oon-35ss/ss/23n.oisoso2.oo/o Tiiz JOURNAL OP PHARMACOLOGY AND EXPEIUMINTAL Thzwsunics CopyrightO 1986by The American Society for PharmacOlogy and Experimental Therspeutics

The possible role of the alpha-2 adrenoceptors in xylazine-kduced vomithg and in moon ckness was investigated. Cats were divided into two groups according to motion sickness susceptibility and were observed after s.c. injections of xylazine. The incidence of vomiting increased with the dose, and at each dose, the high susceptibility group had a greateremetic incidence than the low susceptibility group. In another expenment with cats divided into two groups according to motion sickness susceptibility, s.c. administration of yohimbine effectively antag-onized the xylazine-induced emesis in both susceptibility groups. The cats in the latter experiment were then challenged with a motion sickness stimulus after s.c. pretreatment with yohimbine. Yohimbine fsiled to prevent moticn sickness but did occasion an unexplained variability In the incidence of vomiting. These find-ings suggest that the emetic effect of xylazine results from stimulaticn of a!pha-2 adrenoceptors but that these receptors are not fundamental to feline motion sickness. The fact that susceptibilities to xylazine-induced emesis and to motion sick-ness are correlated suggests a point of interaction other than the area postrema, which is known to be essential for xylazine-induced vomiting but not for motion sickness in the cat. One strategy for studying the neurotransmitters involved in motion sickness is to examine the properties of substances that have emetic potencies varying with the sensitivity to motion sickness. The mechanism of emetic action of such agents may suggest the fundamental receptors involved and indicate antag-onists to be tested for antimotion sickness efficacy. This was the strategy used here. Xylazine [Rompun; BAY 1470; 2-(2,6-dimethylphenyl-amino)-4H-5,6-dihydro-1,3-thiazine] elicits vomiting in cat