Sleep, Memory and Learning - Science topic

Interesting question. I agree with the previous response. Surely I cannot imagine how to totally separate learning from memorizing. Any improvement in the pedagogy focuses on more effective learning, but still cognitive goals are important, along with skills, psychomotor and affective.

For example it is well supported that the more you implement something, the better you learn, or memorize it.

Please go through the following RG link and PDF attachments.

Dear Adriana! There are various and sometimes conflicting opinions on the subject. Please read manuscripts in the annex to my letter.

Vladimir

Thanks!

There are a few tests out there. The most notable ones that I know of are the Corsi Block Test, which tests memorization of visuo-sptial information and sequencing. The Visual Pattern Test (or Task) does the same but without the sequencing aspect. Some research has found that the Corsi test engages different cognitive functioning than the VPT due to the absence or presence of sequencing. Another task I just read about asks the participant to compare patterns to one provided, bringing in decision-making and more executive functioning, as opposed to raw VS working memory. Personally, I'll be using the VPT, because sequencing adds another layer of cognitive processing.

Thank you Ms Nirmala

I shall definitely see these links

Asif

Dear Maria! Mr. Narendra Modi - the incumbent Indian PM sleeps 3 hours per day; the former PM of India Mrs. Indira Gandhi slept in an average 4 hours per night, so also the British PM, Margaret Thatcher. All these personalities are/were extremely energetic in their daily lives. I sleep about 4-5 hours per night and many are long sleepers like you. In a nut shell, sleep requirement varies as function of individual subject.  I remember I presented a paper at Akko entitled, "Long sleepers tend to be nondippers: Is it a paradox? Pati AK, Kar A, Sultana R, Vaidya N and Parganiha A (2009). The Third International Congress of Applied Chronobiology and Chronomedicine, Akko, Israel, May 17-22, p. 76; wherein I showed that both short sleepers and long sleepers are at the disadvantageous position. Unfortunately this work has not yet been published. Coming straight to your question a subject herself/himself can find out how much sleep is adequate for her/him. The ideal sleep length should have the minimum sleep latency and also the minimum sleep inertia along with the feeling of freshness on awakening.

I support the views of Vladimir also.

@ Nirinjini, just thinking out loud. In addition to your suggestion, would sleep deprivation protocols work out in this case? For example, disk over water method?

@ Marie, Although we are not sure about the experimental design; I wonder if these rodents have been prepared for chronic recording (e.g. surgical implantation of electrodes with head-mounted?). I am aware that head-restrained cats do sleep naturally in stereotaxic instruments for chronic recording. 

Perhaps, you could get s second opinion with Deborah Suckecki. 

I find the following very helpful: Geeraerts, Dirk (ed.). 2008. Cognitive Linguistics: Basic Readings. Berlin: de Gruyter, Mouton. (=Cognitive Linguistics Research ; 34)

From the publisher's website:

"Cognitive Linguistics: Basic Readings brings together twelve foundational articles, each of which introduces one of the basic concepts of Cognitive Linguistics, like conceptual metaphor, image schemas, mental spaces, construction grammar, prototypicality and radial sets. The collection features the founding fathers of Cognitive Linguistics: George Lakoff, Ron Langacker, Len Talmy, Gilles Fauconnier, and Charles Fillmore, together with some of the most influential younger scholars. By its choice of seminal papers and leading authors, Basic Readings is specifically suited for an introductory course in Cognitive Linguistics. This is further supported by a general introduction to the theory and, specifically, the practice of Cognitive Linguistics and by trajectories for further reading that start out from the individual chapters."

Dear Rebecca,

Very interesting question for us. We are working in normalization of the affective words originally translated by Hinojosa. Our normalization is being held in México with the affective words in spanish, we are measuring emotion-attention interference.

I am now attaching the affective-word database that we are using, the words are both, spanish and english. We built up out attention-emotion model using SuperLab, based on the Stroop effect.

