جستجوی مقالات مرتبط با کلیدواژه "mecamylamine" در نشریات گروه "پزشکی"

It is well known that morphine influence learning and memory processes. The Nucleus accumbens (N.ac) which has an important role in reward participates in morphine-induced impairment of memory retention. Considering the cholinergic system is involved in the effects of morphine on learning and memory, in the present study, the effects of intra-N.ac injections of acetylcholine receptor antagonists alone or with morphine on memory retention and morphine-induced memory has been investigated in rats. In this original research animals were bilaterally cannulated in the N.ac and a step-through passive avoidance task was used for the assessment of memory retention. Post-training subcutaneous administration of morphine dose dependently decreased the learning and induced amnesia. The administration of the same dose of morphine as pre-test treatment induced state-dependent learning. Pre-test intra- N.ac administration of atropine, scopolamine and mecamylamine in different doses alone cannot affect on memory retention. While, pretest intra- N.ac injection of these drugs before the administration of morphine dose dependently inhibited morphine state-dependent learning. The level of statistical significance was set at p<0.05. The processes of learning in animals can be affected by morphine and the opioids produce state-dependent learning. Moreover, it can be concluded that inactivation of the muscarinic and nicotinic acethylcoline receptors in the N.ac are involved in mediating morphine state-dependent learning.

Nitric oxide and mecamylamine have an important role in anxiety-like behavior. Determining the site of action in the brain and interaction between these agents need to be investigated. Therefore، this study aimed to investigate the possible interaction between mecamylamine and nitric oxide in dorsal hippocampus using the elevated plus-maze test of anxiety. This experimental study was performed on 180 male NMRI mice. Mice were anaesthetized with ketamine and xylazine and two cannuale were inserted stereotaxically into the CA1 region of the dorsal hippocampus. All animals were allowed to recover for 1 week before the beginning of the behavioral testing. The elevated plus-maze was used to test the anxiety-like behavior. Bilateral intra-dorsal hippocampal injections of mecamylamine، L-arginine or L-NAME induced the anxiogenic effects. Intra-dorsal hippocampal injection of ineffective dose of mecamylamine before different doses of L-arginine or L-NAME potentiated the anxiogenic effects of L-arginine or L-NAME. Results reveal that both nitric oxide and mecamylamine not only play a part in the modulation of anxiety in the dorsal hippocampus of mouse but also have demonstrated a complex interaction as well.

Many evidence indicated that glucocorticoids enhanced memory consolidation n a variety of tasks, but the underlying mechanism(s) are not clear. The aim of this study was to determine the role of cholinergic system in glucocorticoids-induced enhancement of memory consolidation in mice. In this experimental study were performed on 100 male albino mice (about 30 g). The animals were trained in an inhibitory avoidance task (0.5 mA shock for 3 seconds). In Experiment 1, effects of corticosterone were determined. Immediately after training, the animals received of vehicle or corticosterone (0.3 mg/kg). In Experiments 2 and 3, effects of corticosterone were examined in the presence of absence of atropine, a blocker of muscarinic cholinergic receptors, (0.5 and 2 mg/kg) or Mecamylamine, a blocker of nicotinic cholinergic receptors, (0.5 and 2 mg/kg), respectively. In all experiments, memory retention tested 48 hr later. Results indicated that Corticosterone enhanced memory consolidation significantly (P<0.01). Blockade of muscarinic cholinergic receptors by atropine suppressed the glucocorticoids response dose-dependently. Blockade of nicotinic cholinergic receptors by Mecamylamine did not change the glucocorticoids response. Also both blockers alone did not change memory consolidation as compared with control group. Finding above showed that the memory enhancing effects of corticosterone, at least in part; may mediate via muscarinic cholinergic receptors.