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Learning and Memory - Science topic

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Does anyone know any research addressing the relationship between non-conscious perception such as subliminal priming and procedural learning/memory that relies on the basal ganglia and its related circuitry in the brain?
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Chen Si Thank you for sharing your research. This is an indirect way to grasp the relationship between non-conscious perception and procedural learning.
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Human is searching the reward to verify some questions, while human predict the answers based on large learned memory.
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Tong,
Here are two articles that may help.
Good luck.
Don P.
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I do LTP recording in rat hippocampus slices. I have been doing it for a while but off late I am facing a couple of strange issues.
1. The slice is thinning out with time while it is in the recording chamber. I use 400 um thick slices and do surface recovery for 2.5hrs before I transfer it to the recording chamber. While placing it in the chamber, the slice looks healthy. I then do a 20mins in-chamber recovery after placing the electrodes and then start the input-output to figure out where to clamp the current. Everything goes fine till this step. Once I start the baseline recording, the slope remains steady for 5-10 mins and then starts to fluctuate a lot. I have seen a trend where it increases with time. When I look into the microscope to check if the slice has moved or is in normal state, I see that the slice has almost become transparent because of thinning out. It's as of the upper layers of it have been scraped off. A couple of times it had become so thin, I literally had to scrap it off the floor of the recording chamber. I cannot figure out why it could be happening. No one in my lab had experienced this before. The first time it happened, I suspected there could some some detergent residue in the aCSF container. So I have been washing it several times with milliQ water before use. Yet the problem continues.
2. Several times, even at very low current, bubbles appear in the slice near stimulating electrode. I have observed this happening at higher current, but this is happening at very low current lately. Not just that, last two stimulating electrodes broke in a very weird manner. I am attaching the pictures of them. In past, electrode got damaged due to physical mishandling, but usually the tip gets bent or the two electrodes are not parallel to each other. But never have I seen an electrode break in this manner. It was more like it got corroded. The second electrode was made just 2 days ago and was used for just 2 experiments. Neither of them hit the floor or the walls of the chamber and yet got damaged.
I cannot figure out why this could be happening. No one I know has ever seen anything like this. If someone has experienced the same, I would be grateful to know how you could fix the issues. I would also be grateful if you can help understand the possible reasons for why this could happen.
Thank you in advance.
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Hi Deepti,
This seems to be an issue with the stimulation electrode or the isolation box. At least, based on the 2nd point. Try to replace each one at a time to see where the problem is emerging. I think the current you are giving is much more than what it should be. Is this an interface or submerged chamber? In the interface chamber the stimulation intensity you need to give is much less than the submerged condition.
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I have collected rats blood plasma, and serum & stored it at -4°C but the problem is that the serum and plasma have preserved more than 1 month.
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Yh you can, once the route of collection and the processes are right
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  • Brain tomography and nuclear magnetic resonance emission tomography, are able to identify areas of the brain that are activated during more participatory learning, and these are related to emotions?
  • Learning and verbal memory is the least remembered the short term?
  • The brain area of emotions in students are not activated or are refractory to the classroom lessons, lectures or conferences?
  • The emotions related area is more active when the student participates in learning and this is related or meaning to the real world?
  • Videoconferencing algorithms, allusive outlines a certain topic with brief captions; and mental and conceptual maps the brain area activated more emotions, that lectures and master classes?
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Sure
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I was wondering if I fear condition my rats, and then train them in Morris Water Maze (spaced training), will the rats show weaker or no long term spatial memory? I tried to look for relevant literature, but could not find many papers directly addressing this sort of question. If I missed them, could someone send me those papers? Thank You.
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From your question it's not really clear, do you aim to test such a hypothesis or to avoid unwanted effects of one task on another?
Fear conditioning in rats can be quite stressful, so the effects of stress modulators (corticosterone, noradrenaline) can definitely affect learning in the next task. But the effects will depend on shock intensity, the timing of each task etc.
If you could be more specific I'd love to provide more literature recommendations.
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I am planning to do learning and memory tests using the Morris water maze and passive avoidance tests in young rats.
I was wondering if it is possible to perform two behavioral tests at the same period of time or I should perform one behavioral test at a time?
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All answers up to this point suggest not doing them at the same time and to space by 24 hours. While I fundamentally agree with both of these, there are times when these options aren't possible (e.g. treatments or training regimens).
The best practice if you want to run two tests in one day is to at least space them apart from one another by 30-90 minutes (depending on tasks, treatments, etc) and, most importantly, to counterbalance the order of the tests across all animals in each group. The interval allows for stress hormones to extinguish and the counterbalancing controls for order effects.
Hope this is helpful!
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Can we perform in vitro learning and memory activity. Please suggest me the material and method to check the activity
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If you mean that you would like to know whether it is possible to investigate the induction of LTP for instance, as an indicator of memory enhancement, yes! But you would need to design supplementary experiments in vivo too.
Fir example, you can record EPSPs or induce LTP in hippocampal organotypic slices (in vitro) or perform patch clamp recording, optogenetic stimulation, etc. But if you would like to expand your study to test behavior (in this case learning and memory), you need to perform learning and memory tasks on animal models to provide behavioral evidence.
For rodents, in terms of testing learning and memory and depending on what type of learning (aversive, goal-oriented, drug or reward-seeking...) or memory (working, reference, fear, ...) features you would like to study you can perform a wide spectrum of paradigms such as passive avoidance learning with shuttle box, y maze or T maze for decision making, orbital and Morris water maze for spatial memory...
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Problem-based learning (PBL) is the most significant innovation in education for the profession for many years . Some argue that it is the most important development since the move of professional training into educational institutions
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The best curriculum is the curriculum that addresses the local needs of each country i.e contextual, and should also satisfy the professional needs and the learners' needs.
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Hello.
If someone could kindly direct me in the direction to research one significant key study in learning, memory, attention and perception, which cognitive psychology has contributed to in our scientific understanding of these areas.
Thank you.
Sonia
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Do you know where can I get/buy a T maze for Planarian memory and learning experiments, particularly the simple T Maze used by McConnell in his planarian studies? Or does anyone know how to create a makeshift T maze for Planarian learning and memory experiments? Thank you very much!
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I can help you with that! e-mail me at chloe@behaviorcloud.com
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central cholinergic signaling via muscarinic receptor is implicated in learning and memory. one of the mechanism by which cholinergic signaling influence cognitive has been assumed to be directly cholinergic stimulation of pre- and postsynaptic hippocampus neuronal receptors. muscarinic receptor is one of the kind of acetycholine receptor. My principal target is this receptors by checking for d activities of my bioassays guided isolated compounds on this receptor. I am looking for muscarinic activating receptor biochemical guided assay. Thanks.
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Thanks@Bahman for your gesture contribution. I went through the articles and i found it interesting.
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Exercise, diet, CBT in relation to neural plasticity, neurogenesis, Long term potentiation and learning and memory. looking for papers to support my assignment
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Thank you Bahman, I will take a look
Kind regards, Kate
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Does anyone have familiarity with switching from normal light/dark (L/D) cycle for rats to reverse L/D ? Our lab is considering, it but I have a number of questions.
Does any exposure to normal light even if brief disrupt the rats circadian rhythm once they are on the reversed cycle?
How do the animals use/respond to extra maze cues if they are being tested in red light and presumably can't see them? Or do you test in normal but very dim light and only the colony room is kept red?
We do learning and memory tasks (T maze alternation / Radial arm maze) does the reversing of cycle actually make a difference in these tasks?
