Nicotine psychopharmacology in animals

Abstract

Two methods were used to assess nicotine-induced antinociception: tail-withdrawal from a hot water bath and hind paw withdrawal from a hot plate. Doses of nicotine which produced 75–80% maximum response were 0.75 mg/kg (free base) for tail-withdrawal and 0.35 mg/kg for hot-plate. The peripheral blocker chlorisondamine (CHLOR; 0.1 mg/kg, sc) was as effective as the central/peripheral antagonist, mecamylamine (MEC; 1 mg/kg, sc) in blocking nicotine-Induced antinociception as measured by the tail-withdrawal method, suggesting that this measure depends on either the action of nicotine at peripheral receptors or the functional integrity of those receptors (e.g., uninterrupted impulse flow at sympathetic ganglia). In contrast, nicotine-induced antinociception, as measured by the hot-plate method, was blocked by MEC but not CHLOR. These results indicate that the two methods of assessing nicotine-antinociception involve at least partially separate pathways and cannot be used interchangeably. In an initial study to further determine the pathways mediating nicotine’s antinociceptive effects, rats were pretreated with MEC or the ß-adrenergic blocker; propranolol and tested using the tail-dip paradigm. As before, MEC completely blocked nicotine-antinociception but propranolol was without effect. Supported by DA07546