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What are the working physical definitions of thoughts and memories? I understand that this is an area of science that is still developing, but are there basic definitions that would work to physically describe thoughts and memories?

 

More specifically, do thoughts arise from electrical signals being passed through certain areas of the brain? If so, would memories then be some neuron characteristics that would then be changed (by the electricity) to "remember" the thought?

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Well, certainly neurons interact, or communicate, using electrical 'signals'. These are nothing like what happens in an electrical network of real metal, where signals travel a lot faster.

 

The network, or mesh of interconnected neurons isn't that efficient at signal transmission, but it does the job. Also the 'slowness' of the actual propagation time of the spikes that travel along an axon seems to be overcome somewhat by the sheer number of 'switching elements', or relays, and the thousands of connections each makes with other neuron 'units'. But it still takes tens or hundreds of msec to get a signal from a 'pain' neuronal assembly when you stub your toe (and reconfigure a few stress proteins, and trigger a signalling cascade). You "remember" the pain for a while. It's got to do with strengthening certain pathways, and its reliant on certain feedback cycles, which are themselves controlled by other stuff.

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Thanks. I think I got the answer I needed but to clarify..

Could it be said that a thought existing at one time is physically represented by the charge distributed between neurons in the brain?

 

But it still takes tens or hundreds of msec to get a signal from a 'pain' neuronal assembly when you stub your toe

 

Different injuries seem to travel at different speeds as well. Clean cuts can be painless for quite awhile.

 

signalling cascade

 

What does this mean?

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Hi Quartile,

 

While Fred does a fun job of explaining things poetically, you must note that he is really oversimplifying much of the above, and speculating on some.

 

The only true answer is that we don't yet know. We can tell which regions are active in memory and which regions are active for certain thoughts. That's it so far. Your questions are more to do with consciousness than thought itself, although the two are very related.

 

 

In sum, any conclusions you try to make will be very weak, and there are no easy answers yet to your very difficult questions.

 

The best thing you can do is study on what is being researched and try to refine your questions once you've learned more about what we do and do not know.

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would memories then be some neuron characteristics that would then be changed (by the electricity) to "remember" the thought?

 

Although I agree with iNow about the little is known on this subject and the complexity of the question, I think that a summarized and simplified answer could be given:

I believe that a significant physical change produced in memory formation is the establishment of new synapses between neurones. This process, by means of which new communications between neurones are built, is known as “Long Term Potentation (LTP)” and the main implicated neurotransmitter is glutamate.

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Although I agree with iNow about the little is known on this subject and the complexity of the question, I think that a summarized and simplified answer could be given:

I believe that a significant physical change produced in memory formation is the establishment of new synapses between neurones. This process, by means of which new communications between neurones are built, is known as “Long Term Potentation (LTP)” and the main implicated neurotransmitter is glutamate.

 

When you say "I believe," what does that mean, exactly? Are you a neuroscientist and that is your professional opinion? Is that more-or-less established science that you're simply saying you trust? Is it just another way of saying "if I recall correctly?" I know almost nothing about the subject, so these are genuine questions.

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When you say "I believe," what does that mean, exactly? Are you a neuroscientist and that is your professional opinion? Is that more-or-less established science that you're simply saying you trust? Is it just another way of saying "if I recall correctly?" I know almost nothing about the subject, so these are genuine questions.

 

Sorry, I can’t express myself fine in English:doh: . When I use “I believe”, I refer to “I believe is a significant physical change”, it could not be considered a significant physical change…

 

I’m a biochemist and I am working in neurochemistry (in Spain there’s not a profession called neurochemistry). So, it’s my professional opinion that for memory formation new synapses must be established by means of LTP, which works thanks to glutamate receptors activation.

 

There is not something new, you can find this in any good neurochemistry book.

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signalling cascade

 

What does this mean?

Epac Mediates a cAMP-to-PKC Signaling in Inflammatory Pain: An Isolectin B4(+) Neuron-Specific Mechanism

 

"A dose–response curve established that 1 uM isoproterenol produced translocation in a maximal number of cells. Translocation of PKC was transient, peaking at 30s, decaying by 90s, and returning to baseline after 5 min.

 

Induction of translocation by isoproterenol was mediated by 2-AR as it was inhibited by the 2-AR-specific antagonist ICI. ICI is described as an inverse antagonist not only blocking receptor activation but also reducing its baseline activity (Bond et al., 1995), reflected by the decrease in baseline PKC translocation.

...

