Memory-improving actions of glucose: Involvement of a central cholinergic muscarinic mechanism

摘要: Post-training intraperitoneal administration of α-D[+]-glucose (10–300 mg/kg) facilitated 24-h retention, in male Swiss mice, a one-trial step-through inhibitory avoidance task. The dose-response curve was an inverted U. Glucose did not increase the retention latencies mice that had received footshock during training. effect glucose (30 mg/kg, ip) on time-dependent, which suggests drug memory storage. facilitation induced by prevented atropine (0.5 administered after training, but 10 min prior to treatment. In contrast, neither methylatropine ip), peripherally acting muscarinic receptor blocker, nor mecamylamine (5 or hexamethonium two cholinergic nicotinic antagonists, effects post-training retention. Low subeffective doses central anticholinesterase physostigmine (35 μg/kg, immediately and (10 given acted synergistically improve were influenced neostigmine ip). Considered together, these findings suggest could result from enhancement brain acetylcholine synthesis and/or its release that, turn, might modulate activity mechanisms are critically involved