Detail of "104076-38-2"

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Potentiation of 2-deoxy-D-glucose antinociception, but not hyperphagia by zolantidine, a histamine (H2) receptor antagonist

Potentiation of 2-deoxy-D-glucose antinociception, but not hyperphagia by zolantidine, a histamine (H2) receptor antagonist. Koch, James E.; Hough, Lindsay B.; Bodnar, Richard J. (Dep. Pharmacol., Mount Sinai Sch. Med., New York, NY 10029, USA). Pharmacol., Biochem. Behav., 41(2), 371-6 (English) 1992. CODEN: PBBHAU. ISSN: 0091-3057. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Antagonism of the histamine (H2) receptor reduces antinociception induced by naloxone-resistant foot-shock, naloxone-sensitive foot-shock, and morphine with a rank-order potency similar to their H2 antagonism. The antimetabolic glucose analog 2-deoxy-D-glucose (2DG) produces antinociceptive and hyperphagic responses that dissoc. from each other and are in part mediated by opioid systems. The present study detd. the effects of the brain-penetraing H2 receptor antagonist zolantidine (ZOL) on 2DG antinociception on the tail-flick and jump tests, as well as on 2DG hyperphagia, in rats. ZOL (0.01-1 mg/kg) potentiated the antinociceptive responses induced by a moderate (450 mg/kg) dose of 2DG, but had lesser effects upon antinociception induced by a lower (100 mg/kg) 2DG dose.There are some commonly used reagents with their cas registry numbers 104076-38-2 and 154-17-6 in this article. ZOL itself slightly increased jump thresholds, but not tail-flick latencies. Combinations of ZOL and 2DG produced supraadditive antinociception, even though ZOL failed to shift the 2DG dose-response curve to the left. In contrast, ZOL failed to alter basal intake or 2DG hyperphagia, supporting previous evidence implicating the H1 but not the H2 receptor in these effects. These results further dissoc. the antinociceptive and hyperphagic effects of 2DG, and also support previous results indicating both pro- and antinociceptive roles for H2 receptors. .