Memory Consolidation In Mice Research Articles

Effects of rubidium chloride and piracetam upon consolidation of memory in mice

Effects of rubidium chloride and piracetam upon consolidation of memory in mice

Effects of volatile anesthetics on memory consolidation in mice

Effects of volatile anesthetics on memory consolidation in mice

Possible interaction between central cholinergic muscarinic and opioid peptidergic systems during memory consolidation in mice

Naloxone (0.01-1.00 mg/kg, ip) facilitated retention of a one-trial inhibitory avoidance task, when administered to male Rockland mice immediately after training, as indicated by performance on a retention test 48 hr later. The dose-response curve was an inverted U in this range of dose. In these conditions naloxone did not lengthen latencies to step-through during the retest of unshocked mice. Higher doses of naloxone (3.00 and 10.00 mg/kg, ip) tended to increase latencies to step-through of both shocked and unshocked mice. These facts rule out an aversive effect of naloxone for low and moderate doses but not for high doses. The influence of naloxone (0.10 mg/kg, ip) on retention was time dependent, which suggests that naloxone facilitated memory consolidation processes. The effects of naloxone were prevented by morphine in both an amnesic and a nonamnesic dose (1.0 and 0.5 mg/kg, ip, respectively). Therefore, naloxone probably facilitated retention as a function of its opiate antagonist properties. The memory facilitation induced by naloxone (0.10 mg/kg, ip) was antagonized by atropine (0.5 mg/kg, ip) but not by methylatropine (0.5 mg/kg, ip), mecamilamine (5 mg/kg, ip), or hexametonium (5 mg/kg, ip). Further, there was a mutual potentiation for both naloxone (0.01 mg/kg, ip) and the muscarinic agonist oxotremorine (6.25 and 12.5 micrograms/kg, ip) administered simultaneously, in doses which had no effect on their own. Moreover, an amnesic dose of atropine (10.00 mg/kg, ip) prevented the enhancement of retention induced by naloxone, while an amnesic dose of morphine (1.00 mg/kg, ip) did not modify the facilitatory effect of oxotremorine (50 micrograms/kg, ip) on retention. An inhibitory modulatory role for endogenous opioid systems on the activity of central cholinergic muscarinic systems during memory consolidation is suggested.

Influence of physostigmine upon consolidation of memory in mice.

The influence of physostigmine upon the consolidation process was investigated in a series of four experiments. Male mice of a DBA/2J strain were trained to escape shock in a Y-maze. In Experiment 1, physostigmine (.4 mg/kg, ip) impaired a previously learned task 2 days after initial learning but improved performance 11 days after initial learning. In experiments 2 and 3, it was determined that the impairment of memory found on Day 3 was transitory and no longer evident once the drug was no longer active in an animal's system. The findings of Experiment 4, in which the Day 12 facilitory effect was examined, were essentially the same as those of Experiments 2 and 3. The results of the experimentation tend to support an inhibitory or motivational hypothesis rather than a consolidation hypothesis.

Comparative effects of cycloheximide and puromycin on cerebral protein synthesis and consolidation of memory in mice

Cycloheximide was injected intracerebrally in mice in amounts which produced 94–95% inhibition of cerebral protein synthesis in the interval between 5 and 8 h after administration. Such animals learned to escape or avoid shock by choosing the correct limb of a T-maze normally 5 h after injection and had normal retention when tested 3 h later. In contrast, mice injected with puromycin in a dose which inhibited protein synthesis less than cycloheximide, had marked impairment of memory 3 h after training. Addition of cycloheximide to the puromycin solution antagonized its amnesic effect. The puromycin effect on memory 3 h after training is, therefore, probably not based on inhibition of synthesis of a protein required for memory storage. A possible role of protein synthesis in ‘consolidation’ of memory in mice is not supported by these experiments.