Involvement of ionotropic glutamate receptors in the appearance of arecoline tremor in mice.

Neuroscience and Behavioral Physiology
N Ya LukomskayaL G Magazanik

Abstract

Administration of the muscarinic cholinoreceptor agonist arecoline (6 mg/kg, s.c.) to mice induced long-lasting tremor. The ability of non-competitive antagonists of ionotropic glutamate receptors to suppress the onset of tremor was studied. These antagonists, i.e., adamantane and phenylcyclohexyl derivatives, selectively blocked NMDA-type receptor channels (monocations) or both NMDA-and AMPA-type channels (dications). Both types of blocker weakened arecoline tremor, though the dose-response relationships were different for mono-and dications. The effects of dications appeared only at low blocker doses (0.0001-0.01 micromol/kg) but gradually disappeared on dose elevation. These data lead to the conclusion that the mechanism of pathogenesis of arecoline tremor predominantly involves NMDA-type receptors. Moderate blockade of AMPA-type receptors could potentiate the preventive effect of mixed-action antagonists (anti-NMDA+anti-AMPA), though predominance of blocking action against AMPA-type receptors prevented this effect.

References

Apr 17, 1998·European Journal of Pharmacology·W Löscher
Mar 7, 2002·Trends in Pharmacological Sciences·Wolfgang Löscher
Sep 13, 2003·Journal of Neurochemistry·K V BolshakovL G Magazanik
Dec 24, 2004·Drug News & Perspectives·C G ParsonsG Quack
Jul 6, 2005·Neuropharmacology·K V BolshakovL G Magazanik
Dec 27, 2005·Current Opinion in Pharmacology·Alan C Foster, John A Kemp

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