Dear Ziad

Long Term Memory can be:

a. Explicit memory :

Depends on structures of the medial temporal lobe ( including the hippocampus, entorhinal cortex and parahippocampal cortex to ) and the diencephalon . Moreover, the septum and the fiber bundles arriving from the basal forebrain to the hippocampus also appear to have important functions. Although both episodic memory and semantic structures depend on the medial temporal lobe , is important to emphasize the relationship of these structures to other . For example , elderly patients with dysfunction of the frontal lobes have more difficulty than episodic memory to semantic memory . Already lesions in the left parietal lobe have impairments in semantic memory .

b . Implicit memory :

The learning of motor skills depends on cortical afferents from sensory association areas to the striatum or the basal ganglia . The caudate and putamen receive cortical projections and send them to the globus pallidus and other structures of the extrapyramidal system , providing a connection between stimulus and response . The conditioning of skeletal muscle responses depends on the cerebellum, while the conditioning of emotional responses depends on the amygdala. Changes in blood flow have been described, the raising and lowering of the cerebellum, striatum at the beginning of the acquisition process of a skill . Already during this process , the flow is that the striatum was increased . The neo - striatum and cerebellum are involved in the acquisition and planning of actions , therefore being through connections between the cerebellum and thalamus and between the cerebellum and the frontal lobes , links between the implicit and explicit system .

Molecular basis of memory storage

The mechanism used for the storage of memories in living beings not yet known . Studies indicate LTP ( long - term potential ) or potential long term as the leading candidate for such a mechanism . LTP has been discovered by Tim Bliss and Terje Lomo in a study on the ability of synapses between hippocampal neurons of storing information . Found that a short period of high-frequency electrical activity artificially applied to a hippocampal pathway produced an increase in synaptic effectiveness . This type of facilitation is what we call LTP . The mechanisms for the induction of LTP can be associative or non- associative types .

LTP has several characteristics that make it a very suitable candidate for the mechanism of long-term storage . First occurs in each of the three main routes by which the information flows in the hippocampus : a perforante route, via mossy fibers and via the Schaffer collaterals . Second , it is rapidly induced and, finally , after being induced stable. This allows the conclusion that LTP presents characteristics of the process of memory itself , or may be formed quickly in the appropriate synapses and lasts for a long time . Remember that despite the LTP have characteristics in common with an ideal memory process , you can not prove it to be the mechanism for memory storage .

Referrals:

-Lent, R. Cem Bilhões de Neurônios-conceitos fundamentais em neurociência, Ed. Atheneu 2005

- Machado, A. Neuroanatomia Funcional, Ed. Atheneu 2006

Mathematical Models of Human Memory

Jeroen GW Raaijmakers

01/2008; In book: Cognitive Psychology of Memory. Vol. 2 of Learning and Memory: A Comprehensive Reference, Chapter: 25, Publisher: Elsevier, pp.445-466.

Dear Ziad

Long Term Memory can be:

a. Explicit memory :

Depends on structures of the medial temporal lobe ( including the hippocampus, entorhinal cortex and parahippocampal cortex to ) and the diencephalon . Moreover, the septum and the fiber bundles arriving from the basal forebrain to the hippocampus also appear to have important functions. Although both episodic memory and semantic structures depend on the medial temporal lobe , is important to emphasize the relationship of these structures to other . For example , elderly patients with dysfunction of the frontal lobes have more difficulty than episodic memory to semantic memory . Already lesions in the left parietal lobe have impairments in semantic memory .

b . Implicit memory :

The learning of motor skills depends on cortical afferents from sensory association areas to the striatum or the basal ganglia . The caudate and putamen receive cortical projections and send them to the globus pallidus and other structures of the extrapyramidal system , providing a connection between stimulus and response . The conditioning of skeletal muscle responses depends on the cerebellum, while the conditioning of emotional responses depends on the amygdala. Changes in blood flow have been described, the raising and lowering of the cerebellum, striatum at the beginning of the acquisition process of a skill . Already during this process , the flow is that the striatum was increased . The neo - striatum and cerebellum are involved in the acquisition and planning of actions , therefore being through connections between the cerebellum and thalamus and between the cerebellum and the frontal lobes , links between the implicit and explicit system .

