Long-term memory
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Long-term memory (LTM) is memory in which associations among items are stored, as part of the theory of a dual-store memory model. The division of long term and short term memory has been supported by several double dissociation experiments.[1] According to the theory, long-term memory differs structurally and functionally from sensory memory, working memory, short-term memory, and intermediate-term memory. While short-term and working memories persist for only about 20 to 30 seconds, information can remain in intermediate-term memory for 5 to 8 hours, and in long-term memory indefinitely. This differs from the theory of the single-store retrieved context model that has no differentiation between short-term and long-term memory. Long term memory is an important aspect of cognition. LTM can be divided into three processes: encoding, storage, and retrieval.[1] Encoding of long-term memory occurs in the medial temporal lobe, and damage to the medial temporal lobe is known to cause anterograde amnesia.[2]
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Dual-store memory model[edit]
According to Miller, whose paper in 1956 popularized the theory of the “magic number seven”, short-term memory is limited to a certain number of chunks of information, while long-term memory has a limitless store.[3]
According to the Atkinson–Shiffrin memory model, a dual-store memory model set forth by Atkinson and Shiffrin in 1968, memories can reside in the short-term “buffer” for a limited time while they are simultaneously strengthening their associations in long-term memory. When items are first presented, they enter short-term memory, but because it has limited space, as new items enter, old ones leave. However, each time an item is rehearsed while it is in short-term memory, it is also increasing its strength in long-term memory. The longer an item stays in short-term memory, the stronger the association becomes in long-term memory. In long-term store, items are recalled through retrieval cues in a two-step process. First, context is used as a cue to probabilistically select an item to be potentially recalled. Second, that item is probabilistically determined to be recalled or not.[4]
The transfer of items from short-term to long-term memory is called consolidation. Theories on consolidation are supported by concussion studies. The claim is that concussions completely knock out the working memory as well as the consolidation process, which is critical because if something interrupts this process the subject will have a very poor memory of what happened prior. One study has confirmed this theory.[5]
In 1974 Baddeley and Hitch proposed an alternative theory to the Atkinson–Shiffrin memory model: Baddeley's model of working memory. According to this theory, short-term memory is divided into different slave systems for different types of input items, and there is an executive control supervising what items enter and exit those systems.[6][7] The slave systems include the phonological loop, the visuo-spatial sketchpad, and later Baddeley added the episodic buffer.[8]
Biologically, short-term memory is a temporary potentiation of neural connections that can become long-term memory through the process of rehearsal and meaningful association. Not much is known about the underlying biological mechanisms of long-term memory, but the process of long-term potentiation, which involves a physical change in the structure of neurons, has been proposed as the mechanism by which short-term memories move into long-term storage. The time scale involved at each level of memory processing remains under investigation.
As long-term memory is subject to fading in the natural forgetting process, several recalls/retrievals of memory may be needed for long-term memories to last for years, dependent also on the depth of processing. Individual retrievals can take place in increasing intervals in accordance with the principle of spaced repetition. This can happen quite naturally through reflection or deliberate recall (also known as recapitulation), often dependent on the perceived importance of the material.
Encoding of information[edit]
Long-term memory encodes information semantically for storage, as researched by Baddeley.[9] In vision, the information needs to enter working memory before it can be stored into long-term memory. This is evidenced by the fact that the speed with which information is stored into long-term memory is determined by the amount of information that can be fit, at each step, into visual working memory.[10] In other words, the larger the capacity of working memory for certain stimuli, the faster will these materials be learned.