• Epac Activates PKC in Nociceptors

 

Because cAMP activates PKA (Neves et al., 2002), we used the well

established activator of AC, forskolin, to test for its involvement

in the signaling cascade leading to PKC epsilon translocation. With a

maximal response time of 30s, forskolin also induced the translocation

of PKC epsilon to the plasma membrane."

--Tim B. Hucho, Olayinka A. Dina, and Jon D. Levine

National Institutes of Health Pain Center, University of California, San Francisco, San Francisco, California 94143

 

 

Review: neuronal-glial interactions in central sensitization

 

Abstract

 

"Pain facilitation has conventionally been viewed as being created and maintained solely by neurons, whereas glia (microglia and astrocytes) were not considered to be involved. Current views of glial function include a dynamic role within the spinal cord dorsal horns to create and maintain enhanced pain. This review summarizes how spinal cord glia are now implicated in diverse exaggerated pain states by proinflammatory cytokines and other potential mediators of glia-neuron communication. Glial activation is shown to be necessary and sufficient to create pain facilitation in laboratory animals. The implications for potential clinical therapeutic treatment is discussed. "

 

--Erin D. Milligan PhDa, Corresponding Author Contact Information, E-mail The Corresponding Author, Steven F. Maier PhDa and Linda R. Watkins PhDa

a Department of Psychology and the Center for Neurosciences, University of Colorado at Boulder, Boulder, Colorado, USA

 

Any clearer, at all?

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iNow: I dont appreciate your post. From what high place are you talking down to me? I know plenty about the current state of science with regards to the physiology of the human brain and I have yet to understand why the most basic questions have not yet been answered. One of the most basic questions is the one I have asked here and it almost seems that science is lacking the initiative to come up with a solid answer to it: what function does electric charge serve in the human brain? Regardless, I am sure you meant well in your post. Thanks.

 

If this post is speculative because of the nature of the question and its relation to unproven science then so be it, respond with speculations and theories. This does not make the question any less worthy of being asked, indeed I would say it makes it more so.

 

zule: I am familiar with LTP and glutamate's roll in plasticity but I failed to make the correlation between these factors and memory storage. Is it possible, however, for glutamate to build new synapses on its own? I would think that it would be necessary for the synapse to be "activated" by electricity before it is "solidified" by glutamate... that is, we have to think a thought before it can become a memory?

 

Fred: Yes that is a little clearer. I was really only curious about the precise use of the word "cascade" and wasnt sure if it was only a clever way to describe a "flood" of activity.

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iNow: I dont appreciate your post. From what high place are you talking down to me?

Okay. You are clearly right. Let me approach this like Fred did so as to make you happy.

 

Unicorns did it.

 

Better now? :doh:

 

 

If you ask a specific question, I will help you out where I can. If I sense that somebody has given you only half truths, I will point those out. If I think your question is too broad, I will request clarification. You need to cool down, and try to express your question a little more clearly. What types of thoughts? What types of memories? Are you refering to proprioception, or some specific sense, or math or movement or memories triggered by scent or the ability to recall or... What? If you'd rather move forward on speculation and prefer I not participate, that's fine. Just say so. If you want actual science, I will try to point you in a direction that will help you learn.

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Okay. You are clearly right. Let me approach this like Fred did so as to make you happy.

Hey man Im just asking you to level with me. My question does have to do with consciousness as I believe that leaving consciousness out of scientific studies of the brain is defeating the purpose.

 

Are you referring to...

Aren't these things all caused by electricity moving through different parts of the brain?

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he is really oversimplifying much of the above, and speculating on some.

OK, my turn for some pointless quibbling.

Are you prepared to present my oversimplified version of a speculative model of consciousness against your version? Or are you just going to keep warning everyone about morons?

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Aren't these things all caused by electricity moving through different parts of the brain?

 

Chemoelectrical conduction throughout the entire nervous system. The thought about pain in your foot is different from the thought about the origin of the universe is different from the thought about sexual intercourse. They are all some emergent property of several chemoelectrical signals, some phenomena due to the activation of the neural and circulatory web, but they are NOT limited to the brain.

 

 

Here's a neat primer to help you with the terminology:

 

http://www.wooster.edu/biology/dfraga/BIO_305/Lectures/BIO305_SigTrandGProt.ppt

 

 

Here's a good high-level overview on the basics:

 

http://www.maui.net/~jms/brainuse.html

 

 

Here's a good page with graphics on the CNS:

 

http://library.med.utah.edu/WebPath/HISTHTML/NEURANAT/NEURANCA.html

 

 

Here's a link with lots of informative sites. If you are truly curious, spend some time exploring these:

 

http://www.mnsu.edu/comdis/kuster2/newbasics.html

 

 

 

 

OK, my turn for some pointless quibbling.

