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Access and decay time of long-term memory

Access and decay time of long-term memory


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As for STM (short-term memory), access time is 70 ms and decay time is 200 ms.

Is there any calculated time for LTM (long-term memory) also?

And does LTM really decay with the passage of time?


Long-Term Memory

Long-term memory (LTM) the final stage of the multi-store memory model proposed by the Atkinson-Shiffrin, providing the lasting retention of information and skills.

Theoretically, the capacity of long-term memory could be unlimited, the main constraint on recall being accessibility rather than availability.

Duration might be a few minutes or a lifetime. Suggested encoding modes are semantic (meaning) and visual (pictorial) in the main but can be acoustic also.

Using the computer analogy, the information in your LTM would be like the information you have saved on the hard drive. It isn’t there on your desktop (your short-term memory), but you can pull up this information when you want it, at least most of the time.


Odor Memory and Perception

Jacob A. Berry , Ronald L. Davis , in Progress in Brain Research , 2014

4 Forgetting is Regulated by Rac and the Cytoskeleton in the MBs

The actin cytoskeleton, a network of filamentous actin polymers and regulatory proteins, allows cells to build their fundamental shape and architecture. For neurons, the cytoskeleton is required to form axonal and dendritic processes and to form synaptic connections between neurons. Importantly, the cytoskeleton is a critical mediator of synaptic plasticity, being essential for both long-term potentiation and long-term depression ( Fifková and Delay, 1982 Matsuzaki et al., 2004 Okamoto et al., 2004 ). In order for the cytoskeletal network to function in synaptic plasticity, it must be dynamic and regulated. Dynamic regulators of the cytoskeleton include the Rho family of small GTPases that function as molecular switches by alternating between GTP-bound active forms and GDP-bound inactive forms (for review, Etienne-Manneville and Hall, 2002 ), transducing signals from extracellular stimuli to the cytoskeleton network (for review, Luo, 2000 ). The roles for these GTPases in neuronal development have been well studied, but their roles in mature neurons for learning and memory remain ill defined.

Recently, a study looking for Drosophila lines that retained aversive odor memories longer than normal animals, that is, had slower rates of forgetting, found that the small GTPase Rac, a member of the Rho family, is critically important for forgetting ( Shuai et al., 2010 ). In particular, they found that blocking Rac activity, via adult expression of a dominant-negative Rac protein, slow memory decay for aversive odor associations. Conversely, increasing activity of Rac, via adult expression of a constitutively active Rac protein, accelerates the rate of memory decay. Furthermore, modulation of Rac activity has no effect on the animal’s ability to acquire and form aversive odor memories thus, Rac activity functions specifically in forgetting. The authors also measured endogenous Rac activity in wild-type flies after learning and found that Rac activity significantly increases in the fly brain 1 h after learning before returning back to baseline levels at 3 h. This indicates that learning itself activates Rac and increases the rate of forgetting postacquisition. While the Rac protein is widely distributed throughout the adult brain, Rac activity regulates the forgetting of aversive odor memories only when manipulated within the MBs. Specifically, blocking Rac activity in a large combined population of γ and α/β KCs is required to regulate memory decay. Shuai et al. showed that, although blocking Rac activity produces a memory lasting more than 24 h, this extra memory is still labile and sensitive to cold shock. Therefore, it appears that Rac activity does not inhibit the consolidation process, but instead acts specifically to remove early labile memory after learning, similar to the dopaminergic-based forgetting mechanism.

The role of Rac in retroactive interference was assayed using the reversal learning paradigm described above. Similar to the results found for the flies lacking the DAMB receptor, when Rac activity is blocked in a reversal learning paradigm, flies have decreased retroactive interference from reversal learning. Additionally, an interference paradigm was employed where flies are conditioned to a set of odors C and D after the standard training to odors A and B (with A as a CS + and B as a CS −), and then tested with odors A and B. In this interference paradigm, the flies will first form an aversive memory to odor A, then subsequently form a new memory to odor C, and then will be tested for memory of odor A. In control animals, this new learning about odor C causes significant forgetting of the first memory to odor A. Remarkably, if Rac activity is blocked, this retroactive interference-based forgetting is completely inhibited. These data are consistent with a general role for Rac in interference-based forgetting, in addition to its role in early memory decay.

