Hippocampal memory encoding and retrieval: Difference between revisions

Revision as of 19:55, 13 November 2015

Revision as of 19:55, 13 November 2015

Line 21:

===Reconsolidation Hypothesis===

The [[reconsolidation hypothesis]] claims that objects encoded into long term memory experience a new period of consolidation, or the time and resource expended to stabilize a memory object, upon each recollection. This is in opposition to the classical consolidation hypothesis which regards consolidation as a one-time event, following the first encoding of a memory. A memory item in this hypothesis, upon reactivation, destabilizes for a brief period and thereafter invokes the neuronal processes requisite for stabilization.<ref name=d>Morris, R. G. M., Inglis, J., Ainge, J. A., Olverman, H. J., Tulloch, J., Dudai, Y., & Kelly, P. A. T. (2006) Memory reconsolidation: Sensitivity of spatial memory to inhibition of protein synthesis in dorsal hippocampus during encoding and retrieval. Neuron,50(3), 479-489. doi:http://dx.doi.org/10.1016/j.neuron.2006.04.012</ref>

The reconsolidation hypothesis has lingered since the 1960s; however, a 2000 study, entitled “Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval”, examining fear conditioning in rats, has provided evidence in its favor.<ref name=e>Nader, Karim, Glenn E. Schafe, and Joseph E. Le Doux. 'Fear Memories Require Protein Synthesis In The Amygdala For Reconsolidation After Retrieval'. Nature 406.6797 (2000): 722-726. doi:10.1038/35021052</ref> After receiving post-retrieval an intra-amygdalar infusion of a known amnesic agent, anisomycin, rats failed to recall a rapidly learned fear memory.<ref name=e /> Hippocampal lesions formed post-retrieval affected the rats' fear conditioning in a similar manner.<ref name=e />