Are you prepared to present my oversimplified version of a speculative model of consciousness against your version? Or are you just going to keep warning everyone about morons?

 

Fred - Perhaps you'd not sound like such an idiot if you realized how much point there was in such "quibbling." Again, what you've presented thus far is the equivalent of "unicorns did it." I don't need to have to have my own theory of consciousness in order to successfully counter yours.

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How is strengthening in neuronal pathways and persistence due to a signal cascade equivocal to unicorns... as you claim (and you are definitely equivocating, calling it "what I've presented" i.e. two articles from recognised research pubs. What are you going to tell everyone about the research they did, exactly, unicorns again, is it, or parrots this time?

 

Decreased ERK-mediated modulation of A-type potassium currents in DN MEK mice

To further investigate whether there is a functional deficit of the MEK-ERK cascade specifically in spinal cord neurons of the DN MEK mice, we asked whether ERK regulation of a downstream target, the transient A-type potassium channel, is altered in these mice. ERK is known to phosphorylate Kv4.2, an A-type potassium channel subunit [27], and we have previously shown that MEK inhibitors (U0126 or PD 98059) enhance A-type potassium currents in dorsal horn neurons of the spinal cord [19]. Dorsal horn cultures were prepared from either wild type or DN MEK mice, and the effect of bath application of 20 μM PD 98059 was examined. Neurons from the DN MEK mice were significantly less sensitive to modulation by the MEK inhibitor PD 98059. These results confirm a reduced function of the MEK-ERK cascade in dorsal horn neurons from the DN MEK mice.

-Mol Pain. 2006; 2: 2.

Published online 2006 January 16. doi: 10.1186/1744-8069-2-2.

Copyright © 2006 Karim et al; licensee BioMed Central Ltd.

 

Group I metabotropic glutamate receptor NMDA receptor coupling and signaling cascade mediate spinal dorsal horn NMDA receptor 2B tyrosine phosphorylation associated with inflammatory hyperalgesia.

Guo W, Wei F, Zou S, Robbins MT, Sugiyo S, Ikeda T, Tu JC, Worley PF, Dubner R, Ren K.

 

Department of Biomedical Sciences, Dental School and Program in Neuroscience, University of Maryland, Baltimore, Maryland 21201, USA.

 

Hindpaw inflammation induces tyrosine phosphorylation (tyr-P) of the NMDA receptor (NMDAR) 2B (NR2B) subunit in the rat spinal dorsal horn that is closely related to the initiation and development of hyperalgesia. Here, we show that in rats with Freund's adjuvant-induced inflammation, the increased dorsal horn NR2B tyr-P is blocked by group I metabotropic glutamate receptor (mGluR) antagonists [7-(hydroxyimino)cyclopropa chromen-1a-carboxylate ethyl ester (CPCCOEt) and 2-methyl-6-(phenylethynyl)-pyridine (MPEP), by the Src inhibitor CGP 77675, but not by the MAP kinase inhibitor 2'-amino-3'-methoxyflavone. Analysis of the calcium pathways shows that the in vivo NR2B tyr-P is blocked by an IP3 receptor antagonist 2-aminoethoxydiphenylborate (2APB) but not by antagonists of ionotropic glutamate receptors and voltage-dependent calcium channels, suggesting that the NR2B tyr-P is dependent on intracellular calcium release. In a dorsal horn slice preparation, the group I (dihydroxyphenylglycine), but not group II [(2R,4R)-4-aminopyrrolidine-2,3-dicarboxylate] and III [L-AP 4 (L-(+)-2-amino-4-phosphonobutyric acid)], mGluR agonists, an IP3 receptor (D-IP3) agonist, and a PKC (PMA) activator, induces NR2B tyr-P similar to that seen in vivo after inflammation. Coimmunoprecipitation indicates that Shank, a postsynaptic density protein associated with mGluRs, formed a complex involving PSD-95 (postsynaptic density-95), NR2B, and Src in the spinal dorsal horn. Double immunofluorescence studies indicated that NR1 is colocalized with mGluR5 in dorsal horn neurons. mGluR5 also coimmunoprecipitates with NR2B. Finally, intrathecal pretreatment of CPCCOEt, MPEP, and 2APB attenuates inflammatory hyperalgesia. Thus, inflammation and mGluR-induced NR2B tyr-P share similar mechanisms. The group ImGluR-NMDAR coupling cascade leads to phosphorylation of the NMDAR and appears necessary for the initiation of spinal dorsal horn sensitization and behavioral hyperalgesia after inflammation.