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Yes, this is a new question but the issue is not new. I think not much study is there. But, the question is important as some specilist pilots, engineers & long distance train drivers carry out their duties only during night time. Do the suffer any physiological changes or they get some benefit although the fact remains that man is not nocturnal.
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The Elevated Plus Maze Model (EPM) is basically tested for the anti-anxiety activity. Currently, I am working on learning and memory activity in rats by the Barnes Maze and EPM test. Is the EPM reliable for nootropic activity? whether the electrophysiology of hippocampus part of rats brain suitable or not to know the mechanism of action for tested drugs?
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Our linear maze is a good instrument for memory tasks. I attach a picture in my paper (page 125). All measures are added. Ope4en-field is also pictured and it is is a good apparatus for fear and anxiety:
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I am doing research on learning and memory activity in rats. I have bought piracetam injection which is used for IM and IV route in human but I want to give through IP route in rats. can I do this?
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I think the injection which is available commercially would not be a decent experimental drug to test in animals because of the presence of other compounds in it.
Best thing to do would be buy the pure drug from a good company like sigma and reconstitute it with normal saline or whatever vehicle instructed to inject it intraperitoneally to the rats. This would be a proper way to study the effect of a particular drug.
Some of the nootropics have also used per oral in animal studies.
You should go through studies in the PubMed and then decide.
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I will do first-time electrophysiology of rats hippocampus. How can I interpret the learning and memory activity in rats by electrophysiology graph?
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In the hippocampus a well-known correlate of learning and memory is long-term-potentiation.
An electrophysiological correlate of working memory is e.g. persistent activity.
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In the elevated plus maze , Barnes maze test and many more behavioral models it is mentioned that 70 percent of ethanol is used for cleaning of maze. Is there any rationality behind it.
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Hi MSc Sharma, most studies use ethanol 70% because this is enough to eliminate any olfactory cues present in the apparatus used. If any cues remain, the next animal tested may repeat the behavior of the predecessor or at least have its behavior altered. But if you use ethanol 70%, you have to dry out the ethanol (paper towel) before placing the next animal because, otherwise, the smell of the alcohol could be very strong and also alter behavior. Some studies use more diluted concentrations of ethanol, like 10 or 20%, to avoid that the apparatus smells a lot like alcohol. Some studies even don't use the ethanol because they want to leave the olfactory cues between animals. I think it depends on what you're trying to answer.
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Hi, I'm analyzing behavioural mice data, such as locomotivity, anxiety and learning and memory. by qq plot I confermed that the data I collected have a considerable variability. I runned normality test and confirm this variability. But I have a large number of animals by group: 3 groups; n=25, 22, 23. So I have two questions regarding wiht. is animal number larger enought to consider a normal distribution?, and if yes, there is another observation: those animals are outbred, and I have riden an article that mentioned that outbred mice tend to have more variability in behaviour. so in the case I can run a parametrical test, Do I have to be present the mouse strain?. I really appreciate your suggestions
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Although I do not have a direct answer to your question on the normal distribution, if you are doing parametric group comparisons, you could calculate the effect size (such as partial eta squared) and conduct a power analysis using Cohen's d (the e-book, power analysis for the bevhavioral sciences, is accessible through google scholar), to determine the number of subjects required to obtain a statistically significant effect. There are also many online calculators to determine sample size given your effect size and power estimates. Here's a site that has an overview of power and sample size calculators:
Hope this helps,
BD
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Shouldn't I provide a shorter (or graduated) way to see what I am all about?
Well, here is an attempt at that :
I (myself) avoid (eschew?) defining anything, I have viewed attention as an aspect of working memory or/and an aspect of the episodic buffer (usually or always both). Both change a lot and frequent (both are very "dynamic") . It is hard to see how attention would not be similarly dynamic (as well as a guiding factor for those 2 memory aspects or types of memory). That being the case, it seems to me it would be well nigh impossible to factor "attention" out. (And "we" should define nothing; the Subject should define all -- as it was with the classical ethologists of the 60s and 70s -- AND AS IS THE CASE WITH ALL TRUE SCIENCES.)
An easy (shorter) way to see my outlook is to read the outline and guidelines I provide for AI people (that about 35 pages long) -- and THAT is also what I believe should be roughly, the as-of-yet outline of good behavioral science: cognitive-developmental human ethology, with (always) an eye to contributing towards an ethogram via that which is ALWAYS founded in the sometime present directly observables (as true proximate causes, along with aspects of the present environment, and simultaneous "innate direction" provided). (This is basically a type of classical ethology, which unfortunately even today's "ethologists" do not know, recall or respect.)
Anyhow, if it is good enough to "mechanize" in AI, AND IS NOT A MODEL OR ANALOGY, but a fair and likely necessary outline of our rather well-defined memory facilities (and capacities) (AKA our differ sorts of Memory) -- all based on the best research -- _AND_ the key "containing system" seen as innately guided qualitative shifts IN/by gaze changes, then things 'noticed' (though often unconscious, and thus better termed "patterned-gazes-noticed") , then defined (conscious) attention, and then new processing (for new representations, and soon, new types/hierarchical levels OF THINKING (all the connected cognition there)). The latter is where BOTH psychology and AI need to make discoveries to progress empirically and systematically (and as any kind of decent science). Anyhow, for a short version of my view,
see:
AND also read the COMMENTS below the item,
Data everythinga.doc 0B (Read "A Human Ethogram ..." sometime rig... :
Deleted research item The research item mentioned here has been deleted
AND
And then, read my major Project description:
--------------------------
AND, finally, for MUCH more (for "everything"), if so desired, see:
(160 pages)
and
read my 326-page collection of essays, everythinga.doc_0B.pdf , UNDER
BY clicking the link to that collection (to everythinga.doc_0B.pdf (and, again, read the new additions, as Comments, under that).
Maybe I am wrong, but I give a clear completely empirical approach to see if I am correct or not. It has been correctly said that I am -- as much as a cognitive developmental ethologist could possibly be -- a "methodological behaviorist"; and, all else cited except such behaviorism (<-- as usually understood) ALSO has clear empirically directly observable foundations, at least at the inception of any major new behavior patterns OR qualitative changes thereof.
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Let me try to provide an answer by sharing a relevant essay I wrote to a friend. (This contains that "shortest description".)
Let me answer "What is your definition of 'innate guidance'? " in the only way I ever will answer anything when it comes to a scientific study of human behavior (aka ethology). My answer is I do not define; I never define anything. All is discovered and the Subject (the human) will define what, in any given type of case/circumstance, the innate guidance IS (and what that is like). ("Ditto" for 'learning'.)
This is the only way other ethologists should have things 'defined' . IN FACT: Real and good scientists (in any science) NEVER 'define' anything just with their imagination; no guessing EVER, except just "where to look" -- THEN they find that which is important and worth noting FROM THEIR SUBJECT MATTER).
Everytime (literally) I hear the word "define", I cringe.