Hope this can be useful.

Best regards.

Many authors differentiate between executive control and storage-related functions of WM (e.g. see Baddeley’s framework, or Jonides, Lacey & Nee, 2005) and to my impression, this distinction is quite useful and reasonable. If you quantify WM capacity with behavioral measures, I would assume that your estimate reflects a mixture of executive (attentional) and storage related processes. Hence I would say that memory capacity allows for some inferences about executive control, but there are also other factors that contribute to WM capacity. Note however that some authors (Nelson Cowan, in particular) do not make the distinction between executive control and storage processes. These authors would assume that WM capacity is a direct measure of executive control.

Hope this helps! cheers,

Tobi

I just read that PPT stimulates STN during REM sleep (Fernández-Mendoza et al., 2009) enhancing the fast (15–35 Hz) subthalamic oscillatory activity. So is possible that the firing of REM-on subthalamic neurons then activates SNr and GPi, what causes activation of LHb in REM sleep. This REM (and preREM, shortly before REM) sleep stimulation of LHb helps to suppress dopamine and serotonin release during REM, so prevents switching into waking and SWS state, respectively. Prolonged LHb activation might finally lead to suppression of SUM and theta oscillations in the brain, as LHb projects to SUM, which I predict is suppressed by LHb. In addition the SNr inhibits PPT, although is not clear of just the wake-on PPT neurons (those PPT neurons stimulate VTA) or also the REM-on neurons of PPT.

Thanks for your ideas!

I am not sure what exactly are you looking for, but I think Bernard Staresina's PNAS paper from 2013 (he has two; check the one with Kriegeskorte) might assist you.

They report (nearly) immediate post-encoding changes in BOLD pattern similarity.

Another relevant study is that of Lorena Deuker, from the Axmacher group, from 2013 in JoN.

They don't relate it directly to consolidation, but it's one of the earliest measurements of post-encoding activity, and it does not have to do with network dynamics.

That's the kind of thing I was hoping for!  The abstract is very clearly written and already has given me some insight, so I'm expecting to enjoy the full text article.  Thanks!

HI Ran.

so given that you have the same mice and treatment it should not happen however 10% of freezing variation is in the normal range because of error in the software scoring or intralab manual scoring differences (inactivity vs. freezing).

That being said what footshock level do you use? you are using adult mice and your labmate is using developing mice so there might be a difference because young mice has different pain perception (lower).

Last but not least, different cohort do you get the mice from your animal house or vendor? if they come from the vendor sometimes they have  different houring conditions.

So in order I would check:

1) Is scoring correct? Freezing vs. -immobility?

2) Footshock intentities use (above .4 mA induces generalisation)

3) Are they coming from the same vendor/ barrier?

Thanks.

Best Regards,

SG

My take on your question is that someone spends the entire dream experience with a deceased relative - without appreciating that the person is dead.

 Whatever your question, this topic seems like a perilous undertaking for a dissertation since you have no control of the nature of your subject's dreams or their likelihood of remembering them.

Before you commit yourself to this topic, why not do an online survey to see what kind of answers you get?

PS. If you're interested in understanding change blindness, a good population to study is those on the Autistic spectrum. Literature suggests they show a reduced susceptibility . By exploring their ability to notice various  types of information which changes- position in the visual field, duration of the exposure, interpolated information (visual, sound, tactile) , you may get some sense of how the differ from the non ASD population. 