 

- J Neurosci. 2004 Oct 13;24(41):9161-73

 

It's a really big show, evr'body...

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I know plenty about the current state of science with regards to the physiology of the human brain.

It is not my intention to upset you, but I would swear, basing on what you have wrote in this thread, that you don’t know anything about basic brain physiology. I think you want to start the house for the roof… But don’t worry; I neither think that Fred56 knows what he is talking about.

 

 

 

zule: I am familiar with LTP and glutamate's roll in plasticity but I failed to make the correlation between these factors and memory storage. Is it possible, however, for glutamate to build new synapses on its own? I would think that it would be necessary for the synapse to be "activated" by electricity before it is "solidified" by glutamate... that is, we have to think a thought before it can become a memory?

Nervous transmission is not only electric transmission; part of the time, the impulse is transmitted electrically and part of the time chemically (by neurotransmitters). Once the impulse arrive at a glutamatergic neuron (presynaptic neuron), prompts the release of glutamate to the synapses. This glutamate joints to glutamate receptors in the postsynaptic neuron, prompting a signal cascade. In the first link that iNow have put, you can see an example of signal cascade. Although this example shows the pathway of metabotropic receptors ad in the case of glutamate the main implicated are the ionotropic receptors, while metabotropic ones are modulators, I think this could serve as explanation.

 

At the end of the signal cascade, we get, through the activation of proteins the “Short Term Memory”. For example, we are going to dial a phone number, someone tells us that number and we immediately dial it. But 10 minutes after that, we don’t remember that number.

 

If we want to remember that phone name for dialling it other day, we have to concentrate and repeat that number. On this way, we made a “Long Term Potentiation” or a “Long Term Depression”: we are prompting repeated stimulations of the glutamatergic neuron and so repeated release of pools of glutamate and activation of the signalling cascades. This lead to activation of several genes that will prompt the phenomenon of synaptic plasticity: it will be a variation in interneuron connexion (the physical change) and we have got the “Long Term Memory”

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I neither think that Fred56 knows what he is talking about.

I think you might have meant to say you do think that, but no worries (even if you did, it doesn't actually matter, does it?). Looks like you're doing this very thing, unless you really are saying that you disagree with four different research groups who are looking at the way neurotransmitters and cytokines are involved in those cascades and signal pathway strengthening, involved with short and medium term analgesic reactions i.e. memory, of pain?

 

However what I was first talking about is how we understand some of what goes on in there, but as another thread I started in Psychology section talks about, there's a lot more going on than just electrical signals zipping around a network.

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Hey man Im just asking you to level with me. My question does have to do with consciousness as I believe that leaving consciousness out of scientific studies of the brain is defeating the purpose.

 

Looking back on your post, I fully agree with your quoted text above. You are absolutely correct. But... tell me... what is consciousness? How is it defined? How is it measured? What parameters to we use to quantize it?

 

This is why I referenced unicorns. The "what is consciousness" question is a speculative and philosophical one, not (yet) a scientific one. This is why I was pushing you to better define your question, break into into smaller parts so we can have a chance at solving those... and, ultimately, arrive closer to the answer you seek.

 

 

 

For others who may not know what zule is referring to with neural plasticity and LTP, here is a better high level overview than those I shared above:

 

http://faculty.washington.edu/chudler/plast.html

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you don’t know anything about basic brain physiology.

Not as much as you but I bet I could describe the basic mechanisms with legitimate accuracy :P

 

tell me... what is consciousness? How is it defined? How is it measured? What parameters to we use to quantize it?

 

Maybe to be conscious is to be aware of the relationship between you and your environment? That is, how do I sustain/benefit myself here so that I dont die?

 

A good measurement would be an organism's black body radiation or an account of energy exchange with the environment. An apparent contradiction with the definition arises here. Whether or not a multicellular organism is readily aware of the full extent of their consciousness, the individual cells that make up their organs have to keep functioning for the whole organism to remain alive. So thinking with the brain is as conscious an act as digesting with the stomach - they both serve the same purpose.

 

Is that any good? Tear it to shreds! lol

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Towards a "lexicon of neural biochemistry".

And an adjunct "offering"

 

Maintenance (late phase) of LTP and central sensitization.

The mitogenactivated protein kinase (MAPK) cascade is activated in both hippocampal and dorsal horn neurons.

 

The receptors and signaling pathways in dorsal horn and hippocampal neurons are indicated. Activated extracellular signal-regulated kinase (ERK; a MAPK) is translocated to the nucleus and activates the transcription factors cAMP-response-element-binding protein (CREB) and Elk-1, causing them to bind to cAMP-response elements (CRE) or serum-response elements (SRE) on gene promoter regions, respectively.

