Nervous system signals and their implications, con.

While I agree that rehearsing a concept that was tricky enough the first time around twice (or even three times) can be frustrating and confusing, I kind of respect an appreciate what Professor Grobstein was doing here.

The NBS concentrators-forum last week included questions about how we thought researchers choose their topics and form their questions. This got me thinking about why researchers don't chose the topics they don't. It's very easy to remain within the limits of your biases, and even moreso to allow the backgroud truths provided by your language and culture go unquestioned. The Bryn Mawr College Intro Bio culture supports only one "truth" or account of how an action potential travels down an axon. It would be very easy to assume that this event can only be thought of in those terms, which would significantly limit the questions you could approach the topic with or the language you could use to describe it.

In breaking the uniform perception of "this is how neurons work," Professor Grobstein is providing a new approach and asking us to think in a manner to which we are not accustomed. I can relate from personal experience that an invaluable lab skill is the ability to generate your own new approaches to scenarios you thought you understood: thinking about the problem in a manner to which your are not accustomed. By providing two accounts of the same event, he is also reminding us of the loopy, story-telling nature of science. Many of the hard and fast "laws" of science are simply ways of describing what was observed; the formula for velocity is just one way to describe an object moving through space. Just becuase one account was taught first doesn't mean that it's explanatory power is somehow better (or worse). Also, language is imperfect and limited, so the more ways a concept is related, the more likely one is to understand the nuances of the process.

i am surprised to read that my peers are still so concerned with the battery analogy mentioned in class to represent the relationship of an impulse traveling through a medium, or the action potential flowing through an axon. i dont have much of a background in biology so this idea is very comprehensive for me. what im not so clear about is the concept of a resting potential, which we havent covered yet but i am interested to learn more about. resting potential seems to contradict the idea that ions are constantly in motion, and i wonder if it simply means that the sodium potassium pumps are inhibitted so that permeabillity is halted? i also still have my question from earlier which asked why the propogation simulation extendedin both directions when the middle node is pressed. i was under the impression that messages only propogate down the axon?

i also wonder about inputs which are obstructed during the action potential. what consequences arise when inputs are not propogated? is the output different? is there no ouput? what sorts of outside factors can influence the propogation of an action potential or make it less sufficient?

i noticed a lot of people are interested in myelin so to keep the conversation going i had a quick question about problems in myelination and what this could mean for the input-output connection. what happens when there is too much myelin? what happens when there is too little? (i think epilespy is an outcome of decreased amounts of myelination, causing information to be crossed among neurons causing seizures). can the myelin be punctured since it is simply a thin lipid layer? what happens if the myelin does not cover the whole axon?

I agree that the battery analogy works better when removed from the literal embodiment of a Duracell battery, but I still don’t think that it is a particularly useful analogy. To begin with the word “battery”, whether we want it to or not, will always be associated with the little metal things that power stuff.  The word itself is just far too loaded.  If a literal battery isn’t what is being discussed then that shouldn’t be what we call it.

Regardless of the wording I think that my main problem with using this analogy is that we don’t need it. The analogy would be useful if we were just learning about the nervous system for the first time, but we aren’t.  We all should have a basic understanding of what an action potential from intro bio.  I find that trying to force myself to understand this analogy just makes me lose sight of what I already know.  I already knew that there was a charge across the membrane, and that is all the battery tells us. Maybe there is some deeper meaning that has not been revealed, but as of right now I just don’t see why we need the battery. 

I was interested in the role the myelin plays in quickening the pace at which an impulse moves through a neuron.  Because the rate at which signals move through the body seems to be an important factor in determining the overall robustness of a nervous system, I decided to look into the myelin a little bit more.

I found that demyelination is the underlying disorder for such diseases as multiple sclerosis. While researching online, I came across this website http://www.mult-sclerosis.org/demyelination.html.  In this website, it states that a demyelinated axon can transmit nerve impulses ten times slower than a myelinated axon.  In some cases, demyelinated axons can become re-myelinated.  However, due to the nature of demyelination and the tendency for scarring along the axon, the re-myelinated axons transmit signals at a slower pace than a normal myelinated axon. In extreme cases, demyelination also leads to degeneration of the axon.  So, it can be concluded that demyelination, although not always, can be an irreversible event with detrimental results.  Of course, there is a lot of information out there about demyelination and its ties to MS and other neurological disorders.

