is not an ago-nist at GABAB receptors that are functional in baclofen-induced antiallodynia in the postoperative pain model invivo and in GIRK channel activation in ventrolateral PAGneurons in vitro.
- 中文關鍵字: --
- 英文關鍵字: --