Molecular basis of memory storage

The mechanism used for the storage of memories in living beings not yet known . Studies indicate LTP ( long - term potential ) or potential long term as the leading candidate for such a mechanism . LTP has been discovered by Tim Bliss and Terje Lomo in a study on the ability of synapses between hippocampal neurons of storing information . Found that a short period of high-frequency electrical activity artificially applied to a hippocampal pathway produced an increase in synaptic effectiveness . This type of facilitation is what we call LTP . The mechanisms for the induction of LTP can be associative or non- associative types .

LTP has several characteristics that make it a very suitable candidate for the mechanism of long-term storage . First occurs in each of the three main routes by which the information flows in the hippocampus : a perforante route, via mossy fibers and via the Schaffer collaterals . Second , it is rapidly induced and, finally , after being induced stable. This allows the conclusion that LTP presents characteristics of the process of memory itself , or may be formed quickly in the appropriate synapses and lasts for a long time . Remember that despite the LTP have characteristics in common with an ideal memory process , you can not prove it to be the mechanism for memory storage .

Referrals:

-Lent, R. Cem Bilhões de Neurônios-conceitos fundamentais em neurociência, Ed. Atheneu 2005

- Machado, A. Neuroanatomia Funcional, Ed. Atheneu 2006

Hi Ziad,

I did some research on that topic last year, but I am not a professional. Therefore, I keep it short and simple.

What I basically found was that new neurons are generated by neurogenesis (even in adult brains), their connections can be strengthened by a process called LTP (basically building more postsynaptic-receptors to receive signals and also causing the sending synapse to grow) and that these connections can be reduced by a process called LTD. The connections are working with electric potential whereas the neurons receive chemical signals.

I cannot find the source anymore, but I also read that during sleep short term memories are converted from an electric format into chemical long-term memories.

I hope that helps,

Jaqueline

Thanks Nelson for this elaborate discussion.

Thank you for your comments - For me, a major difficulty remaining reside in the plurality of the terms employed for a given form of memory. Often, different terms designate the same type of memory. As an exemple: Explicit memory & Implicit memory - what is correspondence of these terms with declarative memory & procedurale memory......

We are at a step where a clarification is absolutely necessary. A lot of time is constantly lost, just to define what are saying the authors.

R.C

Storage in memory is the more or less passive process of retaining information in the brain, whether in the sensory memory, the short-term memory or the more permanent long-term memory. Each of these different stages of human memory functions as a of filter helping to protect the human brain from an overflow of information. Humans are confronted with overflow conditions on a daily basis hence, to avoid overloads of information helps us to keep sane. The more information is repeated or used, the more likely it is to be retained in our long-term memory.

Since the early neurological work of Karl Lashley and Wilder Penfield in the 1950s and 1960s, it has become clear that long-term memories are not stored in just one part of the brain, but are distributed over the cortex. After consolidation, long-term memories are stored over the brain as groups of neurons primed to fire together in the same pattern that created the original experience. Each component of a memory is stored in the brain area that initiated it (e.g. groups of neurons in the visual cortex store a view, neurons in the amygdala store the associated emotion, etc).

It seems that they may even be encoded redundantly, hence several times, in various parts of the cortex, so that, if one memory trace (engram) is wiped out, duplicates (backups), or alternative pathways, elsewhere, are still available in memory and can still be retrieved.

Therefore, contrary to a popular notion, memories are not stored in our brains like books on library shelves, but must actively be reconstructed from elements scattered around in various brain areas by the encoding process. Memory storage is therefore an ongoing process of reclassification (defragmentation in ICT terminology) as a result of continuous changes in our neural pathways, and parallel processing of information in several brain partitions.

There are indications that in the absence of disorders due to trauma or neurological disease, the human brain has the capacity to store (almost) unlimited pieces of information indefinitely. The process of forgetting, therefore, is most likely the result of incorrect or incompletely encoded memory partitions. A common experience is that when we try to remember something once and then fail. However, We often manage to remember the same item later on. The information was therefore clearly still in storage. However, some kind of a mismatch can occur (temporarily) between a retrieval process and the original encoding of the information.

