ABSTRACT
Introduction: Recent studies suggest that glucocorticoids modulate memory reconsolidation. Moreover, cholinergic system is involved in memory reconsolidation. Since glucocorticoids interact with brain cholinergic system in modulating memory processing, we investigated whether glucocorticoid influences on the reconsolidation of emotionally arousing training depend on the cholinergic system
Methods: Mice were trained [1mA, 3s footshock] in an inhibitory avoidance task. Forty-eight hours after training, memory reactivation was occurred [Test 1], and different treatments were given. Two [Test 2], five [Test 3], and seven days [Test 4] after memory reactivation [Test 1], animals were retested for fear memory retention
Results: In the first experiment, we observed that administration of corticosterone [CORT, 0.3, 1 and 3 mg/kg] following memory reactivation impaired subsequent expression of memory in a dose-dependent manner. In the second experiment, we found that CORT-induced impairment of memory reconsolidation was reversed by the muscarinic receptor antagonist atropine [0.5 and 2 mg/kg]. In the third experiment, the nicotinic receptor antagonist mecaylamine [0.5 or 2 mg/kg] was not able to block the corticosterone response
Discussion: These findings indicate that glucocorticoids impair memory reconsolidation by a muscarinic cholinergic mechanism
ABSTRACT
Reconsolidation memory is defined as a process in which the retrieval of a previously consolidated memory returns to a labile state which is then subject to stabilization. Previous studies have shown that mineralocorticoid receptors [MRs] modulate distinct phases of learning and memory, which display a high concentration and distinct distribution in the hippocampus. Moreover, we found no studies that examined the role of hippocampal MRs in fear memory reconsolidation. Here, we investigated the effect of MRs blockade on fear memor reconsolidation in rats. Additionally, to test whether blockade of protein synthesis would disrupt fear memory reconsolidation in our paradigm, we tested the effect of cycloheximide, an inhibitor of protein synthesis after memory reactivation. Results indicated that systemic as well as intra-hippocampal administrations of the MR antagonist spironolactone immediately following memory reactivation did not affect on post-retrieval long-term memory. Cycloheximide given after the reactivation treatment produced a strong impairment that persisted over test sessions. These findings indicate that MRs are not required for reconsolidation of fear-based memory