Sleep[edit]
Some theories consider sleep to be an important factor in establishing well-organized long-term memories. (See also sleep and learning.) Sleep plays a key function in the consolidation of new memories.[11]
According to Tarnow's theory, long-term memories are stored in dream format (reminiscent of the Penfield & Rasmussen’s findings that electrical excitations of cortex give rise to experiences similar to dreams). During waking life an executive function interprets long-term memory consistent with reality checking (Tarnow 2003). Also, that the information stored in memory, no matter how it was learned, can affect performance on a particular task without the subject being aware that this memory is being used. Newly acquired declarative memory traces are believed to be reactivated during NonREM sleep to promote their hippocampo-neocortical transfer for long-term storage.[12] Specifically new declarative memories are better remembered if recall follows Stage II non-rapid eye movement sleep. The reactivation of memories during sleep can lead to lasting synaptic changes within certain neural networks. It is the high spindle activity, low oscillation activity, and delta wave activity during NREM sleep that helps to contribute to declarative memory consolidation. In learning before sleep spindles are redistributed to neuronally active upstates within slow oscillations.[11] Sleep spindles are thought to induce synaptic changes and thereby contribute to memory consolidation during sleep. Here, we examined the role of sleep in the object-place recognition task, a task closely comparable to tasks typically applied for testing human declarative memory: It is a one-trial task, hippocampus-dependent, not stressful and can be repeated within the same animal.[13] Sleep deprivation reduces vigilance or arousal levels, affecting the efficiency of certain cognitive functions such as learning and memory.[14]
The theory that sleep benefits memory retention is not a new idea. It has been around since Ebbinghaus's experiment on forgetting in 1885. More recently studies have been done by Payne and colleagues and Holtz and colleagues.[15] In Payne and colleague's[16] experiment participants were randomly selected and split into two groups. Both groups were given semantically related or unrelated word pairs, but one group was given the information at 9am and the other group received theirs at 9pm. Participants were then tested on the word pairs at one of three intervals 30 minutes, 12 hours, or 24 hours later. It was found that participants who had a period of sleep between the learning and testing sessions did better on the memory tests. This information is similar to other results found by previous experiments by Jenkins and Dallenbach (1924). It has also been found that many domains of declarative memory are affected by sleep such as emotional memory, semantic memory, and direct encoding.[16]
Holtz[15] found that not only does sleep affect consolidation of declarative memories, but also procedural memories. In this experiment fifty adolescent participants were taught either word pairs (which represents declarative memory) and a finger taping task(procedural memory at one of two different times of day. What they found was that the procedural finger taping task was best encoded and remembered directly before sleep, but the declarative word pairs task was better remembered and encoded if learned at 3 in the afternoon.[15]
Types of memory[edit]
The brain does not store memories in one unified structure, as might be seen in a computer's hard disk drive. Instead, different types of memory are stored in different regions of the brain.[citation needed] Long term memory is typically divided up into two major headings: declarative memory and implicit memory (or procedural memory).[17] Computer programs store information similarly, with a separate data section and code section.
- Explicit memory/Declarative memory refers to all memories that are consciously available. These are encoded by the hippocampus, entorhinal cortex, and perirhinal cortex, but consolidated and stored elsewhere. The precise location of storage is unknown, but the temporal cortex has been proposed as a likely candidate.[citation needed] Declarative memory also has two major subdivisions:
- Episodic memory refers to memory for specific events in time, as well as supporting their formation and retrieval. Some examples of episodic memory would be remembering someone's name and what happened at your last interaction with each other.[18][1] Experiments conducted by Spaniol and colleagues indicated that older adults have worse episodic memories than younger adults because episodic memory requires context dependent memory.[19]
- Semantic memory refers to knowledge about factual information, such as the meaning of words. Semantic memory is independent information such as information remembered for a test.[1] In contrast with episodic memory older adults and younger adults do not show much of a difference with semantic memory, presumably because semantic memory does not depend on context memory.[19]
- Implicit memory/Procedural memory refers to the use of objects or movements of the body, such as how exactly to use a pencil, drive a car, or ride a bicycle. This type of memory is encoded and it is presumed stored by the cerebellum and the striatum.[citation needed] The basal ganglia is believed to mediate procedural memory and other brain structures and is largely independent of the hippocampus.Procedural memory is considered non-declarative memory or unconscious memory which includes priming and non-associative learning.[1][20]
There are various other categorizations of memory and types of memory that have captured research interest. Prospective memory (its complement: retrospective memory) is an example.
Emotional memory, the memory for events that evoke a particularly strong emotion, is another. Emotion and memory is a domain that can involve both declarative and procedural memory processes. Emotional memories are consciously available, but elicit a powerful, unconscious physiological reaction. They also have a unique physiological pathway that involves strong connections from the amygdala into the prefrontal cortex, but much weaker connections running back from the prefrontal cortex to the amygdala.[citation needed]
Working memory is not part of long term memory, but is important for long term memory to function. Working memory holds and manipulates information for a short period of time, before it is either forgotten or encoded into long term memory. Then, in order to remember something from long term memory, it must be brought back into working memory. If working memory is overloaded it can affect the encoding of long term memory. If one has a good working memory they may have a better long term memory encoding.[21][22]
Disorders of memory[edit]
Minor everyday slips and lapses of memory are fairly commonplace, and may increase naturally with age, when ill, or when under stress.[23] Some women may experience more memory lapses following the onset of the menopause.[citation needed] In general, more serious problems with memory occur due to traumatic brain injury or neurodegenerative disease.