NOW: This may not be easy to understand, or understand as I intend, but I have written 500 pages explicating, elaborating, and justifying the following view:
From what I said before: I can only tell you where I would look and hope for the discovery of what is at the INCEPTION of new 'seeing' new things and differently (that then eventually leads to new representation, then to new thinking): IN PARTICULAR: This (coming up) is how I will look for the proximate causes OF the behavioral shifts, in BOTH directly observable overt behavior patterns AND in the associated directly observable aspects of the current environment (and WITH the special sort of associative/discriminative learning that THEN OCCURS; and THAT along with other behaviors -- some developed in just this same type of way in the past, which now function in some similar way to when the behavior was overt, though now covert). I hypothesize, and it is now testable and verifiable (yes or no) with new eye-tracking technology and computer assisted analysis :
That "perceptual shifts" are the overt behavioral patterns aspect(s) WITH the innate guidance that there is/are at the inception of a transition starting a qualitatively different level/stage of representation . Such an inception, of course, includes (for contextualization) what is brought forward from our Memories -- to have the new environmental aspect(s) meaningfully seen . The perceptual shifts will result in finding and using "things" thus discovered (by the organism), BEGINNING with the perceptual shift(s) FOR new elements processed from the environment which allow the key new/additional "ingredients" that need to be added to existing cognitive abilities' contents (the latter, existing already, at a lower level of the hierarchy), to begin to move to the next higher hierarchical level/stage-type behavior (behavior including not only necessary overt aspects, but also existing cognition <-- understood, in important part, by seeing similar perceptual shifts beginning earlier stages; THUS: you have to do investigations longitudinally, beginning just after infancy; you must track the relevant ontogeny).
You will note I use the word WITH very intentionally: that is because the innate guidance (which, in a sense can be seen as manifested in the perceptual shift) IS ALSO OCCURRING SIMULTANEOUSLY WITH new LEARNING, IMMEDIATELY (or in effect, immediately) ALSO INVOLVED at the same time as the perceptual shift occurs. (In short,' innate' and 'learned' occur literally (OR, IN EFFECT) SIMULTANEOUS, TOGETHER -- there is no dualism, this is that 'problem' solved. If you really want to say BOTH the innate and learned are always involved, then this is what you mean.)
I think this is the only brief 2 paragraph version I can provide. To really know more:
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A summary of Human ethology is most often expressed as follows: Homo sapiens is the creation of the Creator, Nature and Society. Atheists deny the first component of Human ethology. Those who do not know about the effect of Mowgli, those people will deny the last component of the definition. There will be skeptics who criticize genetic patterns. Therefore, explanations are required, in connection with which your 500 pages of the manuscript may help to understand the essence of the problem. All the best in 2018!
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Hi dear colleagues I need to record AMPA and NMDA currents of CA1 neurons in p21-p32 mice but I do not know what internal solution to prepare. There are papers that use CsCl, other Cs-Glu and other K-Gluc and differ in the use of QX314 (besides that they use different reactants). I really do not know what internal solution is better for this type of records and I am starting in the patch-clamp world. Also, is it possible that you can recommend a publication that supports the use of your internal solution? What care should I have when preparing the internal solution (ATP / GTP) and during the electrophysiological record? I appreciate your help very much
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Hello!
For voltage-clamp recordings the Cs-Methanesulfonate based solution is used in our lab.
127 CsMeS, 10 NaCl, 5 EGTA, 10 HEPES, 6 QX314, 4 ATP-Mg, and 0.3 GTP; pH adjusted to 7.25 with CsOH
It allows to record synaptic currents in pyramidal neurons in slices for prolonged period of time. As it contains the blockers of potassium and sodium channels, the input resistance in whole-cell configuration is rather high (about 250-400 MOhm). I would recommend to voltage-clamp the cell at -50 - -20 mV most of the time during the experiment. Prolonged recordings at more negative voltages decrease the cell viability during the recording. This solution can't be used for current-clamp recordings.
For current-clamp recordings the K-Gluconate based solution is used:
135 K-gluconate, 10 NaCl, 5 EGTA, 10 HEPES, 4 ATP-Mg, and 0.3 GTP (with pH adjusted to 7.25 with KOH)
It allows to record membrane voltage and action potentials in pyramidal neurons in slices. However it does not perform too well in voltage-clamp mode, as the input resistance in whole-cell configuration is quite low (60-180 MOhm depending on cell type). If you use it in voltage-clamp recordings I would recommend to clamp the cell at -90 - -60 mV most of the time during the experiment.
Both of the solutions are prepared in the same manner. First we dissolve all the components in water, except ATP and GTP. After that we rougly adjust pH. Then we rapidly add ATP and GTP, make a final adjustment of pH (ATP decreases the pH) and freeze the solution in 1 ml tubes. The osmolarity of the resulting solutions is about 300 mOsm (for better patching it should be a little lower than the osmolarity of the extracellular solution).
Good luck with your experiments.
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No one could really expect to outline (then research) ALL the species-typical behavior of the human (or any advanced animals, such as mammals and birds) AT ONCE. WE SIMPLY ARE NOT omniscient (and not capable of ever becoming or being so -- though, in time, perhaps TOGETHER we can approximate this state).
Thus, a good start for a human ethogram IS ITSELF the beginning of the human ethogram. Of course, you must have a correct start: Look for the always-involved capabilities which basically is a "containing system" for all other interesting things -- things less pervasive and less-flexibly-and-openly applied (by themselves) (like emotions and language). Yet it must be essential aspects of real particular human behavior.
I chose (for the first and ONLY human ethogram, in existence): the cognitive-development behavioral system AS IT UNFOLDS AND DEVELOPS in ontogeny; I posit such a study can be done grounding everything (at the root, in very key ways) in behavioral patterns and the environmental aspects involved. BUT, in addition, one must understand the nature of our types of memories , and how awesome amounts of perspective and context can be brought forward with that. YET, at the same time, the INCEPTION of anything (including new ways to represent and conceptualize and eventually think) will themselves have real (overt directly observable) environment aspects required at least at the beginning (inception) [ as well as some clear overt, directly observable behavior PATTERNS, acting at the inception ] -- THIS would be true of any SIGNIFICANT new DEVELOPING behavior patterns (including the inception of 'abstract" thought) : this is simply sensible empiricism, which MUCH BE ASSUMED AND SOMETHING A SCIENTIST SEES as necessarily "worth a try", because there simply is NO alternative for an empiricist.
The likely BEHAVIORAL PATTERNS INVOLVED (along with these environmental aspects, at the inception of significant new behavior PATTERNS) not only could simply be perceptual shifts (see first link below) BUT VERY LIKELY WOULD BE _AND_ now these very things are investigable (verifiable, provable, replicable) using the new eye-tracking technology (likely along with computer-assisted analysis). Now the citations: First what I see as the likely phenomenological nature OF these very perceptual shifts, which occur with each hierarchical and new stage/level of thinking:
[ (please IGNORE the incoherent Answers to this Question by Nathan Latvaitis -- an uneducated person with no publications (and not likely under any sort of good mental control) -- one who believes he can simply take on any topic with his mind, no education or discipline needed) ].
THEN: see the overall position, for the role of these perceptual shifts during child development, by reading the paper (Research Item) "A Human Ethogram ...: :
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It would likely also be good for people to see:
(also see my THIRD Answer to this Question)
[ P.S. Please ignore the 2 very largely off-topic and incoherent "Answers" actually SPAMS (along with a lot of plagiarism)
by an uneducated, unpublished and undisciplined individual going by the name Nathan Latvaitis . ]
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When dynamically reactivated through pedagogy, can learning memory embedded for reveal the contemporary relevance and future potentialities of adult learners online?
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Thank you Stephen and, like Eduard, I think this is a very interesting question. My response is not to offer an answer but rather to suggest that questions like  the one you pose need to be answered not on the basis of individuals simply offering their own personal opinions/beliefs about the matter but by undertaking empirical research that is designed to answer clear research questions.  
Best wishes,
Ian
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We talk about "boundaries of intonation units" and that language is a "code". And if we go in the direction of "categorial perceptions" and "motor theories," could it be expected that speech pauses (rather hesitations than breath pauses) can draw attention to the listener and thus promote the performance of remembrance? At which point could one expect a discriminating point at the pause length in relation to the rate of articulation? Imagine a Morse Code, e.g. SOS: We say three times short, three times long, three times short, but nobody talks about the silence between the individual units, right? Someone in distress at sea might have a different frequency of all units including pauses than someone on a deserted island who has been sending this code for weeks or months. How does the receiver discriminate between the individual units (in these cases, of course, we hope that there is a receiver at all ;-) ) and how does he know that it is an SOS signal? Can this model-like idea be applied to the language? And does it make any sense to think about the long-term memory? Or does it only concern the short-term memory and what is actually stored in the brain are generated emotions?