To determine whether Rac-mediated forgetting occurs through its conventional role in cytoskeleton remodeling, aversive memory decay was measured after modulating downstream targets of Rac. The accelerated forgetting that occurs in constitutively active Rac mutants was observed to be blocked if binding to Cdc42/Rac1 interactive-binding (CRIB)-motif effector proteins is eliminated by a second mutation in Rac. Thus, activated Rac must bind to CRIB-motif effectors proteins to cause forgetting of aversive odor memories. In addition, the Cofilin protein, a potent actin depolymerizing factor, is known to be regulated by Rac activity ( Bamburg, 1999 ). Flies also display enhanced memory retention similar to blocking Rac activity when expressing a mutant form of Cofilin that is independent of Rac regulation. Therefore, Rac likely mediates the forgetting of aversive odor memories by modulating cytoskeleton remodeling through a Cofilin-based mechanism.


Contents

The term "decay theory" was first coined by Edward Thorndike in his book The Psychology of Learning in 1914. [3] This simply states that if a person does not access and use the memory representation they have formed the memory trace will fade or decay over time. This theory was based on the early memory work by Hermann Ebbinghaus in the late 19th century. [4] The decay theory proposed by Thorndike was heavily criticized by McGeoch and his interference theory. [5] This led to the abandoning of the decay theory, until the late 1950s when studies by John Brown and the Petersons showed evidence of time based decay by filling the retention period by counting backwards in threes from a given number. This led to what is known as the Brown–Peterson paradigm. [6] [7] The theory was again challenged, this time a paper by Keppel and Underwood who attributed the findings to proactive interference. [8] Studies in the 1970s by Reitman [9] [10] tried reviving the decay theory by accounting for certain confounds criticized by Keppel and Underwood. Roediger quickly found problems with these studies and their methods. [11] Harris made an attempt to make a case for decay theory by using tones instead of word lists and his results are congruent making a case for decay theory. [12] In addition, McKone used implicit memory tasks as opposed to explicit tasks to address the confound problems. They provided evidence for decay theory, however, the results also interacted with interference effects. [13] [14] One of the biggest criticisms of decay theory is that it cannot be explained as a mechanism and that is the direction that the research is headed.

Researchers disagree about whether memories fade as a function of the mere passage of time (as in decay theory) or as a function of interfering succeeding events (as in interference theory). [15] Evidence tends to favor interference-related decay over temporal decay, [1] yet this varies depending on the specific memory system taken into account.

Short-term memory Edit

Within the short-term memory system, evidence favours an interference theory of forgetting, based on various researchers' manipulation of the amount of time between a participant's retention and recall stages finding little to no effect on how many items they are able to remember. [15] Looking solely at verbal short-term memory within studies that control against participants' use of rehearsal processes, a very small temporal decay effect coupled with a much larger interference decay effect can be found. [1] No evidence for temporal decay in verbal short-term memory has been found in recent studies of serial recall tasks. [1] Regarding the word-length effect in short-term memory, which states that lists of longer word are harder to recall than lists of short words, researchers argue that interference plays a larger role due to articulation duration being confounded with other word characteristics. [16]

Working memory Edit

Both theories are equally argued in working memory. One situation in which this shows considerable debate is within the complex-span task of working memory, where a complex task is alternated with the encoding of to-be-remembered items. [15] It is either argued that the amount of time taken to perform this task or the amount of interference this task involves cause decay. [15] A time-based resource-sharing model has also been proposed, stating that temporal decay occurs once attention is switched away from whatever information is to be remembered, and occupied by processing of the information. [17] This theory gives more credit to the active rehearsal of information, as refreshing items to be remembered focuses attention back on the information to be remembered in order for it to be better processed and stored in memory. [17] As processing and maintenance are both crucial components of working memory, both of these processes need to be taken into account when determining which theory of forgetting is most valid. Research also suggests that information or an event's salience, or importance, may play a key role. [18] Working memory may decay in proportion to information or an event's salience. [18] This means that if something is more meaningful to an individual, that individual may be less likely to forget it quickly.

System interaction Edit

These inconsistencies may be found due to the difficulty with conducting experiments that focus solely on the passage of time as a cause of decay, ruling out alternative explanations. [1] However, a close look at the literature regarding decay theory will reveal inconsistencies across several studies and researchers, making it difficult to pinpoint precisely which indeed plays the larger role within the various systems of memory. It could be argued that both temporal decay and interference play an equally important role in forgetting, along with motivated forgetting and retrieval failure theory.