Everyday memory problems[edit]
The everyday experience of memory problems is the problem of failed recall, forgetting. The tip-of-the-tongue phenomenon is particularly frustrating because the person trying to remember feels that the memory is available. Failing to remember something in the situation in which it would have been useful leads to regret.
Traumatic brain injury[edit]
The majority of findings about memory have been the result of studies that lesioned specific brain regions in rats or primates, but some of the most important work has been the result of accidental or inadvertent brain trauma. The most famous case in recent memory studies is the case study of HM, who had parts of his hippocampus, parahippocampal cortices, and surrounding tissue removed in an attempt to cure his epilepsy. His subsequent total anterograde amnesia and partial retrograde amnesia provided the first evidence for the localization of memory function, and further clarified the differences between declarative and procedural memory.
Neurodegenerative diseases[edit]
Many neurodegenerative diseases can cause memory loss. Some of the most prevalent (and, as a consequence, most intensely researched) include Alzheimer's Disease, Dementia, Huntington's Disease, Multiple Sclerosis, Parkinson's Disease, and Schizophrenia. None act specifically on memory; instead, memory loss is often a casualty of generalized neuronal deterioration. Currently, these illnesses are irreversible, but research into stem cells, psychopharmacology, and genetic engineering holds much promise.
Those with Alzheimer's disease generally display symptoms such as getting momentarily lost on familiar routes, placing possessions in inappropriate locations and distortions of existing memories or completely forgetting memories. Researchers have often used the Deese–Roediger–McDermott paradigm (DRM) to study the effects of Alzheimer's disease on memory. The DRM paradigm presents a list of words such as doze, pillow, bed, dream, nap, etc., with a theme word that is not presented. In this case the theme word would have been sleep. Alzheimer's disease patients are more likely to recall the theme word as being part of the original list than healthy adults. There is a possible link between longer encoding time and increased false memory in LTM. The patients end up relying on the gist of information instead of the specific words themselves.[24] Alzheimer's leads to an uncontrolled inflammatory response brought on by extensive amyloid depostion in the brain, which leads to cell death in the brain. This gets worse over time and eventually leads to cognitive decline, after the loss of memory. Pioglitazone may improve cognitive impairments, including memory loss and may help protect long-term and visiospatial memory from neurodegenerative disease.[25]
Parkinson's disease patients have problems with cognitive performance; these issues resemble what is seen in frontal lobe patients and can often lead to dementia. It is thought that Parkinson's disease is caused by degradation of the dopaminergic mesocorticolimbic projection originating from the ventral tegmental area. It has also been indicated that the hippocampus plays an important role in episodic and spatial (parts of LTM) memory and Parkinson’s disease patients have abnormal hippocampuses resulting in abnormal functioning of LTM. L-dopa injections are often used to try to relieve Parkinson's disease symptoms as well as behavioral therapy.[26]
Schizophrenia patients have trouble with attention and executive functions which in turn affects long term memory consolidation and retrieval. They cannot encode or retrieve temporal information properly, which causes them to select inappropriate social behaviors. They cannot effectively use the information they possess. The prefrontal cortex, where schizophrenia patients have structural abnormalities, is involved with the temporal lobe and also affects the hippocampus, which causes their difficulty in encoding and retrieving temporal information (including long term memory). Schizophrenia patients are very hard to treat. Their symptoms can be controlled with medication, but as many schizophrenics are paranoid, they believe the medication is to hurt them not help them[27]
Biological underpinnings at the cellular level[edit]
Long-term memory, unlike short-term memory, is dependent upon the construction of new proteins.[28] This occurs within the cellular body, and concerns in 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.[29] For more information, see long-term potentiation (LTP).
One of the newly synthesized proteins in LTP is also critical for maintaining long-term memory. This protein is an autonomously active form of the enzyme protein kinase C (PKC), known as PKMζ. PKMζ maintains the activity-dependent enhancement of synaptic strength and inhibiting PKMζ erases established long-term memories, without affecting short-term memory or, once the inhibitor is eliminated, the ability to encode and store new long-term memories is restored.