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Hi, we wrote a whole series of papers which investigate this issue, looking at disfluent "er", repetition, and silence (in English).  In brief, "er" and silence increase recognition memory for words which follow disfluencies (Corley, MacGregor, and Donaldson, 2007; MacGregor, Corley, and Donaldson, 2010); repetitions do not (MacGregor, Corley, and Donaldson, 2009).  In the case of "er" and silence, there is an associated attenuation of an N400 ERP effect at the target word, suggesting that people's expectations about what they will hear have been affected.  Importantly, Collard, Corley, MacGregor and Donaldson (2008) use a P300 ERP paradigm to show that this altered expectation is accompanied by an attentional modulation (as you suggest above).
A synthetic view of these studies might be that disfluency is detected when the signal becomes "non-linguistic" (hence not repetitions), and acts as a signal that the speaker is unlikely to utter a predictable word (N400 modulation).  This causes the listener to heighten attention to the signal (reliance on bottom-up information; P300 modulation), resulting in a greater recognition memory for the subsequent (target) word.
Hope that helps!
--MC
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What are some of the main disadvantages to the simple systems research approach in neuroscience?
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Hi. The main problem of the use of invertebrate systems is the reduce number of interneurons in those biological systems on the nervious system. Ramón Alvarado in UNAM worked with neuroendocrine systems with crayfish (Procambarus clarkii), a well known invertebrate model for neurophysiological and endocrine studies. He studied the day-night cycle, but also worked with unpublished models of muscular reaction, similar to the work that you want to do. The reduce number of interneurons makes that the simple reaction of an invertebrate could not explain clearly the human mmechanisms, but could be a first approximation fo the problem. I left to you articles about techniques of cell culture and in vivo work with crayfish. Maybe other invertabrate model could be helpful fot your work. Good luck.
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I thought about how the term scaffolding which was originally a term often used in the field of construction techniques, by Wood and friends later developed by Anghillari and other experts so that a term which may be brought also to the world of education.
on computer systems often delays in the call data. It happened (one of them) because the memory on the disk fragments (position data is a mess). To avoid further delays, perform the defragmentation (arrangement).
In humans (human memory) is also often a delay in calling the information that has been studied, either because the information previously forgotten or not well understood. Can this condition is associated with the term disk fragmentation on the computer?
This becomes interesting, because if it makes sense, the defragmentation can also be done in humans so, improvements will occur over the maximum.
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Yes, I think the total concept has some sence. I also think that such operation is long, so it may occur during sleep. But I think that more correctly to speak about the restructuring of the information from the worrking memory.
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I am currently working on a memory association tool to help build better understanding of various learning models or concept. Any help will be greatly appreciated. Many thanks 
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Thank you Anastasia for sharing these resources. I will look into all of them. 
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I particularly hope to find research on what happens if you elaborate on factual content (e.g. a fact or a concept) on long-term retention. Imagine if I have to remember a definition of what an earthquake is (concept) or a year in which a major earthquake took place (fact), what would elaborating on this do to my memory relative to less active processing strategies such as restudy?
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One of the most effective leaning strategies for remembering, hence,  retrieval from long term memory is the so called testing effects or retrieval practice. I would guess that there are more than 400 publication on the topic. With support from both behavioral an neuroscience studies.  Below is a review of 10 different learning techniques, among other retrieval practice. Note that Dunlosky et al denotes retrieval practice as practice testing. See also  Karlsson Wirebring for neuroscientific  evidence, focusing on the difference between repeated study and retrieval
Dunlosky, J., Rawson, K. A., Marsh, E. J., Nathan, M. J., & Willingham, D. T. (2013). Improving Students’ Learning With Effective Learning Techniques: Promising Directions From Cognitive and Educational Psychology. Psychological Science in the Public Interest, 14(1), 4-58. doi:10.1177/1529100612453266
Karlsson Wirebring, L., Wiklund-Hörnqvist, C., Eriksson, J., Andersson, M., Jonsson, B., & Nyberg, L. (2015). Lesser Neural Pattern Similarity across Repeated Tests Is Associated with Better Long-Term Memory Retention. The Journal of Neuroscience, 35(26), 9595-9602. doi:10.1523/jneurosci.3550-14.2015
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I am trying to investigate learning and memory consolidation over sleep/wake using brain stimulation. Multiple studies have used the paired-association list learning task in the context of sleep; however, only one study has used tDCS and Sleep with this paradigm. Unfortunately, this study made use of German words. Can someone recommend an English database for me to design this experiment?
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Depending on what variables you want to control (word frequency, part of speech, number of letters, etc.), you might try any of the following:
MRC Psycholinguistic Database (http://www.psych.rl.ac.uk/)
University of South Florida Free Association Norms (http://w3.usf.edu/FreeAssociation/)
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Although the importance of enabling students to create episodic and semantic memories during the learning process has long been acknowledged, this issue has not been adequately addressed in educational research. This is particularly true for the 'social contagion of memories' which refers to the memories implanted by others (e.g., teachers, friends, parents) via social interactions. In fact, this implantation process almost entirely occurs in an implicit manner and has important conclusions for learning because, for example, students' memories may be contaminated by others' knowledge, perceptions, beliefs, and emotions during the learning process. If this is the case, I strongly believe that we may benefit from the effects of the mentioned social process (i.e., social contagion of memory) by using memory contagion strategies in educational settings such as classrooms. Yet, at this point, an important question arises: What are these strategies?   
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Dear Altay, 
There is extensive research on the effects of "Self-Development" which results to better cognitive abilities and interpersonal skills. 
I recommend you look for Effects of Transcendental Meditation on cognition/memory and/or education. You will love it! :) Most of the research is done in the US, some in northern EU. 
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I'm wondering if there is a plateau in derivative of learning once you reach a certain level of expertise (say Gladwell's 10K hours) or do people continue to get linearly better at whatever they do? I.e. is growth something like sigmoidal or rather exponential?
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I suspect it would vary with the number of different frameworks or paradigms in what is being learned. In Thomas Kuhn's Theory of Scientific revolutions he makes the comment that the skills learned in the old paradigm do not usually transfer to the new one.  An expert may in fact need to unlearn a way of thinking to learn new ideas.
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hello... I want to know which is the best model to investigate the memory enhancing/restoring effect of any test compound.. Literature has mentioned many models, which makes it difficult to choose one particular model.. Thanks
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Hi Sandeep,
In my opinion many different aspects should be taken in account:
1.which type/kind of learning/memory impairment ? In other words which behavioral test?
2.as mentioned by Fiona, which condition ? Genetic/wild type ?
3.which type of drug ? A novel compound ? a compound acting on specific (mammalian/specific) targets ? an oral administered compound ?
4.Do you need a dose/effect specific curve ?
For instance, I'm working on flies. They have a very sophisticated behavior, although colleagues working on higher models sometimes superficially consider this. The advantage is a huge number of individuals analysed in the same moment. Consider if they are mutants. On the contrary, a curve dose/effect is more complicated and, although 70% homology, there are differences with humans.
In other words you should choose the best for your scientific problem, rather than the best model at all. I'm a MD, PhD, and I worked with a lot of models including humans (patients....former neurologist) and I found that you can reach beautiful results with the apparently less important models.