There seems to be a literature in this area

Dear Alexander, 

Cortisol levels peak between 8 and 9 AM

Psychoneuroendocrinology Research Trends

Martina T. Czerbska

Waking up earlier in the morning increases the response.[8]

Shift work: nurses working on morning shifts with very early awakening (between 4:00–5:30 a.m.) had a greater and prolonged cortisol awakening response than those on the late day shift (between 6:00–9:00 a.m.) or the night shift (between 11:00 a.m.–2:00 p.m.).[9] However another study found this attributed this greater respose to increased stress and impaired sleep quality before an early work shift.[10]

Naps: students taking a nap of one to two hours in the early evening hours (between 6:45–8:30 p.m.) had no cortisol awakening response, suggesting cortisol awakening response only occurs after night sleep.[9]

Waking up in the light: cortisol awakening response is larger when people wake up in light rather than darkness.[11][12]

Noise: there is no cortisol rise after nights with traffic-like low-frequency noise.[13]

Alarm clock vs. spontaneous waking: there is no difference on days when people woke up spontaneously or used the alarm clock.[1]

Aspirin has been found to reduce the response probably through an action upon ACTH.[14]

Hello Joe,

I came across one interesting study which might be relevant to your question and may generate some additional hypothesis.  Italian researchers recently reported on the existing relationship between the amygdala measures and the perceptual and emotional aspects of dreams.

De Gennaro L, Cipolli C, Cherubini A, Assogna F, Cacciari C, Marzano C, et al. Amygdala and hippocampus volumetry and diffusivity in relation to dreaming. Hum Brain Mapp. 2011;32:1458-70.

 We know that the activation of amygdala is higher during REM sleep that during wakefulness:

Maquet P, Peters J, Aerts J, Delfiore G, Degueldre C, et al. Functional neuroanatomy of human rapideye-movement sleep and dreaming. Nature.1996; 383:163–6.

At the same time, earlier brain imaging study has reported that the activation of the amygdala at encoding predicts later memory for emotional stimuli:

Canli T, Zhao Z, Brewer J, Gabrieli J, Cahill L. Event-related activation in the human amygdala associates with later memory for individual emotional experience. J Neuroscience, 2000; 20 RC99.

Although this study did not indicate that the enhanced amygdala activation at encoding is related to altered encoding, this is possible.  Therefore, theoretically emotion as a result of dreaming can alter the nature of the stimuli for memory retention. At the same time, amygdala structure can affect its activity, both during wakefulness and REM sleep.

Kind regards,

Tatyana

There are several methods. Please, evaluate one of this.

Dr. Friedberg's answer is spot on. My only addition would be that Bis is a very poor predictor of patient movement in response to stimuli, as such movement is cord mediated rather than centrally mediated.  Thus, in the absence of neuromuscular blockade, patients may exhibit  Bis signs of adequate hypnosis while moving in response to surgical stimulus.  We did some research concerning implicit memory formation during anesthesia in which we used the bis monitor, and some of the background information in the article might be of use, see attached.

All the best

Rich

The sturdyness of the unit, reliability and validity of actigraphy would have come into consideration when researchers at Portsmouth University commissioned the purchase of several Phillips Respironics II and Spectrum actiwatch watches. We will be using these in our upcoming pilot and feasibility study on testing the effects of Respiratory Muscle Training on Quality of Sleep and Snoring.

Hello Vladimir,

One can hypothesize that the relationship exists between neurobehavioural  variables, including those related to memory, and endogenous circadian rhythmicity.  Blind people who are deprived of light perception have desynchronization of their biological rhythm to free running. Therefore, it is feasible that the loss of circadian rhythmicity and/or sleep homeostatic drive can result in disturbance of sleep architecture,  i.e., lack of sleep stages  believed to be necessary for memory consolidation, producing neurobehavioural deficits.

I do not recall studies that support these hypotheses, however.

Kind regards,

Tatyana

Jacob, given that Fortier-Brochu et al. published a meta-analysis in 2012, you would need to provide a good argument for why a new review in 2015 is required. One reason might be that there has been an explosion of research in this field which needs reviewing systematically. Another may be that your question is different from that posed by Fortier-Brochu. Perhaps you wish to focus, in depth, on a particular aspect of cognition. For example, you may wish to review just the literature on episodic memory deficits. If there are sufficient studies, you could then divide the papers by type of episodic memory (e.g. visual, verbal, visuo-spatial, or learning, cued-recall, free-recall, recognition, etc). Forgive the self-promotion, but that is we did for episodic memory and for executive function in Obstructive Sleep Apnoea, if you want to see the sort of argument I am proposing above, applied in a review.