Also, BDNF is important for the persistence of long-term memories.[30]
Contradictory evidence[edit]
A couple of studies have had results that contradict the dual-store memory model. Studies showed that in spite of using distractors, there was still both a recency effect for a list of items[31] and a contiguity effect.[32]
Another study revealed that how long an item spends in short-term memory is not the key determinant in its strength in long-term memory. Instead, whether the participant actively tries to remember the item while elaborating on its meaning determines the strength of its store in long-term memory.[33]
Single-store memory model[edit]
An alternative theory is that there is only one memory store with associations among items and their contexts. In this model, the context serves as a cue for retrieval, and the recency effect is greatly caused by the factor of context. Immediate and delayed free-recall will have the same recency effect because the relative similarity of the contexts still exist. Also, the contiguity effect still occurs because contiguity also exists between similar contexts.[34]
See also[edit]
Footnotes[edit]
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- ^ Axmacher, N.; Cohen, M. X.; Fell, J.; Haupt, S.; Dümpelmann, M.; Elger, C. E.; Schlaepfer, T. E.; Lenartz, D. et al. (2010). "Intracranial EEG Correlates of Expectancy and Memory Formation in the Human Hippocampus and Nucleus Accumbens". Neuron 65 (4): 541–549. doi:10.1016/j.neuron.2010.02.006. PMID 20188658.
- ^ Miller, George A. (1956). "The magical number seven, plus or minus two: some limits on our capacity for processing information". Psychological Review 63 (2): 81–97. doi:10.1037/h0043158. PMID 13310704.
- ^ Atkinson, R.C.; Shiffrin, R.M. (1968). "Chapter: Human memory: A proposed system and its control processes". The psychology of learning and motivation 2: 89–195.
- ^ Carlson, N., Buskist, W., Heth, C., & Schmatlz, R. (2009). Psychology: The Science of Behaviour 4th Canadian Edition
- ^ Baddeley, A.D. (1966). "The influence of acoustic and semantic similarity on long-term memory for word sequences". The Quarterly Journal of Experimental Psychology 18 (4): 302–309. doi:10.1080/14640746608400047. PMID 5956072.
- ^ Baddeley, A.D.; Hitch, G.J.L (1974). "Working Memory". Q J Exp Psychol 18 (4): 302–9. doi:10.1080/14640746608400047. PMID 5956072.
- ^ Baddeley A (November 2000). "The episodic buffer: a new component of working memory?". Trends Cogn. Sci. (Regul. Ed.) 4 (11): 417–423. doi:10.1016/S1364-6613(00)01538-2. PMID 11058819.
- ^ Baddeley, A. D. (1966). The influence of acoustic and semantic similarity on long-term memory for word sequences. The Quarterly Journal of Experimental Psychology, 18, 302–309.
- ^ Nikolić, D. and Singer, W. (2007) Creation of visual long-term memory. Perception & Psychophysics, 69: 904–912.
- ^ a b Ruch, S., Markes, O., Duss, B. S., Oppliger, D. Reber, P. T., Koenig, T., Mathis, J., Roth, C., Henke, K.(2012). Sleep stage II contributes to the consolidation of declarative memories. Neuropsychologia, 50(2012), 2389–2396
- ^ Bergmann,, T. O.; Molle, M., Diedrichs, J., Born, J., & Siebner, H. R. (1). "Newly acquired declarative memory traces are believed to be reactivated during NonREM sleep to promote their hippocampo-neocortical transfer for long-term storage.". NeuroImage 59 (3): 2733–2742. doi:10.1016/j.neuroimage.2011.10.036.
- ^ Binder, S; Baier P, Mölle M, Inostroza M, Born J, Marshall L. (February 2012). "Sleep enhances memory consolidation in the hippocampus-dependent object-place recognition task in rats.". Neurobiology Of Learning And Memory 2 (97): 213–219. doi:10.1016/j.nlm.2011.12.004.
- ^ Martella,, D.,; Plaza, V., Estévez, A. F., Castillo, A., & Fuentes, L. J. (2012). "Minimizing sleep deprivation effects in healthy adults by differential outcomes". Acta Psychologica 139 (2): 391–396. doi:10.1016/j.actpsy.2011.12.013.