I hope to have helped you, at least, to watch the problem from another side 
:-) AM
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I will look at to the effect of aging on learning and memory in rat (using Morris Water Maze test).
The rat will be performed the testing when they reach the age of 8, 12, 16, 20 months.
Is it possible to use the same rat for testing?
The previous testing (at 8 month age) will interfere the result of the later testing (at 12 or 16, 20 month age) , or not?
or I should separate the rat into 4 group?
What is the minimum of time interval between the two testing (in case of Morris water maze test) can be performed?
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Dear Taratorn,
regarding re-testing of the same animal in various repetition of the test, it is possible however, you have to take that into accound when you do your statistical analysis as well as your results interpretations.
In particular in a learning task like the Morris Water Maze, where some procedural learning is present as well as spatial learning.
In particular some "training" effect might shadow your age-induced deficit.
If you keep that in mind there is no reason you should not re-use the same animals, especially considering that you seem to plan to test them every 4 months, which should be enough to reduce the impact of each repetition of the test.
In an attempt to reduce the transfert of learning from one iteration to the next, you could consider testing them in different room (if feasible) or changing the distal and local cues used during the visual learning and spatial learning phase of the task.
I hope it helps
best 
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      Baddeley (1983) said it clearly, that working memory is the temporary retention of recent information for the performance of a task or the solution of a problem.  Yet the future perspective of working memory is commonly ignored and, with it, the essence of its definition and the key to understanding its brain mechanisms.   Indeed working memory is essentially prospective, like other executive functions of the prefrontal cortex.  They are prospective and preadaptive.  So, in a certain sense, working memory is teleological.  Psychologists and neuroscientists, however, like all other scientists, abhor teleology because it reverses the temporal course of causality, an absurdity.  They even have a hard time accepting teleonomy (Monod 1971), which posits that life itself has future “purposes”: to preserve and to propagate itself.
      On close analysis, working memory can be shown to be prospective, future-oriented, yet not strictly speaking teleological.  The evidence is now overwhelming that working memory consists of activated long-term memory that has been updated for the achievement of a goal in the near future.  The updating may be prompted by an external or internal stimulus, but the content of working memory is not just that stimulus but also its history.  Therefore, working memory is not a special form or system of memory, but the active state of a temporarily reconfigured cortical network of long-term memory toward a goal in the near future.
Baddeley, A. (1983). Working memory. Phil. Trans. R. Soc. London. B302, 311-324.
Monod, J. (1971). Chance and Necessity. (New York: Knopf).
Fuster, J. M. (2015). The Prefrontal Cortex, fifth Edition.  (London: Academic Press).
 Fuster, J.M. and Bressler S.L.  (2015).  Past makes future: Role of pFC in prediction.  Journal of Cognitive Neuroscience, 27: 639-654, 2015.
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Dear Tobi,
 You have addressed most directly the two assumptions on which my question was based.  And you have reasoned persuasively for both: (a) WM is a prospective function, and (b) its content consists of a portion of LTM (semantic, episodic or other) that has been updated, reconfigured, and given present relevance for a prospective action.
With indispensable caution and respect for all those who have intelligently participated in this discussion, here I wish to make a few points regarding those two principal tenets:
 1.  The in-depth discussion of WM makes no sense, either psychologically or neurobiologically, by taking this function out of the perception-action (PA) cycle, the circular and dynamic interaction of the organism with its environment in goal-directed behavior and language.  WM mediates cross-temporal contingencies in that cycle (“if now this then later that; if earlier that then now this”).  That cybernetic cycle processes information from the environment through subcortical structures, the cortex, and back to the environment in the form of action.  It has cognitive as well as emotional components.  The cycle can be set in motion anywhere within it in addition to the environment: sensory receptors, internal milieu, limbic system (notably amygdala, insula or hippocampus), motor systems or associative cortex.
2.  The action that WM prospectively mediates can take many forms:  the response to an emergency, the correct answer to the tester, a mental arithmetical operation, etc.   Further, it can be part of a larger plan--with several PA cycles in it--toward a behavioral or linguistic goal.
3.  The evidence for the prospective property of WM is reviewed in the publications cited under the original post of my question.  Here is a tiny bit of it from our lab (Quintana and Fuster, 1999).  During the delay (retention) period of a WM task, while the discharge of some prefrontal neurons decays, that of others ramps up in anticipation of, and preparation for, the delayed choice to an ambiguous stimulus.  What’s more: the slope of that ramp is proportional to the degree of predictability (Bayesian certainty or probability) of the specific characteristics of that impending choice.
4.   The evidence for the LTM content of WM is also reviewed in those publications.  To reiterate, WM is a portion of LTM retrieved and activated by association (as also by association LTM was originally made, through a STM stage), updated to present context, and retained for a prospective action.  Without these qualifications, discussions of WM can become utterly fruitless or simplistic.
5.  Yes, WM can be viewed as a form of metacognition because it is a knowledgeable “manipulation” of knowledge.  Its content can be infinitely diverse, like LTM or knowledge (semantic memory).  No, there is nothing entirely new under the sun for WM.  The content of WM in a WM test or operation may be a sequence of letters making up a non-sense word, but the letters are part of an alphabet, which is very much a part of semantic LTM.  That piece of the alphabet has been reconfigured, updated, for present use in present context, within the PA cycle.  The sequence may be new, but the components are old.  What defines the content of that WM is the order, the relations (spatial or temporal) between its elements, the Gestalt, like all cognition and metacognition.
6.  As in any executive function, and as the highest stage of the PA cycle, the prefrontal cortex plays a critical role in WM.  It performs that role, however, in close coordination with subcortical, limbic and cortical structures.  It most certainly is not the “store” of WM.  An apt analogy is that of the director of orchestra.  
7.  WM has a temporal decay.  This has been amply substantiated in human and nonhuman primates, psychologically and neurobiologically.  What determines the “WM load” and the course of that decay is the complexity of the content being retained, not just the number of items in it, which may vary considerably about 7 (I am a proud holder of the Miller Prize for cognitive science).
I hope someone will find this helpful.  Cheers.
With kind regards,
Joaquin
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Oral administration of aluminium chloride (AlCl3) in a dose of 17 mg/kg body weight daily for 45 days, which induced AD-like pathology in male rats. Any reference for what should be the molar concentration of AlCl3 to be administered.
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sawati  , How are you  ? can you tell me how  you made induction of AD ? and how  you prepared  ALCL3 for oral adminstration in Rat?                                                                                         thanks in advance
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Dear fellow researchers,
I just started doing field stimulation in the CA3 region of wild-type (WT) SVE129 mice (2-4 month old) to record long-term potentiation in the CA1 region. However, I have major problems seeing LTP in young sve129 mice slices. Instead of an instant excitatory postsynaptic potential (EPSP) elevation, which is maintained at least 30min (typical LTP), I see a slow incline over 5 to 10 min. I already tried to improve my slicing, double checked my solutions and changed batteries in the stimulator. I would be grateful for your help and advice how to fix it.
Thanks!!
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 Dear Flo Hi, please send me your e.mail address so that I can send, in privet, a dedicated paper concerning to your question or difficulties. 
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in the field of education
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Usually, researchers have revealed the role of free unsaturated fatty acids on learning memory. I am very curious whether the saturated fatty acids have any function on learning and memory formation. If you have any idea or access of research article, are welcome to share.
Thanks in advance.
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Can you please show the difference between them? it is related to reflective practice.
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i am interested in recent empirical  studies on early memories and career interests, following the Adlerian approach. does anyone know? 