Revisions in decay theory are being made in research today. The theory is simple and intuitive, but also problematic. Decay theory has long been rejected as a mechanism of long term forgetting. [5] Now, its place in short term forgetting is being questioned. The simplicity of the theory works against it in that supporting evidence always leaves room for alternative explanations. Researchers have had much difficulty creating experiments that can pinpoint decay as a definitive mechanism of forgetting. Current studies have always been limited in their abilities to establish decay due to confounding evidence such as attention effects or the operation of interference. [1]

Hybrid theories Edit

The future of decay theory, according to Nairne (2002), should be the development of hybrid theories that incorporate elements of the standard model while also assuming that retrieval cues play an important role in short term memory. [19] By broadening the view of this theory, it will become possible to account for the inconsistencies and problems that have been found with decay to date.

Neuronal evidence Edit

Another direction of future research is to tie decay theory to sound neurological evidence. As most current evidence for decay leaves room for alternate explanations, studies indicating a neural basis for the idea of decay will give the theory new solid support. Jonides et al. (2008) found neural evidence for decay in tests demonstrating a general decline in activation in posterior regions over a delay period. [20] Though this decline was not found to be strongly related to performance, this evidence is a starting point in making these connections between decay and neural imaging. A model proposed to support decay with neurological evidence places importance on the firing patterns of neurons over time. [20] The neuronal firing patterns that make up the target representation fall out of synchrony over time unless they are reset. The process of resetting the firing patterns can be looked at as rehearsal, and in absence of rehearsal, forgetting occurs. This proposed model needs to be tested further to gain support, and bring firm neurological evidence to the decay theory. [20]


Contents

The term "decay theory" was first coined by Edward Thorndike in his book The Psychology of Learning in 1914. Α] This simply states that if a person does not access and use the memory representation they have formed the memory trace will fade or decay over time. This theory was based on the early memory work by Hermann Ebbinghaus in the late 19th century. Β] The decay theory proposed by Thorndike was heavily criticized by McGeoch and his interference theory. Γ] This led to the abandoning of the decay theory, until the late 1950s when studies by John Brown and the Petersons showed evidence of time based decay by filling the retention period by counting backwards in threes from a given number. This led to what is known as the Brown–Peterson paradigm. Δ] Ε] The theory was again challenged, this time a paper by Keppel and Underwood who attributed the findings to proactive interference. Ζ] Studies in the 1970s by Reitman Η] ⎖] tried reviving the decay theory by accounting for certain confounds criticized by Keppel and Underwood. Roediger quickly found problems with these studies and their methods. ⎗] Harris made an attempt to make a case for decay theory by using tones instead of word lists and his results are congruent making a case for decay theory. ⎘] In addition, McKone used implicit memory tasks as opposed to explicit tasks to address the confound problems. They provided evidence for decay theory, however, the results also interacted with interference effects. ⎙] ⎚] One of the biggest criticisms of decay theory is that it cannot be explained as a mechanism and that is the direction that the research is headed.


Long-term memories are physically robust memory storage does not require sustained electrical activity

Many organisms (including humans) can retain long-term memories while surviving highly disruptive events such as temporary global ischemia (Steen et. al. 1979) or deep hypothermic circulatory arrest (DHCA) (Behringer et. al. 2003, Percy et. al. 2008). Many profound changes take place in the nervous system during these traumatic events, such as loss of the brain’s extracellular space (Thorne & Nicholson, 2006) and complete loss of electrical activity (Raichle 1983), yet long-term memories are still retained. The information of long-term memories must be stored in a durable physical/chemical form that doesn’t depend on the nervous system’s dynamic electrical activity, or else traumatic events like ischemia or DHCA would erase long-term memories.

Note: Long-term memory recall is an active process which requires electrical activity. It should not be confused with storage. Recall is disrupted during DHCA and temporary global ischemia but returns after recovery.

Key papers: (note, click the papers in boxes to expand them and review relevant quotes!)