Finally, I cannot recommend highly enough the guidance on systematic reviewing written by the Centre for Reviews and Dissemination at the University of York, UK. The guide is free for download. Be warned, it's a big file, but makes for good reading. Good luck with this interesting project.

Maybe some of you might like my ideas on this question.

Just have a look! You don't even have to leave RG!

thanks

Good luck!

Olivier,

Sorry for escaping into a parallel e-mail discussion! Now I'm back again on ResearchGate.

I had been confused by your last question! I did not understand why you need high resolution capability of the theta waves. Thank you for clarification!

As I told you, in my holographic hypothesis I don't need at all high temporal and/or spatial resolution for encoding information. For me, 'information' is not encoded in single cells, not even in small cell assemblies. In the holographic analogy 'information' is represented by a comprehensive pattern of waves and oscillations (w/o) distributed over the whole brain, especially distributed over more than one sensory system. 'Information' is reaching the brain as a 'concerted action' of a huge amount of w/o stemming from the outside world and reaching a variety of sensory systems (visual and auditory and/or olfactory and/or tactile, etc.); these w/o representing the 'information' will be recognized instantaneously AS A WHOLE by a comparably huge amount of neurons. This is the very moment where synchronous impact – high temporal correlation of several inputs – is required. Spatially, they are distributed over the whole brain. For me, 'Binding by Synchrony' is an event which takes place when 'informations' – represented by w/o – are entering the sensory systems. The w/o are bundled to 'informations' by synchrony, i.e., they are characterized and identified by synchronous arrival. To emphasize: w/o do not encode information, they ARE the information! The 'inner representation' of an outside world object is equivalent to the sum of all w/o reaching the brain from this and similar objects.

The holographic storage of the w/o reaching the brain from the outside world requires not only the participation of a variety of sensory systems, it always requires, in addition, the involvement of a variety of subcortical regions which we attribute to the EMOTIONS.

In the German text, I posted on ResearchGate, I made an attempt to explain my view. Unfortunately, I did not translate it up to now. Hopefully a can catch up soon.

Ursula

REM parasomnias

1. Recurrent Isolated Sleep paralysis

Dear All,

IMHO, Consciousness evolves biologically at first and then socially, if at all we can call it so. I would like to present a ancient Yogic perspective here which might quite differ from mainstream opinion. Consciousness is the Unified field, very much like the theory of 'Everything'. It manifests everywhere and is the essence of everything. It animates matter and is the cause of the phenomenon we call 'Life'. In 'scientific' circles and jargon, people shy in using the word 'God' and instead use the word Consciousness, preferring instead to indulge in debating over Consciousness as 'It'.

It is the unknown variable 'x' in all equations where the cause is attributed to something unknown, and our ego doesn't accept to ascribe to a higher power.

In Yoga, the Background Consciousness is the essence and substrate of everything. It is the drawing board/blackboard upon which everything happens, and which is not affected by the changes happening. Upon this background, consciousness evolves from the matter state to the Spirit state.

1. In the mineral kingdom, Consciousness is said to be in the sleeping state. Matter is conscious, but the degree of consciousness is low.

2. In the Plant kingdom, the degree of conscious 'awareness' is higher than that of plants.

3. In the animal kingdom, consciousness has more degrees of awareness than the plant. Animals perceive everything in the world and have similar emotions like ourselves, but they are not aware that they 'exist'. They are led by nature through 'instincts' and follow nature's rhythms and patterns-Eating, sleeping, mating only in fixed times and periods.

