The effects of oxotremorine, epibatidine, atropine, mecamylamine and naloxone in the tail flick, hot plate, and formalin tests in the naked mole rat (Heterocephalus glaber)

Citation:
Dulu T.D, kanui T.I., P.K. T, G.M. M, K.S. A. "The effects of oxotremorine, epibatidine, atropine, mecamylamine and naloxone in the tail flick, hot plate, and formalin tests in the naked mole rat (Heterocephalus glaber)." In vivo. 2014;28(1):39-48.

Abstract:

Abstract. The naked mole-rat (Heterocephalus glaber) is a
promising animal model for the study of pain mechanisms,
therefore a thorough characterization of this species is
essential. The aim of the present study was to establish the
naked mole-rat as a model for studying the cholinergic
receptor system in antinociception by investigating the
involvement of muscarinic, nicotinic and opioid receptors in
nociceptive tests in this species. The effects of systemic
administration of the muscarinic receptor agonist
oxotremorine and the nicotinic receptor agonist epibatidine
were investigated in the tail-flick, the hot-plate, and the
formalin tests. The effects of co-administration of the
muscarinic receptor antagonist atropine, the nicotinic
receptor antagonist mecamylamine, and the opioid receptor
antagonist naloxone were also investigated. Oxotremorine
and epibatidine induced a significant, dose-dependent
antinociceptive effect in the tail-flick, hot-plate, and formalin
tests, respectively. The effects of oxotremorine and
epibatidine were blocked by atropine and mecamylamine,
respectively. In all three nociceptive tests, naloxone in
combination with oxotremorine or epibatidine enhanced the
antinociceptive effects of the drugs. The present study
demonstrated that stimulation of muscarinic and nicotinic
receptors produces antinociceptive effects in the naked-mole
rat. The reversal effect of atropine and mecamylamine
suggests that this effect is mediated by cholinergic receptors.
As naloxone increases the antinociceptive effects of
cholinergic agonists, it is suggested that the cholinergic
antinociception acts via a gateway facilitated by opioid
receptor blockage; however, the precise interaction between
these receptor systems needs further investigation.

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