Hippocampal memory encoding and retrieval: Difference between revisions

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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>{{cite journal | last1 = Morris | first1 = R. G. M. | last2 = Inglis | first2 = J. | last3 = Ainge | first3 = J. A. | last4 = Olverman | first4 = H. J. | last5 = Tulloch | first5 = J. | last6 = Dudai | first6 = Y. | last7 = Kelly | first7 = P. A. T. | year = 2006 | title = Memory reconsolidation: Sensitivity of spatial memory to inhibition of protein synthesis in dorsal hippocampus during encoding and retrieval | url = | journal = Neuron | volume = 50 | issue = 3| pages = 479–489 | doi = 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>{{cite journal | last1 = Nader | first1 = Karim | last2 = Schafe | first2 = Glenn E. | last3 = Le Doux | first3 = Joseph E. | year = 2000 | title = Fear Memories Require Protein Synthesis In The Amygdala For Reconsolidation After Retrieval | url = | journal = Nature | volume = 406 | issue = 6797| pages = 722–726 | doi = 10.1038/35021052 | pmid=10963596}}</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 />

The reconsolidation hypothesis does not suppose that subsequent and precedent consolidation phases are necessarily identical in duration or in the neural mechanisms involved. Nevertheless, the commonality that exists in every consolidation phase is a short-lived destabilization of a memory object and a susceptibility for said object to react to amnesic agents—principally protein synthesis inhibitors.<ref name=d /> Morris and colleagues’ experiment indicates that the reconsolidation hypothesis could apply to particular memory types such as allocentric spatial memory, which is either acquired slowly or rapidly. As implied by the authors, however, such an application is feasible only in the case of rapidly acquired spatial memory, the degree to which is influenced by how thoroughly a spatial object is trained.<ref name=d />