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ANESTHETIC PHARMACOLOGY

Modulation of Gamma-Aminobutyric Acid_A Receptor Function by Thiopental in the Rat Spinal Dorsal Horn Neurons

Chuan-Xiu Yang, MS^*, Han Xu, PhD^*, Ke-Qing Zhou^*, Meng-Ya Wang, PhD, and Tian-Le Xu, PhD, MD^*

*School of Life Sciences, University of Science and Technology of China, Hefei; Institute of Neuroscience and Key Laboratory of Neurobiology, Chinese Academy of Sciences, Shanghai; and Laboratory of Cell Electrophysiology, Wannan Medical College, Wuhu, China

Address correspondence and reprint requests to Tian-Le Xu, PhD, MD, Institute of Neuroscience and Key Laboratory of Neurobiology, Chinese Academy of Sciences, 320 Yue-Yang Rd., Shanghai 200031, China. Address e-mail to tlxu{at}ion.ac.cn.

To assess the actions of thiopental at the spinal dorsal horn level, we examined the effects of thiopental using the whole cell patch-clamp technique on mechanically dissociated rat spinal dorsal horn neurons. Thiopental, at large concentrations, elicited a current (I_Thio) through activation of chloride conductance, and its threshold concentration was approximately 50 µM. I_Thio was sensitive to bicuculline, a -aminobutyric acid (GABA)_A receptor antagonist, but not to strychnine, a glycine receptor antagonist. At a clinically relevant concentration (30 µM), thiopental markedly enhanced the peak amplitude of a subsaturating GABA-induced current (I_GABA) but not that of a saturating GABA-induced cur-rent. Furthermore, thiopental prolonged the time constants of both desensitization and deactivation of I_GABA. At a large concentration (300 µM), it inhibited the peak amplitude of I_GABA, which may be the result of open-channel blockade. In addition, at 30 µM, thiopental increased the duration and decreased the frequency of GABAergic miniature inhibitory postsynaptic currents. These results indicate that thiopental enhances GABAergic inhibitory transmission and suggest that GABA_A receptors in the spinal cord are a potential target through which thiopental causes immobility and depresses the response to noxious stimuli.