4. In the human kingdom, we still retain the attributes of animals, from whom we evolved. Accordingly humans are all equal by rights but they are not equal in the degree of Conscious awareness. The humans who have just enetered the human kingdom from the animal, are again sense bound and intent on 'me-first' consumption pattern. They perceive the world as 'what can I get out of it for me' attitude. They use strength and intelligence to grab 'things'. When others are faster, they become unhappy and cause conflict. Everything is 'Action-Reaction'. Slowly nature teaches them the lessons of life. In the second stage of the human kingdom, for the first time, the animal man notices that like himself, others have pain too. Others too have hunger. For the first time, he begins to share. This sharing is limited to those he likes and identifies with. In the third stage, he evolves higher and hepls/shares with everyone irrespective of who they are.

5. There are three stages of evolution higher than man, totaling seven stages in the evolution of consciousness.The final stage of Consciousness is the merger of the limited, 'localized' packet of Consciousness, 'me', the soul, with the super soul(God?), background consciousness, known in various cultures as Liberation/Freedom/Immortality/ Salvation/Nirvana/Moksha, to become One, without any further distinction of 'me' and 'that'.

In Yoga, the tiniest atom, with its miniature structure of nucleus-electron-proton...is a future solar system in waiting. The time scales are huge and our current state of knowledge is insufficient to fathom these large time scales.

Thus, in brief, I have tried to explain the evolution of consciousness according to Yoga. Please note that these time scales have been consistently corroborated by 'modern science'. Current concepts and models of the universe are close replicas of ancient Yogic models.

Comments invited.

Regards

Abstractive approaches require deep knowledge of the target domain and complex substitution rules that require intensive groundwork and corpus specific tagging. You would need extensive semantic and pragmatic information to carry out this type of processing. Due to the domain knowledge requirements I would propose first a template approach from which to study if generalities in procedures can be obtained and then take it from there to see if open domain alternatives are possible.

Just a thought

Hello Sak, We studied the effect of subanesthetic acute dose of ketamine 30mg/kg i.p. in rats on qauantittative EEG. Ketamine decreased spectral power in delta and theta, however increased gamma band power. Also discrete decreases in EEG coherences were seen.

In order to eliminate the anestesia effects on EEG we implantate the electrodes in isoflurane anesthesia and rats have one week for recovery before the experiments.

1. For chronic LFP recording metal electrode would be the first choice. Depending on how much you can spend - platinum-iridium or tungsten :-). The size (surface) of an active tip would determine what would you have in the signal. With a small tip (10-25 µm) you can see also multi-unit spikes. With larger tips spikes would not be visible (due to signal averaging on the electrode large surface).

2. As concern reference - you need to remember that the recorded signal is differential : reference signal is subtracted from 'active' electrode signal. So - whatever you record on reference would be present in you recorded data. If the reference is close to 'active' electrode and its signal is similar - the effect of this subtraction can be almost zero. It is useful in single unit recording - if the reference is recording LFP but not spikes it reduces slow wave component in a signal from electrode with spikes.

However - it is not so good for LFP which you want to record - here you want to have the reference in a place as neutral as possible - it should record all the general fluctuations of the field around the brain but not the neural signal. In a perfect situation it can eliminate all the noise without adding any neural activity from it's location.

Bipolar recording might be sometimes interesting - when you want to see the difference between two recording locations. But today it can be easily obtained with an off-line analysis and 'rereferencing' in the software.

3. Ground - for monopolar recording the same place (like screw in a nasal bone) can be used for connected reference and ground.

regards

ewka

Anybody?

Dear Attilio, we have experience in doing TH staining. Please consider the following paper: Involvement of KCNQ2 subunits in [3H]dopamine release triggered by depolarization and pre-synaptic muscarinic receptor activation from rat striatal synaptosomes.

Martire M, D'Amico M, Panza E, Miceli F, Viggiano D, Lavergata F, Iannotti FA, Barrese V, Preziosi P, Annunziato L, Taglialatela M.

