Tags

Type your tag names separated by a space and hit enter

Retrieval does not induce reconsolidation of inhibitory avoidance memory.
Learn Mem. 2004 Sep-Oct; 11(5):572-8.LM

Abstract

It has been suggested that retrieval during a nonreinforced test induces reconsolidation instead of extinction of the mnemonic trace. Reconsolidation would preserve the original memory from the labilization induced by its nonreinforced recall through a hitherto uncharacterized mechanism requiring protein synthesis. Given the importance that such a process would have in terms of maintaining, as part of the animal behavioral repertoire, a learned response that has been devalued by experience, we analyzed its existence for the memory associated with a one-trial, step-down inhibitory avoidance task (IA), a memory whose consolidation and extinction require protein synthesis in the CA1 region of the dorsal hippocampus (CA1) and involve the participation of the basolateral amygdala (BLA) and entorhinal cortex (ENT). Rats were trained in IA, and 24 h later they were submitted either to a pure reactivation session (retrieval without stepping down), which was unable by itself to initiate extinction of the avoidance response, or to a second training session. Fifteen minutes before or 3 h after either the reactivation or the retraining sessions, animals were infused with the protein synthesis inhibitor anisomycin (ANI) into CA1, BLA, or ENT. Contrary to the prediction of the reconsolidation hypothesis, none of these treatments affected subsequent memory retention. Because reconsolidation is regarded to be a direct consequence of retrieval, one would expect that, when given before a retention test or a pure reactivation session, enhancers of memory expression should permanently improve retention and, therefore, facilitate retrieval both in that and in subsequent sessions. Using two well-known retrieval enhancers, noradrenaline and adrenocorticotropin(1-24), we could not find any evidence suggestive of reconsolidation. Hence, our results indicate that there is no retrieval-induced, protein synthesis-dependent process that would cause reconsolidation of IA memory.

Authors+Show Affiliations

Memory Research Laboratory, Institute for Cell Biology and Neuroscience Prof. Dr. Eduardo de Robertis, School of Medicine, University of Buenos Aires, Ciudad Autónoma de Buenos Aires, CP 1121, Argentina.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15466311

Citation

Cammarota, Martín, et al. "Retrieval Does Not Induce Reconsolidation of Inhibitory Avoidance Memory." Learning & Memory (Cold Spring Harbor, N.Y.), vol. 11, no. 5, 2004, pp. 572-8.
Cammarota M, Bevilaqua LR, Medina JH, et al. Retrieval does not induce reconsolidation of inhibitory avoidance memory. Learn Mem. 2004;11(5):572-8.
Cammarota, M., Bevilaqua, L. R., Medina, J. H., & Izquierdo, I. (2004). Retrieval does not induce reconsolidation of inhibitory avoidance memory. Learning & Memory (Cold Spring Harbor, N.Y.), 11(5), 572-8.
Cammarota M, et al. Retrieval Does Not Induce Reconsolidation of Inhibitory Avoidance Memory. Learn Mem. 2004 Sep-Oct;11(5):572-8. PubMed PMID: 15466311.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Retrieval does not induce reconsolidation of inhibitory avoidance memory. AU - Cammarota,Martín, AU - Bevilaqua,Lia R M, AU - Medina,Jorge H, AU - Izquierdo,Iván, PY - 2004/10/7/pubmed PY - 2005/1/7/medline PY - 2004/10/7/entrez SP - 572 EP - 8 JF - Learning & memory (Cold Spring Harbor, N.Y.) JO - Learn Mem VL - 11 IS - 5 N2 - It has been suggested that retrieval during a nonreinforced test induces reconsolidation instead of extinction of the mnemonic trace. Reconsolidation would preserve the original memory from the labilization induced by its nonreinforced recall through a hitherto uncharacterized mechanism requiring protein synthesis. Given the importance that such a process would have in terms of maintaining, as part of the animal behavioral repertoire, a learned response that has been devalued by experience, we analyzed its existence for the memory associated with a one-trial, step-down inhibitory avoidance task (IA), a memory whose consolidation and extinction require protein synthesis in the CA1 region of the dorsal hippocampus (CA1) and involve the participation of the basolateral amygdala (BLA) and entorhinal cortex (ENT). Rats were trained in IA, and 24 h later they were submitted either to a pure reactivation session (retrieval without stepping down), which was unable by itself to initiate extinction of the avoidance response, or to a second training session. Fifteen minutes before or 3 h after either the reactivation or the retraining sessions, animals were infused with the protein synthesis inhibitor anisomycin (ANI) into CA1, BLA, or ENT. Contrary to the prediction of the reconsolidation hypothesis, none of these treatments affected subsequent memory retention. Because reconsolidation is regarded to be a direct consequence of retrieval, one would expect that, when given before a retention test or a pure reactivation session, enhancers of memory expression should permanently improve retention and, therefore, facilitate retrieval both in that and in subsequent sessions. Using two well-known retrieval enhancers, noradrenaline and adrenocorticotropin(1-24), we could not find any evidence suggestive of reconsolidation. Hence, our results indicate that there is no retrieval-induced, protein synthesis-dependent process that would cause reconsolidation of IA memory. SN - 1072-0502 UR - https://www.unboundmedicine.com/medline/citation/15466311/Retrieval_does_not_induce_reconsolidation_of_inhibitory_avoidance_memory_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/15466311/ DB - PRIME DP - Unbound Medicine ER -