Having said that, though, it seems unlikely that, all information is stored somewhere in the brain, and that it is only in the retrieval process that irrelevant details are “forwarded” over or “purged”. It seems more likely that the information which is stored is in some way edited and sorted. Additionally some of the peripheral details are not stored.

Forgetting, then, is perhaps better thought of as the temporary or permanent inability to retrieve a piece of information that has previously been recorded in the brain. Forgetting typically follows a logarithmic curve. Hence, information loss occurs quite rapid at the start, but becomes slower as time goes on. In particular, information that has been imprinted persistently (like with studying, names, facts, foreign-language vocabulary, etc), will usually be very resistant to forgetting, especially after the first three years of storage. Unlike amnesia, forgetting is usually regarded as a normal phenomenon involving specific pieces of information, rather than relatively broad categories of information.

There is still disagreement over exactly what becomes of the material that is forgotten. Some state that long-term memory does actually decay and disappear completely over time. Others state that a memory trace remains intact as long as we live, but the bonds or cues that allow us to retrieve the trace become broken, due to changes in the organization of our neural network by new experiences, etc. Somewhat comparable as a misplaced book in an immense library is “lost” even though it still exists somewhere in the library, but cannot be found. Of course the book is a physical object. Question is, how do we have to imagine us that book in the human brain? As a set of membrane electro-magnetic potentials, or pH or ion gradients? Who has a clue?

Interestingly, it appears not to be possible to deliberately delete memories at will, which can have negative consequences. For example if we experience traumatic events we would actually prefer to forget these events. In fact, such memories tend to be imprinted even more strongly than normal due to their strong emotional content, although recent research involving the use of beta blockers (such as propanonol) suggests that it may be possible to tune down the emotional aspects of such stored trauma’s , even if the trauma itself cannot be erased. The way this works is that the act of recalling the stored trauma, makes the person with the stored trauma go though the experience once more, as it were during the initial encoding phase. The re-storage can then be blocked by drugs which inhibit the proteins enabling emotional memory to re-save. Hence the emotional connotation is weakened.

Without a doubt, we are just starting to understand the fundamental mechanisms of the brein including its storage mechanisms. I figger that only 1 % of the knowledge is more or less acquired, Hopefully in a well organised library;-)

Cheers,

Frank

Thank you Jaqueline, Raymond, and Frank for your valuable contribution to this question.

Zaid,, you might take a look at the chapter "Learning, Imagery, Tokens, and Types: The Synaptic Matrix" on my RG page. This is a chapter in *The Cognitive Brain* that deals with the basic mechanism for establishing long-term memory in the brain.

One of the storage mechanisms of memory traces may be changes in the DNA. Upon stimulation of neurons in the nucleus occur permanent changes in the distribution of genes:

A. Walczak et al.: Novel Higher-Order Epigenetic Regulation of the Bdnf Gene upon Seizures. Journal of Neuroscience, 2013; 33 (6): 2507

DOI: 10.1523/JNEUROSCI.1085-12.2013

http://dx.doi.org/10.1523/JNEUROSCI.1085-12.2013

Many thanks Arnold!

Many thanks Mariusz!

In our lab, we examine the biological basis of memory. In particular, we study transcription factors (TF), which are specialized proteins, that are responsible for regulating gene expression or repression. Our focus has been on NF-kB, CREB, and Egr, all shown to play critical roles in synaptic plasticity and long term memory. Other families of TF play a role in memory as well, such as AP-1 and C\EBP.

It would be nice if somebody would like to put down a rationale organization of the term employed to designate differents forms of memory.

Thank you - RC

I'll have a go at telling you something about human memory from the perspective of Neuropsychology.