J Neurochem. 2007 Jul;102(1):179-93. Epub 2007 Apr 16

On the difficulty of exploring this with conscious people (from my blog: http://timfawns.com/wordpress/?p=167):

"Studies into how memory works when we are dreaming are more commonly associated with memory consolidation (e.g. Torabi and Zarrindast 2011) than with recall. In a study of almost 300 dream accounts, Fosse et al. (2003) found that only a very small proportion (1-2%) satisfied their criteria for relating coherently to identifiable episodic memories (criteria included: confidence of association with a real experience, and appropriate contextual factors such as location, objects and characters). Although this proportion is likely to go up or down in relation to how strict the applied criteria are, their account shows how difficult it is to map dream accounts neatly onto waking memories. This difficulty arises from the substitution of locations, objects and characters within dreams, as well as the often bizarre behaviours and attitudes held by the dreams’ inhabitants."

- Fosse, M. J., Fosse, R., Hobson, J. A., & Stickgold, R. J. (2003). Dreaming and episodic memory: a functional dissociation? Journal of cognitive neuroscience, 15(1), 1-9. doi:10.1162/089892903321107774

- Torabi, N. M., & Zarrindast, M. (2011). Sleep and Memory Processing: A Solid Relationship. WebmedCentral BRAIN, 2(9).

Kritika, Unfortunately that one is not available from our university subscription. I'm looking for reprint request. Thanks again.

Thanks Bradley. I will try this.

usually, short memory reactivations fail to induce reconsolidation, while long reactivations induce extinction. I think that the reactivation time lenght necessary to induce reconsolidation depend on the kind of memory (and its strenght and age), the kind of reactivation (mismatch or match) and species.

Many thanks to Nishant! This article covers exactly the information I have been reading about and trying to locate in detail. Again, kudos to you!

Aysha Bey

For rats try Matthias suggested dose of 1mg/kg. Not all noted effects may be cognitive.

Check out our old 1996 back to back Behavioral Neuroscience papers: Cain ET al., and Saucier ET al., mainly exploring NMDA antagonism on water-maze learning, but capturing many more behaviors in order to quantify the sensori-motor deficits as differentiated from cognitive deficits. One of our control groups is Scopolamine at 1mg/kg. Can also try Atropine at 10mg/kg for equivalent dose.

Both these papers can be downloaded from my website ww.pageoneuroplasticity.com, under "about Eric" tab and then link to available *.pdf files

Eric is right about all TBI not being equivalent; low-velocity trauma such as penetration with a sharp object and other relatively focal injuries tend to have a different profile. But the majority of severe injury is due to motor vehicle accident or similar magnitude of blunt forces acting on the head that include a coup-contrecoup phenomenon (often involvling both frontal and occipital/cerebellar areas), shearing and DAI, and a preponderance of laceration to the inferior frontal and temporal lobes as notes with a fairly characteristic picture of diffuse ineffeciency of learning and processing that will tend to improve over time. This would seem consistent with the ripples being at first completely then more partially blocked and/or having to find alternative paths that would be less direct. In a milder injury, where there is little permanent cell death/structural damage, but some edema and neurochemical disruption, the recovery would be quicker and more complete.

Wilson, D.A. Single-unit activity in piriform cortex during slow-wave state is shaped by past odor experience, Journal of Neuroscience, 2010, 30: 1760-1765.

Wilson, D.A. and Yan, X. Sleep-like states modulate functional connectivity in the rat olfactory system. Journal of Neurophysiology, 2010, 104: 3231-3239.

Barnes, D.C., Chapuis, J., Chaudhury, D. and Wilson, D.A. Odor fear conditioning modifies piriform cortex local field potentials both during conditioning and during post-conditioning sleep. PLoS ONE, 2011, 6(3): e18130. doi:10.1371/journal.pone.0018130.

