Glucocorticoids have important role in cognitive functions. Evidences indicated that modulating effects of Glucocorticoids on memory, at least in part; mediate via cholinergic system, but the underlying mechanism(s) of these effects on consolidation and reconsolidation are not clear. The aim of this study was to determine the role of cholinergic system in glucocorticoids-induced modulate of memory consolidation and reconsolidation memory in mice.

Experiments were performed on 100 male albino mice (about 30 gr). In consolidation experiments, the animals were trained in an inhibitory avoidance task (0.5 mA shock for 3 seconds). Immediately after training, the animals received of corticosterone (0.3 mg/kg). Then, effects of corticosterone were examined in the presence of absence of atropine (an antagonist of muscarinic receptors, 0.5 and 2 mg/kg) or mecamylamine (an antagonist of nicotinic receptors, 0.5 and 2 mg/kg). In reconsolidation experiments, mice were trained in a passive avoidance task as above. For memory reactivation, mice were returned to the chamber 48 h later. Immediately after reactivation, mice were injected with corticosterone (3 mg/kg) in the presence or absence of atropine (0.5 or 2 mg/kg) or mecamylamine (0.5 or 2 mg/kg). Two, four, and seven days after memory reactivation, rats were returned to the context for 10 min, and step-through latency was recorded.

Our findings revealed that corticosterone significantly improved memory consolidation. This effect was blocked by atropine but not mecamylamine. Conversely, corticosterone impaired memory reconsolidation and this effect was not blocked neither with atropine nor mecamylamine.

It is concluded that glucocorticoids has opposing effects on memory consolidation and reconsolidation. Further, cholinergic system may mediate glucocorticoids on memory consolidation, but not reconsolidation.

Keywords: 

Atropine, Mecamylamine, Glucocorticoids, Memory consolidation and reconsolidation, Mice