Memory consolidation
The second process is systems consolidation, occurring on a much larger scale in the brain, rendering hippocampus-dependent memories independent of the hippocampus over a period of weeks to years.
He noted the "curious fact... that the interval of a single night will greatly increase the strength of the memory," and presented the possibility that "... the power of recollection .. undergoes a process of ripening and maturing during the time which intervenes."
This idea was elaborated on by William H. Burnham a few years later in a paper on amnesia integrating findings from experimental psychology and neurology.
Coining of the term "consolidation" is credited to the German researchers Müller and Alfons Pilzecker who rediscovered the concept that memory takes time to fixate or undergo "Konsolidierung" in their studies conducted between 1892 and 1900.
After Molaison underwent a bilateral medial temporal lobe resection to alleviate epileptic symptoms the patient began to suffer from memory impairments.
Molaison lost the ability to encode and consolidate newly learned information leading researchers to conclude the medial temporal lobe (MTL) was an important structure involved in this process.
[6] These studies were accompanied by the creation of animal models of human amnesia in an effort to identify brain substrates critical for slow consolidation.
Meanwhile, neuropharmacological studies of selected brain areas began to shed light on the molecules possibly responsible for fast consolidation.
[1] LTP can be thought of as the prolonged strengthening of synaptic transmission,[10] and is known to produce increases in the neurotransmitter production and receptor sensitivity, lasting minutes to even days.
LTP is also considered to be an important mechanism in terms of maintaining memories within brain regions,[11] and therefore is thought to be involved in learning.
[10] There is compelling evidence that LTP is critical for Pavlovian fear conditioning in rats suggesting that it mediates learning and memory in mammals.
[18] The standard model of systems consolidation has been summarized by Squire and Alvarez (1995);[19] it states that when novel information is originally encoded and registered, memory of these new stimuli becomes retained in both the hippocampus and cortical regions.
Squire and Alvarez took the temporally graded nature of patients with retrograde amnesia as support for the notion that once a connection has been established within the neocortex the hippocampus is no longer required, but this process is dynamic and extends for several years.
[21] An important point they make while interpreting the results is that activation in the hippocampus was equally as strong regardless of the fact that the memories recalled were as old as 45 years prior to the date of the experiment.
[21] Haist, Gore, and Mao, sought to examine the temporal nature of consolidation within the hippocampus to test MTT against the standard view.
[22] Finally, they state that the initial interview in the scanner acted as an encoding event as such differences between recent and remote memories would be obscured.
[21] Nadel and Moscovitch argue that these retained memories have lost the richness of experience and exist as depersonalized events that have been semanticized over time.
[23] The amygdala, specifically the basolateral region (BLA) is involved in the encoding of significant experiences and has been directly linked to memorable events.
[24] Studies by Gold and van Buskirk provided initial evidence for this relationship when they showed that injections of epinephrine into subjects following a training period resulted in greater long-term retention of task related memories.
[5] This relationship was studied by Packard and Chen who found that when glutamate was administered to the hippocampus, enhanced consolidation was seen during food-rewarded maze tasks.
[5] Rapid eye movement (REM) sleep has been thought of to be an important concept in the overnight learning in humans by establishing information in the hippocampal and cortical regions of the brain.
[37][38] Zif268 is an Immediate early gene (IEG) thought to be involved in neuroplasticity by an up-regulation of the transcription factor during REM sleep after pre-exposure to an enriched environment.
[10] It is believed that post-retrieval stabilization is different and distinct from consolidation, despite its overlap in function (e.g. storage) and its mechanisms (e.g. protein synthesis).
[3] Nader, Schafe, and Le Doux (2000) demonstrated that the reconsolidation process may make memories more malleable than previously believed.
[41] Following the same method that Nader and his associates used, Brunet induced anxiety responses in the patients by having them listen to a 30 second recording describing the circumstances of their traumatic experiences.
The patients were shortly thereafter injected with propranolol, a drug that blocks stress hormone receptors in the amygdala which is implicated in neurologically representing the emotional content of memories.
Under this possibility, traditional disruptions of reconsolidation might actually maintain the original memory trace but preventing the consolidation of extinction learning.
It is also useful to show that the behavioral measure used to assess disruption of memory is not just due to task impairment caused by the procedure, which can be demonstrated by testing control groups in absence of the original learning.
Both consolidation and reconsolidation can be disrupted by pharmacological agents (e.g. the protein synthesis inhibitor anisomycin) and both require the transcription factor CREB.
[51][52][53][54][55] Three of these groups have proposed that the wide variety of different psychotherapies produce permanent change in clients to the extent that they manage to activate this same neurobiological mechanism of reconsolidation in a way that leads to deconsolidation.
