Glucose enhancement of memory is not state-dependent.

Immediate post-training intraperitoneal administration of alpha-D[+]-glucose (10-300 mg/kg) significantly enhanced retention of male Swiss mice tested 24 h after training in an inhibitory avoidance task. The dose-response curve was an inverted U in this range of dose. However, of the doses tested, only 30 mg/kg was effective. Glucose did not affect response latencies in mice not given the footshock on the training trial, suggesting that the actions of glucose on retention performance were not due to nonspecific effects on response latencies. The influence of glucose (30 mg/kg) was time-dependent, which suggests that glucose facilitated memory consolidation processes. Administration of glucose (30 mg/kg) 2 or 10 min prior to the retention test did not affect the retention performance of mice given post-training injections of either saline or glucose (30 mg/kg). These findings indicate that the memory-enhancing effects of post-training administration of glucose are not state-dependent and are consistent with the view that the behavioral effects of glucose are mediated through an interaction with the neural or neurohumoral processes underlying the storage of acquired information.

Facilitation of memory storage by the acetylcholine M2 muscarinic receptor antagonist AF-DX 116.

Post-training administration of the acetylcholine muscarinic M2 presynaptic receptor antagonist AF-DX 116 (0.1-10.0 mg/kg, ip), facilitated 48 h retention, in male Swiss mice, of a one-trial step-through inhibitory avoidance task. The dose-response curve was an inverted U. AF-DX 116 did not increase the retention latencies of mice that had not received a footshock during training. The influence of AF-DX 116 (1 mg/kg, ip) on retention was time-dependent, which suggests that the drug facilitated memory storage. The memory facilitation induced by AF-DX 116 (1 mg/kg, ip) was prevented by atropine (0.5 mg/kg, ip) administered after training, but 10 min prior to AF-DX 116 treatment. In contrast, neither methylatropine (0.5 mg/kg, ip), a peripherally acting muscarinic receptor blocker, nor mecamylamine (5 mg/kg, ip) or hexamethonium (5 mg/kg, ip), two cholinergic nicotinic receptor antagonists, prevented the effects of post-training AF-DX 116 on retention. Low subeffective doses of the central acting anticholinesterase physostigmine (35 micrograms/kg, ip), administered immediately after training, and AF-DX 116 (0.1 mg/kg, ip), given 10 min after training, acted synergistically to improve retention. The effects of AF-DX 116 (0.1 mg/kg, ip) were not influenced by the peripherally acting anticholinesterase neostigmine (35 micrograms/kg, ip). Considered together, these findings suggest that the activation of a muscarinic cholinergic presynaptic inhibitory mechanism, probably by increasing brain acetylcholine release, may modulate the activity of post-training processes involved in memory storage.