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ANESTHETIC PHARMACOLOGY

5-HT₃ Receptors Partially Mediate Halothane Depression of Spinal Dorsal Horn Sensory Neurons

Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut

Address correspondence and reprint requests to J. G. Collins, PhD, Department of Anesthesiology, Yale University School of Medicine, 333 Cedar St., PO Box 208051, New Haven, CT 06520-8051. Address e-mail to j.collins{at}yale.edu

We recently reported that -aminobutyric acid type A- and strychnine-sensitive glycine receptor systems partially mediate halothane depression of spinal dorsal horn low-threshold neurons. Serotonin subtype 3 (5-HT₃) receptors belong to the same ligand-activated ion-channel family as -aminobutyric acid type A- and strychnine-sensitive glycine receptors, so we examined the possible involvement of 5-HT receptor systems in halothane depression of spinal sensory neurons. Extracellular recordings of spinal low-threshold neurons were obtained in decerebrate, spinally transected rats. Receptive field size and brush-induced activity were recorded in the presence or absence of 5-HT antagonists and in the presence or absence of 1.1% (1 minimum alveolar anesthetic concentration) halothane. In the absence of halothane, antagonists had no effect on receptive field size or brush-induced activity. In the presence of halothane, methysergide, a nonselective 5-HT antagonist, and tropisetron, a selective 5-HT₃ antagonist, significantly reversed the halothane-induced reduction in receptive field size but did not alter halothane depression of brush-induced activity. Methiothepin, a 5-HT₁ antagonist, and ketanserin, a 5-HT₂ antagonist, did not reverse halothane depression. These results support the hypothesis that 5-HT₃ receptors partially mediate some inhibitory effects of halothane on spinal dorsal horn neurons.

IMPLICATIONS: The results of this study support the hypothesis that halothane depression of spinal sensory neuronal responses to low-intensity stimuli is mediated, to a minor extent, by serotonin subtype 3 neurotransmitter systems.

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