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Dear colleague, this is a marvelous question and I thank you for posting it.  I too am interested in this topic, but also more broadly interested in the contributions of other psychodynamic schools of thought and how career counselling and psychotherapy converge (McIlveen, 2015). 
I have attached the link to a paper that may interest you (Hoyer & Steyaert, 2015).  It is not Adlerian in focus, instead it takes a Freudian perspective; but I believe it is well worth reading.
Peter
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This is due to me finding that the DVN has improved performance of a visual memory task in one of my PhD studies.
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Thank you both for the article suggestions. Definitely some good ones to read for my PhD!
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I am looking to make a task for adults that tests memory for sentences.
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Not all sentences are equal.  There are issues of syntactic complexity above and beyond sentence length.  Vocabulary would be easier to control for as would be familiarity of content.  It's a matter of what you want to test and which variables you need to control for.
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I want to analyze a performance task over a period of time in animal study, where a particular group of animals is observed for learning curve over a period of 5 days. Is there any trend analysis statistics or other similar analysis that I can perform for this type of dataset? I would like to know how significant the treatment group is as compared to untreated group. Any input or suggestions are welcome.
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Hi Shah,
Probably you could use the repeated measures Two-Way ANOVA. Than you will take in account the performance of the particular group of animal along time and also you can compare both groups. Use as independent variables Time (5 days) and group treatment. You also can add the post-hoc of Bonferroni to compare both groups in each day.
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It is an alternative to memory or stereotype based learning methodologies, more in line with Socratic method. I wonder if any experiments have been conducted and documented with reference to contemporary learning. 
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Studies in metacognition look at the way we think (or think about thinking) and the results have given us more effective ways to acquire knowledge. The link to one recent study that is worth reading is given below. Sometimes it’s not as easy as we would like. Many of us were taught ineffective and even flawed ways to learn new material. If our early years of school were spent using approaches that are contradictory to better learning, it can put us at a disadvantage and affect the messages we give ourselves about our own abilities to learn.
Mark Twain wrote, “I have never let schooling interfere with my education.”
This is a great statement which helps to answer this question. It also leads us into the need for Systems Thinking in our schools. Mark Twain was a proponent of life-long learning and his statement tells us that formal education is just a small part of our learning; but it can also hinder us as well. Formal education is often rigid with boundaries placed on what is expected of us and what is taught based on grade level and other variables.
Many of us learned ineffective and even flawed ways to learn new material. If our early years of school were spent using approaches that are contradictory to better learning, it can put us at a disadvantage and affect the messages we give ourselves about our own abilities to learn. You might take a look at the Center for Educational Neuroscience and the studies based on their computer programs. The link is below.
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Usually we see that when a baby is instruct not to do a particular task, they do that one or want to do that frequently. So far the literature explain in a way of losing control of inhibiting instruction. I suspect that it might be happen to older people (above 60 years of age). It would be highly appreciable if any one can provide me any relevant study in that context. 
Thanks
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Try this, Effects of Emotion and Age on Performance During a Think/No-Think Memory Task Murray et al. 2011 . Hope it helps 
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When does perception end and memory begin? This question is rarely considered but has important implications for the science of psychology.
Folk intuition suggests that perception ends once the object of experience is no longer stimulating the senses. However, this demarcation lacks scientific rigor and is inconsistent with many physical theories of time.
Take for example time considered as a spacetime continuum. Meaningful events that unfold relative to an organism are always defined by time-like intervals. Therefore, the use of spacetime as a model for time in psychology would lead to the conclusion that every experience is memory-based.
I would be happy for any contributions you might have to this discussion!
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Brandon, you might be interested in the surprisingly low information rate of learning novel information (a few tens of bits per second maximum). This would suggest that we retrospectively construct an internal narrative that makes sense of sensations. In addition, the briefest glance can capture around 50 bits of information that is subsequently processed and memorised.
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I am looking for robust theories which explain our ability to know and recall knowledges acquired by drill and practice, but is not obviously somatic. Perhaps knowing the times tables is the best example - similar but also different from learning to ride a bicycle. Thus I know that 42 is the answer to the question "what is six times seven" and I know it instantaneously - without thinking. The body must be involved, just the same as I know some telephone numbers as long as I hold a hand-set and engage in the rhythm of finger-punching them out, but if I try to recall them to mind-alone, I can't. Can anyone help me with a genuine theorisation of these issues?
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Conscious thought isn't necessary for sensory input to be processed by neural mechanisms that mediate learning. Those mechanisms include the brainstem and midbrain sensory nuclei, amygdala and limbic system, hippocampus, striatum, cerebellum, and the so-called "dorsal stream" cortical pathways. These are all unconsciously activated mechanisms, and as a collaborating team are not sufficient for generating conscious states. Conscious states are evidently mediated by frontal executive mechanisms, the activating of which is not obligatory for activating the aforementioned mechanisms mediating learning.
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Bacopa monnieri is one of most studied medicinal herb for memory and cognition. Yet, we have very little scientific evidence (in terms of PK) on the bioactive compounds of the plant. I would like to invite comments on this.
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Thanks for your comment Dr. Gour. The link cites the references to highlight the pharmacological effects of brahmi and its constituents. However, there is still no reference available on the bio-availability and pharmacokinetics of the plant.
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I am trying to understand how depolarisation induced with KCl or glutamate/ NMDA or any such stimuli leads to the balance of actin polymerization: actin depolymerization in neurons. Is it possible that actin depolymerization precedes actin polymerization as an immediate step post depolarization. How does it fit the spine dynamics post depolarization. This relates to temporal dynamics of actin organization in the neurons post depolarization. I think if actin depolymerization precedes polymerization for few minutes (30-1 hr) post depolarization it will help the spines to be flexible and let the movement of receptors and function of other spine machinery possible. It might also help to let the new dendritic mRNA and newly synthesized proteins to enter the spines and take their appropriate functions. Does this concept sound logical? Or are there other possibilities?
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Hi Apurva,
 I think this paper will help your conceptual  questions but this one is more focused and single molecular study but the references will  be more helpful.
Neuron. 2015 Aug 19;87(4):813-26. doi: 10.1016/j.neuron.2015.07.023.
A Temporary Gating of Actin Remodeling during Synaptic Plasticity Consists of the Interplay between the Kinase and Structural Functions of CaMKII.
Kim K1, Lakhanpal G2, Lu HE3, Khan M2, Suzuki A1, Kato-Hayashi M4, Narayanan R4, Luyben TT5, Matsuda T6, Nagai T6, Blanpied TA7, Hayashi Y8, Okamoto K9.
Best
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I have two D'Prime measures - one for baseline memory, and another one for similar but manipulated trials that are of primary interest. Instead of using the actual D'Prime for the condition of interest, I wish to correct it by subtracting the baseline in some way. Is there a definite way of doing this or one of these would work?
- D'Prime Baseline - D'Prime Condition
- (D'Prime Baseline - D'Prime Condition) / (D'Prime Baseline + D'Prime Condition)
Can someone suggest a better way?
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Generally, the difference in two d's is only interpretable under certain conditions. In signal detection theory, d' is the normalized difference between two internal distributions: one for noise and one for signal plus noise. If both of your experimental tasks work on the same continuum (i.e., same decision axis), and if they conceivably share the same noise distribution, then d'1-d'2 gives the differences between S1+N and S2+N. But if the decision axes are not commensurable, then the interpretation depends a lot on how large the standard deviations are on each decision axis, because d' is essentially a measure of effect size.
For instance, you could have d'1 = 1.0 and d'2 = 1.8. If the same decision axis is used in both conditions, then the two S+N distributions lie 0.8 standard deviations apart. If the decision axes are different, you can interpret the difference only as a difference in effect size, but not in a theoretically deeper way. Apples and oranges...
