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The research, authored by Restivo et al, examined the time course of spine formation in the hippocampus and anterior cingulate cortex following contextual fear learning in mice. Based on the widely held hypothesis that declarative memories are “formed” in the hippocampus and slowly transferred to the cortex and other structures (where they are ultimately stored), one might predict that spine density would be increased in the hippocampus soon after learning, and in the cortex only following a long delay (that is, after the memory no longer requires the hippocampus for retrieval). (Confused???). Not one to disappoint, Restivo et al showed that this is indeed the case.
More specifically, they showed increased spine growth in the hippocampus 24 hours after a single session of fear conditioning, whereas spine density in the cortex remained unchanged at this time point. Conversely, 32 days after fear conditioning, spine density was no different from pseudo-conditioned control animals in the hippocampus, but significantly increased in the cortex. When the hippocampus was lesioned immediately after conditioning, both memory and cortical spine growth were impaired. When hippocampal lesions were performed 24 days post conditioning, however, both memory and increased cortical spine density were intact, suggesting the “transfer” of the memory from hippocampus to cortex had been completed. Unfortunately, a cortical-lesion control was not performed.
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The study highlights several interesting questions in the field. For example, when does a particular memory become hippocampal-independent, and how exactly does this happen? One explanation offered by the authors is that, “top-down inhibitory control, presumably arising from cortical regions which are actively engaged in remote memory storage and retrieval” might serve to disengage the involvement of the hippocampus. An additional (and admittedly highly speculative) idea is that neuronal turnover in the hippocampus could place a time limit on the consolidation process, i.e. when neurons coding for a specific memory eventually die off or become integrated in a circuit with newborn cells, the consolidation process also ceases.
An additional question one might ask is, “if the hippocampus is so paramount for all forms of conscious memory, and animals are constantly being exposed to new events and presumably forming new memories, why the heck would one see increased spine density in the hippocampus solely after fear conditioning?” This I don’t have a good answer for, chiefly because it’s my question! But it could be that something as traumatic and rapidly acquired as fear conditioning results in enhanced plasticity in the hippocampus. Regardless, the study adds weight to the idea that the hippocampus is fundamental for transferring and consolidating memories to external structures, and even hints at part of the engram for contextual fear conditioning.
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Aug 07 2009 6:09 pm
in b4 404
Aug 24 2009 11:37 am
So was this a global increase in spine density of the cortex or did they see targeted dendritic spine density in certain areas of the cortex?