Wilson, D.A., Hoptman, M.J., Gerum, S.V., Guilfoyle, D.N. State-dependent functional connectivity of rat olfactory system assessed by fMRI. Neuroscience Letters, 2011, 497:69-73.

This simple question has a very complex answer. First of all there are several forms of memory and each type of memory appears to have mechanisms and processes that are in some cases unique to that particular form of memory. My laboratory focuses on the role of transcription factors in memory that assist in the physiological regulation of memory processing. Transcription factors are specialized proteins that once activated trigger gene expression and new protein synthesis. There are several types of proteins that are required during the memory formation process and transcription factor activity assists in this process. There are in fact many transcription factors involved in memory but current studies focus around 5 main families (CREB, NF-kB, AP-1, C/EBP, and Egr). My laboratory works on NF-kB and Egr proteins and their role in memory. NF-kB has been shown by our lab and other labs to be involved in several time-dependent phases of memory, including memory encoding, memory consolidation, and memory reconsolidation. Understanding the transcriptional regulation underpinning different memory phases should assist in developing new drugs that will enhance memory or help in preventing or reversing memory impairments.

The keyword method is by far the most-researched mnemonic strategy, and I have written about it on my website on several occasions. You might find these articles helpful: a basic description of the method at http://www.memory-key.com/improving/strategies/advanced/mnemonics/keyword-method; Using the keyword method to learn vocabulary at http://www.memory-key.com/improving/strategies/advanced/mnemonics/using-keyword-method-learn-vocabulary; Retrieval practice & the keyword mnemonic (which provides the very important reminder that it's not enough to have an effective mnemonic) at http://www.memory-key.com/improving/strategies/advanced/retrieval-practice-keyword-mnemonic

Thanks for links

Yes i would like but there is many obsticles in the way the main thing is that I'm not a member of any university / institution, it's only my personal project.Because that i searching for more people intresting in this topic to join experience ,knowledge,resources.

My homemade experimentation is never reach the quality of scientific work mainly becouse i expedimenting on myself.

I might put together a larger sample should be 10 Ludcid dremers but still too little,and it to much complication without institution/unoversity support.

In the future I plan to try theta-TDCS on DLPFC(if no one do it before me). Still looking for more information and waiting for better equipment.

In last few yers workong on imporving mental techniques to induce Lucid Dreaming

Hi,

The eye movements have to rapid (hence Rapid Eye Movement: REM), as opposed to rolling eye movements, which are common at the transition from sleep to wake. And you can also see small muscle twitches sometimes.

However, also other sleep stages can have eye movements, and REM sleep can take place without eye movements at all. The be able to determine if REM sleep is really taking place, you need at least 1 EEG lead (C3 or C4 referenced to the opposite ear or mastoid) as well as 2 electro-oculogram (EOG) leads and a submental electromyography lead.

Good luck

Ingrid

Vinita, you ask if memory can be erased. I strongly feel that if you could, you shouldn't. What most people want to erase is actually the feelings they have upon recall, and the bad physiological effects that recall has. It shows that memory does not have one location in the brain, but many, where each of the sensations associated with an event are stored.

Emotion centers will also store information about the event as well, and usually that is where you often wish you could "erase" the memory. In fact, you can train your own mind to "disconnect" the emotion from the memory. I have done this to deal with PTSD, and the panic attacks have been reduced from 1 per 18 sec to 2-3 per day. I simply used the paradigm that there are emotion centers in each section of the brain (using embryonic sections of Telencephalon, Diencephalon, Mesencephalon, Metencephalon, and Myelencephalon) and figured how each emotion center plays a role at each level of representation of the body's functions in the brain (e.g. Myelencephalon controls the body's chemistry and cellular activities, Metencephalon controls the body's tissues and how we interact with the environment around us, Mesencephalon controls the organ level and how our personality is involved with dealing with the environment around us, the Diencephalon controls the interaction between systems of the body and our conscious awareness of this interaction, the Telencephalon controls how we apply internal events to external events). Knowledge of anatomy would greatly help psychologists, I figure.