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I would like to understand how my results fit within the levels of processing framework. However, I am only familiar with the original work that was completed in the 70s.
What sources (preferably review article(s)) might you recommend for obtaining a contemporary understanding of this phenomenon?
Thanks!
Brandon
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Brandon,
Here is great review article that describes the progression of levels of processing.
Baddeley, A. (2012). Working memory: theories, models, and controversies. Annual review of psychology, 63, 1-29.
I don't know much of the contemporary applications of this model, but I'm personally interested in inhibitory control.  The act of retrieving information can render subsequent related items less accessible, also refereed to a Retrieval Induced Forgetting.  This is a popular topic now-a-days and has a nice Wikipedia page that might interest you.
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Specifically, there are two main types of settings for mice: 2mA, 2s and 0.3 mA, 5 s. What is the difference? Which is more sensitive? How Passive Avoidance test results may be different between out bread white mice and C57Bl/J mice?
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Please learn about the experience of other scholars who compared the features of behavioral tests in mice of different lines (as compared with rats). All the best.
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I wonder whether findings on memory recall based on lists of nouns can just be tranferred to other kinds of content, especially numbers. I would think that math problems would be encoded diffently and memory recall would also not be comparable. Any thoughts or hints to literature?
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My guess is if you compare say operations span to reading span (in both they have to remember words) they are very similar, certainly they factor together. Now a math problem is a different question then a list of nouns. 25+13=38, at least for a person who is good at math might be encoded as a chunk as opposed to bird, woman, snow which without training will be encoded separately. A math problem is almost more akin to something like rain+ice=sleet which I think participants would encode as a single idea. Recommended papers are this one on span task by Conway et al. 
And this paper by Herbert Simon on chunking
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Can anyone recommend coordinates (w.r.t bregma) for CA-1 region of the hippocampus in 4 mo old mice (C56/BL6). Also, what is the recommended volume of the dye to be injected for verification purposes?
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Given that the question is tagged under Learning and Memory and Behaviour, it is worth noting that CA1 has functional differences depending on where you implant. I'm most familiar with rats but judging from a quick search on PubMed, the same is true in mice. Basically, the dorsal region of CA1 is linked with spatial learning and memory whereas when you move more ventrally, the CA1 becomes weighted towards anxiety-related behaviour.
My best recommendation is to identify what behavioural tasks you're intending to run or to compare to and find if others have done any electrophysiology or microdialysis in those tasks and adopt their co-ordinates. Failing that, are there lesion studies that look at these behaviours? If you find the co-ordinates for a lesion that affects the behaviour, you can put your electrode into the same place.
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I am looking for specific literature to understand what happens with the calcium levels during early LTP phase and Late- LTP phase. It is very well known Calcium influx is necessary for LTP induction but what happens during the maintenance phase of LTP or late- LTP phase, is my question. Are the calcium levels brought to normal levels during maintenance and if yes, then how?
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You can get the similar or apropriate answer by searching the keyword in the GOOGLE SCHOLAR page. Usually you will get the first paper similar to your keyword.
From my experience, InsyaAllah this way will help you a lot. If you still have a problem, do not hasitate to let me know.
Kind regards, Dr ZOL BAHRI - Universiti Malaysia Perlis, MALAYSIA
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Please do not suggest drilling / weigt-drop device.
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The rats can be anesthetized during delivery of blast.  Lee Goldstein here at the BUSM uses anesthesia in his model.  Use a short acting anesthetic such as isoflurane as longer acting anesthetics may attenuate the induction of apoptosis et cetera.  I believe they induce trauma via air pressure.
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 Greg Miller " Many details of the process of memory recall are not known (or are disputed). Even so, some researchers say it's time to revise some aspects of the standard view—such as the notion that the hippocampus is not involved in retrieving older episodic memories, and that memories become fixed and unchangeable once transferred to the neocortex. Newer work suggests a far more fluid role of memory, and one in which retrieval plays a crucial role in shaping memory over time"
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Maybe some of you might like my ideas on this question.
Just have a look! You don't even have to leave RG!
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It is known testosterone can improve cognitive functions, but less known is whether triggering some kinds of memories can influence testosterone production. 
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Hi Xin,
Hippocampus is one of the region of brain which have adult neurogenesis more than any other region in most mammals. Gonadal hormones are found to be involved in regulation of neurogenesis and modulate the structure and function of the brain and can affect the learning and memory. Also there are growing evidence about the complex interaction between HAP and HPG axes. There might be direct correlation of activity in dentate gyrus as it is densely populated and have enormous amount of neurons carrying receptor for stress related hormones like glucocorticoide receptors, and activity of the neurons having these receptors in dentate gyrus can alter the function of HPA as well as HPG axes. It’s probably the neurons in dentate gyrus and other brain regions form a neural circuit network (intra or interconnectivity with other type of neurons or among the regions) which might control the excitation or inhibition of the release of physiologically relevant hormones and drive the related behavior.
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I am looking to dissociate the functional role of the hippocampus and Striatum in humans and am currently searching for potential tasks that have been used in previous studies. I am particularly interested in the dissociation of stimulus response and action outcome learning.
Thank you very much for your help.
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This is the review article that contains information and references of importance. Note that medial and lateral striatum are different in terms of anatomy, physiology, and behavioral function.
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We plan to do some behaviour experiments such as putting the SD rats into a multiple T mazes and record the path and latency of the subjects to analyze the behavior performance. Some questions:
Is there any latest protocols published in the literatures can be referenced? Wish the experiments can be conducted as the standard protocols and finished smoothly.
How many types of spatial learning are there in the above experiments according to the cognitive psychological theory?
Given that the rat can be delivered with real time reward to its motor actions during running in the maze. What is difference between the group of rats with real-time reward and the rats with the final reward only at the goal position?
Your comments and suggestions are really appreciated. 
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Testing spatial memory means the animal will get rewarded if responding based on spatial location as defined by allocentric, rather than egocentric cues. That is, the animal has respond based on the information provided by multiple cues located around the maze - rater than within the maze; or based on body turns. Thus, you have to be careful to surround the maze with a number of cues, none of which should be placed in close proximity to the location where the animal has to respond.
This paper may be of help. It contains all the references you need.
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By which mechanism does Acetylcholine affect on the learning ability and memory performance ?
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thank you Dr.Ali Abdil Razzaq 
its really helpful 
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I am working on the relationship between working memory and academic achievement among children with intellectual disabilities.
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I'm not sure if this is what you are looking for, but it does measure Spatial Working Memory
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Neger, Rietveld and Janse (2014; attached) recently found that perceptual and statistical learning may rely on the same mental mechanism. Now, fearless of stretching, if we relate that to the issue of symbol grounding in language comprehension (cf. modal/embodied vs. amodal/symbolic accounts), would the previous findings support the mixed proposals that language comprehension is both perceptual and statistical (e.g., Barsalou's Language and Situated Simulation; Louwerse's Symbol Interdependency)?
Thank you very much
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A few additional references for your consideration:
Maye, J., Weiss, D. J., & Aslin, R. N. (2008). Statistical phonetic learning in infants: Facilitation and feature generalization. Developmental Science, 11(1), 122-134.
Keidel, J. L., Jenison, R. L., Kluender, K. R., & Seidenberg, M. S. (2007). Does grammar constrain statistical learning? Commentary on Bonatti, Pena, Nespor, and Mehler (2005). Psychological Science, 18(10), 922-923.
ten Cate, C., & Okanoya, K. Revisiting the syntactic abilities of non-human animals: natural vocalizations and artificial grammar learning. Philosophical Transactions of the Royal Society B: Biological Sciences, 367(1598), 1984-1994.