The distinction between implicit and explicit memory was based on clinical findings that patients with amnesia (resulting from localised damage within Papez circuit: hippocampus, thalamus, mamillothalamic tract) were unable to recall or recognise salient event information but could nevertheless show evidence of learning when assessed using methods that did not require conscious access to the contents. The famous case of Henry M (studied by Milner and Corkin in Montreal) is one example of the amnesic syndrome. On one example of implicit learning he showed that he had acquired of the skill of mirror writing but never knew he had done the task and did not recognise the equipment that he had been using. While skill acquisition is one well documented example of implicit memory, the term subsumes a wide range of memory processes. These range from motor skills to eye-blink conditioning, facilitation of reading in unfamiliar texts, speeded identification of specific degraded words, retention of solutions to complex cognitive problems and even some forms of recognition memory.

The common feature interlinking these types of memory is probably best stated in negative terms. At the psychological level, the memory is Not accessible to introspective awareness and at the neurobiological level the memory does not require the Papez circuit. But we should not be misled by the single term "implicit" to think that there is necessarily a single process or system which is responsible. There are almost certainly multiple brain systems that are involved in supporting the diverse collection of memory processes that can be retained implicitly. Why? well these same skills can often be compromised separately following damage to different areas of the brain.

By the same token there is no single type of memory involved in declarative conscious recollection. Psychologists differentiate between semantic memory (facts and culturally stable information) and episodic memory (memory for events with and without autobiographical reference). Amnesia spares the former and compromises the latter whereas some temporal cortical injuries damage semantic memory while leaving the ability to retain events and episodes intact. Some would further subdivide these broad categories -- at least in the human brain.

But that is another note for another day.

Dear All:

I would like to thank you for providing rich answers to this simple yet very intriguing question. It is very easy to go to a physiology book and read about memory, but that would limits the scope to certain classical findings that were the results of years of research. However, by allowing individuals from around the world to provide their expert opinion about the subject matter yields a rich amalgam of information that once put together will certainly add to the knowledge about human memory.

Kind regards,

Ziad

Dear Ziad,

I believe that one major obstacle to understanding memory is the artificial distinction that is made between memory and cognition.

Memory is a concept that emerges as a result of the relationship between two different information systems - language and cognition.

It is no coincidence that we only really begin to 'remember' our lives once we have language with which to structure our experiences.

Chris

Excellent point Christopher - Thank You!

Christopher, if language is required for memory, how do you explain the evidence for memory in jays and bees?

Arnold, my old fiend!

You should really read my answer. I did not say that there was no such thing as memory. I said that to make an artificial distinction between memory and cognition may stand in the way of a complete understanding.

In my view, cognition can be understood in much the same way as memory. To illustrate what I mean let us compare two different situations:-

In the first situation a subject is presented with a photograph of an unknown person with only one eye. The subject's reaction is an unsettling response to an image that breaks the normal rules of symmetry associated with the cognition of faces generally.

In the second situation the subject is presented with an image of a person that he/she recognizes - again, with only one eye.

The subject's reaction to the second image is of a similar kind but accentuated by personal recognition. When reporting their reaction afterwards a subject may say something like - "I don't remember her having only one eye." or "I remember him when he had two eyes". In either instance the subject is referring to modes of cognition - not 'memories' as they are commonly conceived.

Christopher, when you wrote "... we only really begin to 'remember' our lives once we have language with which to structure our experiences.", I thought you were claiming that language was needed for memory as commonly conceived. My mistake.

Cheers Arnold,

I should have been clearer.

PS - what did you make of the glaucoma paper?

Christopher, the notion of retina --> V1 remapping seems feasible in principle. In application, there may be unanticipated glitches. Has your idea been tested in practice?

Arnold, you have got me thinking now!

I have given some thought about what I seem to do when I navigate from one point to another.

If someone asks me, 'Do you know the way to Mark's house?', my reply is always 'Yes' and this is borne out by the fact that I can always find my way to Mark's house. But, if the truth be known, in reply to the same question, there is always a little voice inside that knows very well that I do not know the way to Mark's house!

How can both these beliefs be true? Well, if I am asked if I know the way to Mark's house the fact of the matter is that I do not have a complete map of all the twists and turns involved in the journey. However, if, at any point along the way, someone were to ask me:- 'What is the way to Mark's house?', I know the answer.

It seems that at any point along the way I can take stock of my surrounds and adopt a particular 'cognitive stance'. I can choose to 'see' my particular surrounds in terms of my destination - in this case, Mark's house.