Each has an emotion center which puts a "weight" on local circuitry because of the emotion associated with it. Thus depression can happen because of a consistent failure in some locations of the body to get the ions it needs (lack of satiety in the myelencephalon). Or it can result from failure in certain tissues that cannot be addressed by local circuitry in the metencephalon. Or it can result from a failure in organs that cannot be addressed by local circuitry in the mesencephalon. The mesolimbic system originates here, and thus failure in local circuitry in two of the above areas to address the problem will automatically be transmitted to the hypothalamus in the diencephalon. If hormones cannot address the failure, then the amygdala steps in to produce depression. Because of its proximity to more conscious circuits, this will cause the telencephalon (emotion center in the prefrontal cortex) to send strong signals to the decision-making center there to do something. All circuits in the Mesencephalon and below are unconscious circuits and operate under much simpler rules than the conscious brain does.

Now why should you NOT erase memory? Mainly because everything that ever happens to you is stored in the brain for a reason. All levels need to recall how the body dealt with a situation in the past to help it prepare for similar situations. At the myelencephalon level, that may involve changing metabolism, or increasing heart rate, or respiration rate at the cellular level. Coordination of the cells involves some regulation at the tissue level (metencephalon), too, so there must be centers associated with blood pressure, heart rate, metabolism and respiration rate there as well, and the same goes for the mesencephalon and the organ level. Memory of the past involves storage of what the body did to react to the event as well as what it predicted should happen before the event occurs. Learning will take place with each event and cannot if that information is not stored at the same time as the visual, auditory, olfactory and other sensations' associations.

All of this is discussed in a book I am writing now on how the brain works down to the details of individual cells and based upon a theory of how the brain is organized anatomically. I rely heavily on embryology and anatomy and some very basic principles that must be operating in the nervous system for it to function at all. I am reinterpreting the results of much of the research that has been done to describe the function of various centers in the brain.

Yes, the brain does some learning during sleep, in fact you can tell by accuracy on tests, that people who are kept active between the time they learn something and the time they are tested are not as good at the tests as they would be if they got at least 2 hours sleep in between.

Experiments done with MEG and EEG seem to suggest that the hippocampus is active during slow-wave sleep, and it reviews knowledge learned during the day. (They found evidence of repeated patterns but running at about 10:1 of the original speed.) This suggests that there is a step where knowledge is recovered from episodal memory, as if it ran a movie of the day an analyzed it for information on time and place.

In all probability areas in the Parietal lobe are monitored by the cerebellum to form sequences or episodes of experiencial information on what the organism did, immediately afterwards the hippocampus reads the sequence and creates indexes to the information that tell where and when it happened. During sleep these episodal sequences are run through the hippocampus again probably multiple times at 10X speeds, and this allows the hippocampus and the entorhinal cortex to fully index all the information stored in the sequence. Then the sequence is stored probably in the Front of the Temporal Lobe for later review.

What this suggests is that the learning done during sleep is probably related to Declarative Memory, but not only does this go on, but some of the internal cellular learning involves chemical pathways that may take weeks to complete their jobs, and of course they must still be working even when we sleep.

At what level do you want to study sleep? and Learning? the level you want to reach determines how much you need to know before you can start.

A Sleep Lab, and at least an EEG are a good start, although a MEG might be useful.

As well you would want a psychology lab where you can administer tests, to see what has made it into long-term memory.

You might be able to share these with others.

Then you would need to design a particular test protocol, such as determining whether a subject learns more words from a list, after sleep than before, and so on.

This might require that you design your own test, or that you use a standard test, such as a standard bank of words, and partial words designed for similar tests.

Then you would have to control for familiarity with the list, for short term rather than long-term memory, for all sorts of other possible confusing factors, so that you know that you are testing only what you think you are testing.

It's all very complicated.