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I am doing a research in Spatial Location Memory in children.  If anyone knows of previous research performed in the subjuct could you please help? 
Thank you
Antonio
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There is a US Science of Learning Center (Spatial Intelligence and Learning Center) in which most of the investigators study some aspect of spatial processing in children: http://sites.temple.edu/risc/projects/navigation/.
Also, Lynn Nadel and colleagues did a series of spatial learning and memory studies in children that were analogous to the sorts of studies done in rodents. Many of these were done in the 1990's.
Good luck with your work!
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Memory is genetically regulated from mother to offspring or its all influence by her experiences during gestational period. What influences or what determines the offspring cognitive process and memory?
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I agree with the previous answers. The question is very interesting. In fact it is the so called Nature vs Nurture problem. Nowadays many scientists focus their attention in epigenetic factors that contribute to CNS development. We know that genes are essential for that development and these genes come from both parents. However, during pregnancy and after delivery, there are several factors that modify gene expression. For example, stress. High cortisol levels in the mother during pregnancy affect brain features of the offspring (they can be more sensitive to stress). The same happens with other hormones. Hence, a male with a low level of testosterone keeps the brain with a female-like structure (and this could be detected in spatial memory tasks). These are just two examples. I’m afraid that the answer to this question involves many factors and it’s not so simple (but we’re trying ;-)
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I'm having some trouble with my mice freezing when they are placed in the Morris water maze. I understand that this is indicative of anxiety, but I'm not sure how best to remove this element when conducting these experiments. I try to handle the mice daily for at least a week prior to commencing the experiment and the water is kept at around 28°C. Any suggestions would be greatly appreciated. 
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Hi Paul
Floating (or freezing) can have several reasons:
  1. Water temp too high (or too low) could reduce motivation to locate and escape; try to lower it, but do not go below 23C, because mice do rapidly cool down. However, keep in mind, changing parameters such as temp during an experiment is impossible, it will distort your results. Our pool temp is between 25-26C, which works very well for us.
  2. Motor defect: some genetic models might have (slight) impairment in motor behavior, and maybe floating is a coping strategy for them (they might learn quickly that they will get out sooner or later)
  3. Anxiety: external factors certainly play an important role, eliminate/reduce extremes, like loud sudden noises, strong odors, fast movements, basically anything unexpected. Also try to remove yourself from view ( including visual, olfactory and auditory cues), make yourself as 'invisible as possible' until the animal is safely on the platform. if you have to transport the animals to the MWM room, give them time to settle down. Your mice should be used of being handled by you (not by someone else), take a few days to handle them, before starting. And stay calm and relaxed yourself.
  4. Age: really old mice will show more often floating behavior. We are working with aged (>12months old) AD models, and floating is frequently observed across genotypes. Adult mice (age 3-9 months) usually do well.
  5. Protocol: Spacing your daily trials to ensure optimal acquisition learning is crucial. The time in between swims should ideally be between 15 and  30 min, enough time to recover but not too long to loose the recall effect. We also place the animals under a IR lamp, and provide ample paper tissue material for them to dry themselves. Rats can also be patted dry, but mice do not always appreciate human touch that much.
  6. Bad luck. Sometimes, despite all measures you will find floaters. If an animal refuses to cooperate, it will also not acquire spatial information and its behavior cannot being interpreted as such. If this is a general phenotype of your i.e. genetic model (see point 2), you just report it as such (without being able to draw any conclusion about spatial learning). If you observe this behavior in one or two animals in your group, it might be learned individual behavior (coping) and you need to exclude them. It is almost impossible to reverse established floating behavior. We have extensive experience with MWM and sometimes, no matter what, they float...
  7. Good luck...
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There are several theories of basal ganglia function, leading many of us to propose segregation of functionally heterogeneous subregions within the dorsal striatum [e.g., see our 2011 review in Neurobiology of Learning and Memory, vol. 96, pp. 95-120]. Given the subregional variation in several neurochemical markers within the striatum, are the functional distinctions related to the compartmental organization of the patch-matrix system?
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Patch - matrix compartments .Defined by neurochemical markers ,this Organization appears to related separated population of Striatal medium spiny Neurons with distinct Input-output connections .
Both patch and Matrix projects to substantia nigra , but patch behaves as  an input to Dopaminergic cells esp in ventral tier of Dopaminegic neurons while matrix neurons provide inputs to the location of the GABAergic neurons in the substantia nigra pars reticulata.
More details and source of my understanding so far is here ,
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pardon "the newbie"  for any mistakes .
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We have been using the Morris Water Maze, but I was wondering if there are any more reliable experiments to test for deficits in ACC function in rats.
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I agree with Tumay, ACC has several different behavioural roles (most of what I'm familiar with is impulsivity) so your task would depend primarily on the function of most interest.
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my question is that,short stressful events (acute stress) always said to be facilitates learning and memory and also chronic stress said to be impair the learning and memory. Can anyone tell what is the reason and how it works?
What is the neuronal plasticity mechanism behind learning and memory during stressful condition?
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When you say plasticity are you talking about LTP and LTD. With neuroplasticity even acute stress can decrease hippocampal LTP. As has been mentioned this is thought to be mediate by the HPA axis via cortisol and glucocorticoid receptors, which are highly expressed in the hippocampus and thus memory is so tightly linked to stress, along with the hippocampal connections to the amygdala. I want to say that mTor is involved downstream of glucocorticoid actiation. Best of luck,
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Is it possible for hypertension to effect any behavioral change (learning memory or motor)? Any reports regarding this?
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I published in 1986 the following paper
MAZZUCCHI A., MUTTI A., POLETTI A., RAVANETTI C., NOVARINI A., PARMA M. Neuropsychological deficits in hypertension. Acta Neurologica Scandinavica, 73, 619-627,1986.
Best regards
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What are best blood and brain biomarkers available to test the animal (rat) cognition and intelligence.
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In my opinion no functional marker is known till date for cognition and memory. But physiological marker is there like reading attention and remembring and there is some scoring system to evaluate the cognitive functionFunctional Cognitive Assessment Scale (FUCAS) is a new reliable (alpha > 0.89 - 0.92) cognitive-behavioral scale that assesses executive function in daily life activities directly in patients with dementia.FUCAS is a useful and reliable diagnostic tool for MCI. Cognitive-behavioral assessment such as that provided by FUCAS can provide objective information that can serve to enhance the quality of clinical decision-makin.
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How do you check the normal intelligence of laboratory animals like rat? What criteria is there and how are the normal healthy animals identified?
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yes, but it´s depend in what kind of study you are thinking to use de animal model, usually animal lab arrived with a health certificated from where they are coming as eg. Charles River. To check how intelligence can be rat for eg. there is many ways to do it, as Stephanie said. but you have to be sure that they are healty animals.
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Is there any work already reported on S-nitrosothiol used against AD in animal models?
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Hi Sharma,
There are other things you can do about it. For example, go to Comparative Toxicogenomics Database (free)
Under search - select Chemical
Enter "S-nitrosothiol" and click on Search
The results page will show a number of tabs on top
Click on the "Diseases tab" - arrange it alfabeticaly by clicking on the arrows next to the disease heading in the tab
Look for Alzheimers disease - it will show two rows for Alzheimer- it contains genes regulated, etc, and also references from where the data is coming from (papers)
This is a starting point but you could explore other resources
I hope this helps
Good luck!
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Tyrosine hydroxylase positive cells are not present in the sample.
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You are welcome. If you need anything else, I will be glad to help.
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