The possibility exists, of course, that at exactly the same place I might instead be asked if I know the way to Simon's house. This time I adopt a different 'cognitive stance'. I see my surrounds in terms of another possible destination and I see things slightly differently.

It is assumed that these alternative cognitive stances are consequent upon the historical experiences of the 'journey man' - in this case, myself.

I believe that cognition consequent upon historical experience and language are sufficient to account for the phenomena of memory.

Arnold,

I will send you the up-to-date status of the glaucoma idea privately.

I am pleased at your response.

Chris

Christopher, regarding your way to Mark's house, see "Composing Behavior: Registers for Plans and Actions" on my RG page.

Will do!

One of the most difficult questions is - how potentiation of a synapse conductance can be maintained for so long time.

In this respect I find very attractive a hypothesis of prion-like proteins as the keepers of memory, which is developed by the group of Erik Kandel.

See this paper and google for others:

http://www.sciencedirect.com/science/article/pii/S0092867403010201

Excellent comment Viatcheslav!

For an additional molecular hypothesis for memory see Marx & Gilou's two-part paper on "The Molecular Basis of Memory". I will attempt to attach a PDF version of those two.

Here is the first part of "The Molecular Basis of Memory".

Many thanks Bruce - Nice articles!

Thanks very much Bruce for the two-part paper.

I would like to discuss the principal possibility of cell's loosing (eliminitaion from network) as a mechanism of long-term memory.

Here is an abstract which contains that idea:

Endogenuos mechanisms of death justified by synthetic evolution: lessons from epilepsy

Authors: Godlevsky, SL, Kresyun, VN, Muratova, TN

Odessa National Medical University, Ukraine

Objective:

To analyze the role of endogenous self-augmenting mechanisms of diseases as instrumentation for heightening of population vital potential.

Methods: evolutional comparative analysis of neurophysiologic and behavioral data

.Results:

A lethal result of serious pathogenic process prevents spreading of putative infectious diseases within a population and eliminate “weak” genotype. The endogenous mechanism of disease aggravation could play a role in survival of the

species and in further evolution. This principle is applicable to brain functioning observed during development of epileptic syndrome. Thus, anti- and proepileptic effects of antiepileptic system activation as well as dual type of action of different metabolits and drugs could be explained with regard to main principles of synthetic theory of evolution.

Being based on rational role of death, it could be supposed that rationality of brain construction and functioning is extended to cell death (apoptosis) ascribing to it an additional functional role. Such role might be contributive to memory mechanisms, which could be based on event- related loosing of neurons in the brain network. Rotational behavior could be regarded as discriminative neurophysiological and neuropharmacological instrument for distinguishing self-damaging and avoiding type of adaptive reactions.

Conclusions:

Reaching individual comprehension in the course of progressive evolution is connected with the comprehension of selfdamaging endogenous systems. Which are in charge of worsening of decompensate states and promoting death

outcome induced by powerful pathogens.

Thanks Godlevskii for your elaborate and interesting contribution to this question!

I think that neuronal activity is controlled by myelin. Memory is linked to energitation, and myelin energized neuron, see our paper "Hypothesis of an Energetic Function for Myelin" Cell Biochem Biophys (2011) 61:179–187. In myelin exist many component tipically mitochondrial, and the impressive work of Tanaka et al "Normal mitochondrial respiratory function is essential for spatial remote memory in mice." Mol Brain. 2008 Dec 16;1:21. doi: 10.1186/1756-6606-1-21, eimostre that long term memory is linked to mitochondrial DNA. I think that our attention must be converted to myelin for new findings about memory. See our web site www.biochemlab.it

I like how the late Gerald Maurice Edelman put it:

"Every act of perception is to some degree an act of creation and every act of memory is to some degree an act of imagination."

http://books.google.com.au/books?id=lV2FG-NlAYcC&pg=PA56&lpg=PA56&dq=gerald+edelman+every+act+of+memory+is&source=bl&ots=Fga4qAmd23&sig=dAtyopuucOW5ceuqMg1fYJbbko0&hl=en&sa=X&ei=j6x9U6mKOpLp8AXNl4HQCQ&ved=0CDkQ6AEwAg#v=onepage&q=gerald%20edelman%20every%20act%20of%20memory%20is&f=false

Dear Alessandro: Many thanks for sharing with us your interesting ideas and references.

