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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Effects of zolantidine a brain-penetrating H2-receptor antagonist, on naloxone-sensitive and naloxone-resistant analgesia.

The action of zolantidine, a histamine H2-receptor antagonist which penetrates the brain, was characterized on the analgesia elicited by brief continuous footshock of 3 intensities. Zolantidine inhibited the analgesia elicited by exposure to 3.5 mA for 3 min, with maximum inhibition observed 30 min after a dose of 5 mg/kg. This inhibition was not dose-related, possibly due to inhibition of the metabolism of histamine in brain by this drug at larger doses. While zolantidine alone, or in combination with naloxone, attenuated this analgesic response, naloxone alone had no such effect, further supporting the non-opiate nature of this response. Conversely, naloxone, but not zolantidine, strongly inhibited the analgesia elicited by 2.0 mA for 3 min, confirming the apparent opiate nature of this analgesic mechanism. Although a combination of zolantidine and naloxone still significantly attenuated this response, a tendency toward reversal of the antagonism by naloxone was observed with this combination of drugs, consistent with previous findings. Furthermore, the analgesia elicited by 2.5 mA for 3 min was resistant to both naloxone and zolantidine, alone or in combination. These results further strengthen the hypothesis that histamine and H2-receptors in brain are important mediators of endogenous antinociception and also support the possible existence of an additional non-opiate, non-H2-analgesic mechanism.[1]


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