- ^ a b c Holz, J., Piosczyk, H., Landnann, N., Feige, B., Spiegelhalden, K., Riemann, D., Nissen, C., Voderholzer, V.(2012). The timing of learning before night-time sleep differentiall affects declarative and procedural long-term memory consolidation in adolescents. PLoS ONE, 7(7), 1–10.
- ^ a b Payne, D. J., Tucker, A. M., Ellenbogen, M. J., Wamsley, J. E., Walker, P. M., Schacter, L. D., Stickglod, R. (2012). Memory for semantically related and unrelated declarative information: the benefit of sleep, the cost of wake. PLoS One, 7(3), 1–8, DOI: 10.1371/journal.pone.0033079.
- ^ "THE BRAIN FROM TOP TO BOTTOM".
- ^ Ranganath, C. C., Michael, B.X., Craig, J.B. (2005).Working Memory Maintenance Contributes to Long-term Memory Formation: Neural and Behavioral Evidence. Journal of Cognitive Neuroscience, 17(7), 994–1010.
- ^ a b Spaniol, J., Madden, D. J., Voss, A. (2006). A Diffusion Model Analysis of Adult Age Differences in Episodic and Semantic Long–Term Memory Retrieval. Journal of Experimental Psychology: Learning, Memory, and Cognition, 32(1), 101–117, DOI: 10.1037/0278-7393.32.1.101
- ^ Holz, J., Piosczyk, H., Landnann, N., Feige, B., Spiegelhalden, K., Riemann, D., Nissen, C., Voderholzer, V.(2012). PLoS ONE, 7(7), 1–10
- ^ Ranganath, C. C., Michael, B.X., Craig, J.B. (2005)Working Memory Maintenance Contributes to Long-term Memory Formation: Neural and Behavioral Evidence. Journal of Cognitive Neuroscience, 17(7), 994–1010
- ^ Axmacher, N., Haupt, S., Cohen, M. X., Elger, C. F., Fell, J. (2010). Electrophysiological signature of working and long-term memory interaction in the human hippocampus. European Journal of Neuroscience, 31(1), 101–117. DOI: 10.1111/j.1460-9568.2009.07041.x
- ^ Reason, J. (1995) Self-report questionnaires in cognitive psychology: have they delivered the goods? in Attention: Selection, Awareness, and Control (Eds.) Alan Baddeley & Lawrence Weiskrantz
- ^ MacDuffie, E. K., Atkins, S. A., Flegal, E. K., Clark, M. C., Reuter-Lorenze, A. P. (2012). Memory distortion in Alzheimer's Disease: deficient monitoring of short-and long-term memory. Neuropsychology, 26(4), 509–516. DOI: 10.1037/a0028684
- ^ Gupta,R.,Gupta,K.L.(2012). Improvement in long-term and visuo-spatial memory following chronic pioglitazone in mouse model of Alzheimer's disease. Pharmacology, Biochemistry, and Behavior, 102 (2012), 184–190
- ^ Costa,C.,Sgobio,C.,Siliqueni,S.,Tozzi,A.,Tantucci,M.,Ghiglieri,V.,Filippo,D.M.,Pendolino,V.,De lure,A.,MArti,M.,Morari,M.,Spillantini,G.M.,Latagliata,C.E.,Pascucci,T.,Puglisi-Allegra,S.,Gardioni,F.,DiLuca,M.,Picconi,B.,Calabresi,P.(2012). Mechanisms underlying the impairment of hippocampal long-term potentiation and memory in experimental Parkinson's diseaseBrain: A Journal of Neurology, 135, 1884–1899. DOI: 10.1093/brain/aws101
- ^ Langraf, S., Steingen, J., Eppert, Y., Neidermeyer, U., Elke, U., Krueger, F. (2011). Temporal Information Processing in Short- and Long-Term Memory of Patients with Schizophrenia. PLoS ONE, 6(10), 1–10. DOI: 10.1371/journal.pone.0026140
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- ^ Neihoff, Debra (2005) "The Language of Life 'How cells Communicate in Health and Disease'" Speak Memory, 210–223.
- ^ Pedro Bekinschtein, Martín Cammarota, Cynthia Katche, Leandro Slipczuk, Janine I. Rossato, Andrea Goldin, Ivan Izquierdo, and Jorge H. Medina (February 2008). "BDNF is essential to promote persistence of long-term memory storage". Proceedings of the National Academy of Sciences of the USA 105 (7): 2711–2716. doi:10.1073/pnas.0711863105. PMC 2268201. PMID 18263738.
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