 

This triggers transcription of immediate-early genes (IEG) and late-response genes (LRG).

 

Abbreviations: bAR, b adrenoceptor; CaMK, Ca2þ/calmodulin-dependent protein kinase; DR, dopamine receptor; Dyn, dynorphin; mAChR, muscarinic ACh receptor; MEK, MAPK kinase; mglu, metabotropic glutamate receptor; NK1, neurokinin 1; PKA, cAMP-dependent protein kinase; PKC, Ca2þ/phospholipid-dependent protein kinase; trkB, tropomyosinrelated kinase B.

 

--Ru-Rong Ji1, Tatsuro Kohno1, Kimberly A. Moore2 and Clifford J. Woolf1

1Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA

2Department of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, CA 94143, USA

Fear Memory Formation Involves p190 RhoGAP and ROCK Proteins through a GRB2-Mediated Complex

p190 RhoGAP phosphorylation by the Src proteins induces its interaction with SH2-containing proteins such as p120 RasGAP (Hu and Settleman 1997 and Roof et al. 1998).

 

A GRB2-p66Shc-RasGAP-p190 RhoGAP complex was observed during early morphogenic events of gastrulation and is modulated by changes in cell contacts (Dupont and Blancq, 1999).

 

The formation of this molecular complex, in LA, may promote the translocation of p190 RhoGAP by Shc or GRB2 to a distinct neuronal area in close proximity to its site of action.

 

For example, GRB2 and members of the Rho GTPase family bind to N-WASP, a protein involved in actin polymerization (Snapper and Rosen, 1999).

 

In addition, extracellular stimulation, such as activation of integrin, induces rapid translocation of p190 RhoGAP to cytoskeleton and membrane ruffling where it colocalized with polymerized actin (Nakahara et al. 1998 and Sharma 1998).

 

It is therefore plausible that fear conditioning couples p190 RhoGAP to the cytoskeleton via GRB2 and induces modulation of actin dynamics as well as changes in dendritic and spine morphology in LA.

 

Actin dynamics are involved in remodeling the morphology of dendrites and spines (Matus, 2000), and these structures have been strongly implicated in synaptic plasticity (Nimchinsky et al., 2002).

--Raphael Lamprecht, Claudia R. Farb and Joseph E. LeDoux

Neuron 14 November 2002, Pages 727-738

 

"...Fred does a fun job of explaining things poetically, you must note... This is why I referenced unicorns."
--?
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"...Fred does a fun job of explaining things poetically, you must note... This is why I referenced unicorns."

--?

 

 

 

Troll. You didn't even quote me properly.

 

 

Hi Quartile,

 

While Fred does a fun job of explaining things poetically, you must note that he is really oversimplifying much of the above, and speculating on some.

 

The only true answer is that we don't yet know. We can tell which regions are active in memory and which regions are active for certain thoughts. That's it so far. Your questions are more to do with consciousness than thought itself, although the two are very related.

 

 

In sum, any conclusions you try to make will be very weak, and there are no easy answers yet to your very difficult questions.

 

The best thing you can do is study on what is being researched and try to refine your questions once you've learned more about what we do and do not know.

 

Looking back on your post, I fully agree with your quoted text above. You are absolutely correct. But... tell me... what is consciousness? How is it defined? How is it measured? What parameters to we use to quantize it?

 

This is why I referenced unicorns. The "what is consciousness" question is a speculative and philosophical one, not (yet) a scientific one. This is why I was pushing you to better define your question, break into into smaller parts so we can have a chance at solving those... and, ultimately, arrive closer to the answer you seek.

 

 

 

For others who may not know what zule is referring to with neural plasticity and LTP, here is a better high level overview than those I shared above:

 

http://faculty.washington.edu/chudler/plast.html

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Well as long as were going to be quoting ourselves..

 

Maybe to be conscious is to be aware of the relationship between you and your environment, evident in the fact that you create change in it? A cell's digestive process makes an effort to change the environment for the survival of the organism.

A good measurement would be an organism's black body radiation or an account of energy exchange (in all physical forms) with the environment. An apparent contradiction with the definition arises here. Whether or not a multicellular organism is readily aware of the full extent of their consciousness, the individual cells that make up their organs have to keep functioning for the whole organism to remain alive. So thinking with the brain is as conscious an act as digesting with the stomach - they both serve the same purpose.

 

I also think that a measure of the total negative entropy of an organism would suffice. How is this not a measurement of the effort that an organism expends to perpetuate itself? Is that not consciousness?

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