Dear Paul:

Thanks for your comment and for your reference on The Brain!

I am a follower of BB Murdock, Baddeley, Craik, Lockhart and a couple of other researchers.

Two notes: memory is an ability or cognitive trait if you like and a retrieved representation is always phenomenological. This is so becuase what we remember are earlier perceptions of events, not the events as such.

We do not remember synapses or cell assemblages. It is obvious that the brain is involved, but in a discussion of such an important human capacity I would prefer if we are clear about what we mean when we use the word "memory".

Many problems regarding the conceptual analysis of memory stems from the computer models introduced in the 60s and 70s. An interesting note regarding the now popular "memory systems theory" is that followers to that paradigm often defines episodic memory as the ability to remember what you had for breakfast: however, to my knowledge no test exists including a question regarding such events. It is also ironic that most people probably had almost exactly the same breakfast this morning as they had the last month, i.e. they only have to check their "semantic memory" regarding their eating habits in order to produce a correct answer. One more irony: habits are most often regarded as belonging to even one more so called "system".

Regarding our own research using alleged "semantic memory" and "episodic memory tests" shows that performance in the tests are always highly correlated.

It is really premature to postulats different memory systems in the brain, and I would say that it has be premature several decades by now.

Should be "assemblies" not assemblages...Funny word processor here...

Welcome aboard Sven-Erik and thank you for your nice contribution to this question.

Ziad O. Abu-Faraj Sven-Erik Fernaeus Paul H Mason Godlevsky L. John Boswell

In genoa in our laboratory we have discovered that the myelin sheath generates the axon and speeds up the CAP. This role greatly simplifies the chemical-physical modalities in the passage from the non-myelinated nerve to the myelinated one. In fact these chemical-physical mechanisms remain unaltered in the passage. We express this concept in our preprint:

Article The Myelin cannot change the basic mechanisms of axonal cond...

Interesting. Note, I have only published theee studies (long ago) on white matter lesions.

We are now doing reanalysis of automatic retrieval related to wmh and Hypoperfusion.

Best regards,

S-E

Well, dear Sven-Erik Fernaeus,

I'm very glad you are considering these novelties. The new vision that emerges is that an injury to white matter precedes axon degeneration. The basic work that demonstrates this is the attached one: "Axon Conduction and Survival in CNS White Matter During Energy Deprivation: A Developmental Study "Fern et al, J. Neurophysiol., 79: 95-105, 1998 I will also tell you that these ours are no longer hypotheses but reality emerged from rigorous 12-year laboratory experiences with numerous papers on this topic. And I will tell you that the world scientific establishment rejects these innovations and I find this unscientific. Given that our vision introduces a radical change, it is the duty of the neurobiologists to verify our data. There is a paper that would deny our vision but only on a theoretical basis (see "Is myelin a mitochondrion?"Journal of Cerebral Blood Flow & Metabolism 2013, 33, 33–36) and we replied with the article "Hypothesis of lipid-phase-continuity proton transfer for aerobic

ATP synthesis" Journal of Cerebral Blood Flow & Metabolism 2013, 33, 1838–1842 , but to deny what we discovered the first article is mentioned and not our counter-reply. I hope in your lab. take this new vision into consideration and set up experiments in the light of these news. I am very interested in your opinion on these ideas. With my best,

Sandro

Very interesting discussion! I just want to point out that psychology allocates many different types of memory based on different criteria: modality, timing, etc. Therefore, tests have been developed to evaluate many types of memory: visual, auditory, tactile; visual, auditory, tactile; operational (working), short-term and long-term memory; emotional memory, motor memory, verbal memory. Although they have analogous brain mechanisms, they are organized and manifest in a specific way because they are related to different types of perceptions (information). Although familiar to science, the memory system remains one of the most complex, since without memory there is no thinking, no perception, no conscious life.

Best regards.