Certain cardiovascular operations require cardiopulmonary bypass and prolonged circulatory arrest to provide an adequate operative field. Profound hypothermia is induced to protect brain function during these periods without cerebral perfusion…

…Electrocerebral silence (ECS), induced by profound hypothermia, is readily recognizable in the EEG…

…The EEG of most patients showed a characteristic evolution with progressive core hypothermia. In all patients, there was initial depression of amplitude and slowing of background rhythms. There was progressive depression of amplitude which, in 17 patients, was preceded by a period of episodic generalized voltage attenuation (suppression-burst activity). This was followed by the development of generalized, periodic, slow-wave transients. The transients were mono- or polyphasic, of moderate voltage, and of relatively long duration (up to 0.5 sec). The intervals between transients became more prolonged, and the transients became progressively less complex and more depressed in amplitude. This eventually led to the onset of ECS…

…Duration of circulatory arrest was 14-109 min (mean, 39 min). The time required for cooling to the onset of ECS was 20-107 min (mean, 41 min)…

This study presents relatively strong evidence that patients with high cognitive needs who underwent aortic surgery using DHCA (deep hypothermic circulatory arrest) experienced no perceptible cognitive change as a consequence of this procedure. This study, using a self-administered questionnaire, supplemented by a familial informant, provides direct subjective feedback by patients who underwent DHCA and their families. Our study found excellent preservation of cognitive function after surgery, according to both patient and informant responses. Although subtle deficits after DHCA might hide in individuals with less intellectually demanding professions, it is unlikely that substantive deficits could remain undetected in our high-cognitive needs group.

…High-cognitive professions were loosely defined, but were essentially limited to physicians, lawyers, doctorates, clergymen, artists, musicians, accountants, and managers…

Our results indicate that there was no significant difference in quality of work generated after surgery between patients who had DHCA and those without. This validates the initial motivation of this study, based on our clinical impression that DHCA did not seem to affect or bias patients’ postoperative performance in their work field.

Interruption of cerebral blood flow results in loss of consciousness within 10 seconds and cessation of spontaneous and evoked electrical activity within 20 seconds. Within several minutes after the loss of electrical activity there are major disruptions of normal tissue ion homeostasis. Ion-sensitive microelectrodes placed in the extracellular fluid space of the brain record a marked increase in potassium concentration and a fall in sodium and calcium concentrations…

…Steen et al recently reported that fasted dogs subjected to complete ischemia could tolerate only 8 to 9 minutes of ischemia and go on to achieve normal electrical activity…


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Procedural Memory

This relates to memories about how to do things. When we need to use motor or cognitive skills, procedural memories are automatically brought to the fore and used to correctly complete the task. Every skill we learn involves procedural memory, from playing a guitar to driving an automobile. This whole process requires no active thinking on our part. This type of long-term memory is also known as ‘implicit memory’.

Though it is a fact that skills we have practiced constantly can be performed effortlessly over time, an interesting exception occurs when great stress is placed on us. This is apparent during occasions when highly-skilled athletes make simple mistakes under pressure they would not normally make. This is also known as ‘choking’ and makes an elite athlete look like a beginner because they have momentarily forgotten how to do something they are accustomed to doing with ease.


Fluoxetine Inhibits Natural Decay of Long-Term Memory via Akt/GSK-3β Signaling

Understanding the mechanisms underlying the natural decay of long-term memory can help us find means of extending the duration of long-term memory. However, the neurobiological processes involved in the decay of long-term memory are poorly understood. In the present study, we examined the effect of acute and chronic treatment of fluoxetine on natural decay of long-term memory and the possible mechanism. Late administration of fluoxetine prolonged the persistence of long-term memory in mice, as demonstrated by object location recognition and Barnes maze tests. Fluoxetine altered Akt/glycogen synthase kinase-3β (GSK-3β)/β-catenin signaling in the hippocampus. Late short- and long-term pharmacological inhibition of GSK-3β mimicked the effect of fluoxetine on memory persistence. Pharmacological inhibition of Akt blocked the effect of fluoxetine on memory persistence. Finally, late infusion of fluoxetine increased hippocampal long-term potentiation (LTP) and pharmacological inhibition of GSK-3β blocked the natural decline in LTP. These results demonstrate that GSK-3β might be a key molecule in memory decay process, and fluoxetine extends the period of long-term memory maintenance via Akt/GSK-3β signaling.

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Footnotes

1 Another line of neural evidence about the separability of short- and long-term memory comes from electrophysiological studies of animals engaged in short-term memory tasks. We review this evidence and its interpretation in The Architecture of Unitary-Store Models section.

2 This carving up of STM processes is also consistent with recent approaches to individual differences in working memory, which characterize individual variation not in terms of variation in buffer capacity, but rather in variation in maintenance and retrieval processes (Unsworth & Engle 2007).

3 The alternative to this strong claim is that memory items outside the focus might also be supported by residual active firing. The empirical results reviewed above indicating load-dependent posterior activation might lend support to this alternative if one assumes that the memory load in those experiments was not entirely held in the focus, and that these activations exclusively index firing associated with the memory load itself.