The final storage is long-term memory, which has a very large capacity and is capable of holding information possibly for a lifetime.
[2] The exact mechanisms by which this transfer takes place, whether all or only some memories are retained permanently, and even to have the existence of a genuine distinction between stores, remain controversial.
One form of evidence cited in favor of the existence of a short-term store comes from anterograde amnesia, the inability to learn new facts and episodes.
[9] Ovid Tzeng (1973) reported an instance where the recency effect in free recall did not seem to result from a short-term memory store.
[10] Koppenaal and Glanzer (1990) attempted to explain these phenomena as a result of the subjects' adaptation to the distractor task, which allowed them to preserve at least some short-term memory capabilities.
[17][18] The slave systems include the phonological loop, the visuo-spatial sketchpad, and the episodic buffer (later added by Baddeley).
Within the first minutes or hours after acquisition, the engram (memory trace) is encoded within synapses, becoming resistant (though not immune) to interference from outside sources.
When you try to remember an experience, perhaps your friend's birthday party a year ago, your brain is activating a certain pattern of neurons.
This kind of remembering is the idea of retrieval because it involves recalling the specific distributed representation created during the encoding of the experience.
During waking life an executive function interprets LTM consistent with reality checking (Tarnow 2003).
Newly acquired declarative memory traces are believed to be reactivated during NonREM sleep to promote their hippocampo-neocortical transfer for long-term storage.
[27] Specifically, new declarative memories are better remembered if recall follows Stage II non-rapid eye movement sleep.
[28] Sleep deprivation reduces vigilance or arousal levels, affecting the efficiency of certain cognitive functions such as learning and memory.
Research by Meulemans and Van der Linden (2003) found that amnesiac patients with damage to the medial temporal lobe performed more poorly on explicit learning tests than did healthy controls.
According to Damien Moore and Paul D. Loprinzi, episodic memory can be improved using long-term potentiation, which is when synapses are made to be more durable with exercise.
The durability and healthiness of the synapses will in time be able to pick up more connections with neurons and eventually help with episodic memory.
The basal ganglia is believed to mediate procedural memory and other brain structures and is largely independent of the hippocampus.
Working memory holds and manipulates information for a short period of time, before it is either forgotten or encoded into LTM.
[34][50] Minor slips and lapses of memory are fairly commonplace and may increase naturally with age, when ill, or under stress.
Alzheimer's disease patients are more likely to recall the theme word as being part of the original list than healthy adults.
It is thought that Parkinson's disease is caused by degradation of the dopaminergic mesocorticolimbic projection originating from the ventral tegmental area.
[54] Schizophrenia patients have trouble with attention and executive functions, which in turn affects LTM consolidation and retrieval.
[56] This occurs within the cellular body, and concerns the particular transmitters, receptors, and new synapse pathways that reinforce the communicative strength between neurons.
The production of new proteins devoted to synapse reinforcement is triggered after the release of certain signaling substances (such as calcium within hippocampal neurons) in the cell.
In the case of hippocampal cells, this release is dependent upon the expulsion of magnesium (a binding molecule) that is expelled after significant and repetitive synaptic signaling.
The temporary expulsion of magnesium frees NMDA receptors to release calcium in the cell, a signal that leads to gene transcription and the construction of reinforcing proteins.
[59] On the molecular level, an increase of the postsynaptic scaffolding proteins PSD-95 and HOMER1c has been shown to correlate with the stabilization of synaptic enlargement.
[61] When such an exposure was experimentally applied, more than 5,000 differently methylated DNA regions appeared in the hippocampus neuronal genome of the rats at one and at 24 hours after training.
[62] These alterations in methylation pattern occurred at many genes that were down-regulated, often due to the formation of new 5-methylcytosine sites in CpG rich regions of the genome.
Instead, whether the participant actively tries to remember the item while elaborating on its meaning determines the strength of its store in LTM.