| Abstract No.: | B-G2196 |
| Country: | Canada |
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| Title: | THE ROLE OF THE ANTERIOR CINGULATE CORTEX IN CONSOLIDATION AND RECONSOLIDATION OF CONTEXTUAL FEAR MEMORIES |
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| Authors/Affiliations: | 1 Einar Einarsson*; 1 Karim Nader;
1 Department of Psychology, McGill University, Montreal, QC, Canada.
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| Content: | Objectives: The standard view of systems consolidation posits that the hippocampus (HC) plays a time-limited role in memory processes, after which the memory can be supported by cortical structures. The anterior cingulate cortex (ACC) has been identified as a key structure in the expression of such remote, HC-independent, contextual fear memory. Recently, it has been reported that reactivation of such HC-independent memories can make them once more transiently sensitive to dorsal hippocampal (dHC)-manipulations, a process termed systems reconsolidation. Here we asked a) whether remote ACC-dependent memories undergo systems reconsolidation, where their expression becomes transiently independent of the structure, and b) whether contextual fear memories undergo cellular consolidation and reconsolidation in the ACC immediately following acquisition and retrieval, respectively.
Materials and Methods: Rats were trained with 8 shocks in a conditioning context.
To test for systems consolidation and reconsolidation the ACC was inactivated with a local infusion of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist, or its vehicle before testing. To test for cellular consolidation and reconsolidation, anisomycin (ANI), a protein synthesis inhibitor, or its vehicle was infused into the ACC immediately following training or memory reactivation.
Results: We found that, consistent with systems consolidation, inactivation of the ACC impaired the expression of a 30 day old memory, but did not affect expression of a 3 day old memory. Systems reconsolidation in the ACC would be demonstrated by showing that reactivation of a remote memory returns performance to being transiently independent of that structure. To test this, we inactivated the ACC before a second test at different time-points after reactivation. Inactivating the ACC at 6 hr after reactivation of the 30 day old memory did not impair the expression of the memory, but did at 24 hours. To test whether the memory expression 6 hr after reactivation could be mediated by either the ACC or the dHC we inactivated either the dHC or the ACC, or both. We found that inactivating either structure did not block the expression of the memory, but inactivating both did. Thus, a subsequent retrieval of a 30 day old contextual fear memory requires either the ACC or dHC 6 hours following the first memory reactivation.
In testing for cellular consolidation, we found that ANI infusions immediately after training resulted in similar freezing to vehicle group 4 hours post-training, but impaired performance 20 hours later. Similarly, ANI infusions following reactivation of a 3 and 30 day old memories resulted in normal freezing 4 hours post-training, but impaired 20 hours later. Thus, contextual fear memory undergoes cellular consolidation in the ACC and reconsolidation at 3 and 30 days following training.
Conclusion: Together, these data suggest that although the ACC is preferentially required for retrieving older memories, the structure is involved in stabilizing a newly acquired memory, as well as restabilizing recent and remote memories. Furthermore, once retrieved, the expression of a remote memory can be transiently supported by either the ACC or dHC. |
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