ABSTRACT
Organophosphorus compounds such as malathion are environmental contaminants that may evoke neurobehavioral responses including anxiety and depression. In this study, after a functional observational battery, rats were tested in an open field and temperature test to better define doses used in subsequent experiments. Then, we investigated the effects of acute and repeated treatment with malathion on elevated plus-maze and forced-swim test, which are validated animal models to observe for anxiety- and depressive-related behaviors, respectively. We found that both acute and repeated malathion administration induced anxiogenic and depressive-like responses at doses that affected neither locomotion nor systemic temperature. Biochemical assays demonstrated inhibition of cholinesterase activity by these effective doses.
ABSTRACT
Cannabinoid receptor agonists significantly inhibit nociceptive responses in a large number of animal models. The present study examined whether mice displaying different basal levels of anxiety in the plus-maze test of anxiety might differ in terms of responsiveness to the antinociceptive effects of Delta(9)-tetrahydrocannabinol (Delta(9)-THC). Further, the involvement of the cannabinoid and/or opioid receptors in Delta(9)-THC-induced antinociception was investigated by using SR 141716A and naloxone, respectively, cannabinoid and opioid receptor antagonists. Delta(9)-THC-induced antinociception was evaluated in the formalin test that involves a biphasic response with an early and a late phase of high paw-licking activity. This characteristic biphasic response was observed in all control animals selected as "anxious" and "nonanxious." Delta(9)-THC (0.5-5 mg/kg i.p.) caused a dose-dependent antinociceptive effect in both groups of mice during the early and late phases. This response was fully reversed by SR 141716A (1 mg/kg i.p.) and partially reversed by naloxone (2 mg/kg i.p.). These findings suggest that mice selected for differences in anxiety-related behavior show similar responses to the antinociceptive action of Delta(9)-THC and that this action involves predominantly cannabinoid mechanisms.