At the end of Thursday’s class, Professor Grobstein said, in conclusion to our discussion, “Behavior happens unless it is inhibited.” This really struck me because it seems since the age of Freudian psychoanalysis, which long-reigned as the pinnacle of behavioral understanding, there is an impetus, socially, medically, culturally, to describe behavior based upon cause and effect. Why do things happen? What “drives” people to behave in certain ways? Freudian theory would have it that there are two “causes” of behavior, sexual impulses and aggressive impulses ( http://www.rpi.edu/~verwyc/FREUDOH.html ). There must be more to behavior than two driving impulses. But, if behavior is rooted in passive current flow and the random movement of ions, there is something that impels us all to “be” and to “do” that is altered by our inhibition of that behavior. In such a paradigm, behaviors we consider aberrant are so much more easily reconciled given that perhaps certain dysfunctional neuronal mechanisms do not allow certain aspects of behavior to be inhibited by certain people. Superficially, one might think that “meaning” is stripped from behavior if viewed as random and the product of passive current flow. However, behavior (and anything else, really) has only the meaning or significance that we ascribe to it.

As Erich Fromm wrote in Man for Himself, “Man must accept the responsibility for himself and the fact that only by using his own powers can he give meaning to his life. But meaning does not imply certainty; indeed, the quest for certainty blocks the search for meaning Uncertainty is the very condition to impel man to unfold his powers. If he faces the truth without panic he will recognize that there is no meaning to life except the meaning man gives to life by the unfolding of his powers…”

I thought mcrepeau's comments on Tourette Syndrome was another interesting direction to take this conversation. I hope in class we can begin to apply what we've learned with our battery theory and action potentials in helping to explain things that are more commonplace. This will only help further our understandings of what a "battery" is, and I agree with Evan as well that it is difficult to think of a battery as not something that is in our remote controls but as a machine itself. But seeing the whole picture, I think the battery example is definitely up to par in explaining action potentials (Although I'm not sure we covered where the "first pulse" comes from; what are sensory transducers? and how do they become stimulated?). Also, I'd like to talk more about the "leaky region of the membrane", and why leakages allow for signals to start and end in the middle of the system. Moreover, what is "the middle" of the system?

I would also be interesting in talking more about multiple sclerosis and loss of myelin.What are the mechanics involved in replacing lost myelin? Why does MS get worse over time?

After reading "Inverting the Relationship", I find I'm still puzzled as to where "meaning" comes in to all this. To me, "meaning" implies volition, and I don't think our neurons are aware of the pulses and depolarization occurring, much less the motor response that is the eventual outcome. But then, that doesn't necessarily mean the occurrences are "random," because there is a system and a pattern. I'm not sure these two things are opposites, or perhaps even comparable. The opposite of random would be planned, or something synonymous, and the opposite of meaning would be pointless. So can something be both random and have meaning? Or planned and pointless? I think so..

This is the topic for my webpaper but I thought it related to well to what we discussed on Thursday. My 3 year old cousin Katie was adopted and spent the first 5 months of her life in an orphanage in rural China. She was diagnosed with autism about six months after my uncle and aunt picked her up, and after communication with the orphanage to try and assess the level of sensory stimulation she received they discovered that Katie had been (like so many other children in these situations) left in a crib in the same room without any toys and was only picked up to have her diaper changed. She had looked at the same walls and ceiling everyday, heard the same sounds and had the same physical contact with her caregivers (essentially no sensory variation, no chances to make summaries of observations etc).

So though we concluded that an action potential can start and end in the middle of a nervous system, I am wondering how that much activity is possible when there have been so few inputs. Katie's inputs were severely limited and thus her development was hindered, so how can the "leaky regions of membrane" idea work in this case when there are so few- if any- sources of stimuli for the brain to work with? Or are these input-independent action potentials the reason why my cousin survived for her first five months?

This has been a topic that I have considered before and thought about it more from this discussion about the brain as a battery. As Professor Grobstein had thrown out, what about the concept of the brain as a computer. I was searching the internet and came across a website(http://faculty.washington.edu/chudler/bvc.html) that is meant for little kids and discusses the similarities and differences between a machine and the brain. I think we are forgetting that metaphors do not mean that two things that are being compared are necessarily the same. Also it is important to remember as many have mentioned above that in order to understand the battery metaphor we would have to redefine what a battery is.

Going over the similarities between the machine and a computer made me realize that the battery metaphor if explained simply can also apply. For example the brain uses chemical signals to transmit information—which can be related to the electrical signals used through the wires in a computer.

Another similarity is that both a computer and the brain transmit information. A computer is binary as it uses switches or commands that are either on or off. Looking at the brain, the neurons are either on or off by either firing an action potential or not firing an action potential. The difference is that neurons are more than binary, as the “excitability” of a neuron is always changing as the neuron is constantly getting information from other cells through synaptic contacts. Also as pointed out in previous weeks that information or inputs across a synapse does not always result in an action potential (output).

Okay...so I get the idea of the battery is stored energy across a synapse...but...I'm still wondering...why is this a more conducive way to look at it? As an alternative way I can accept, but does it open doors for better understanding action potentials?

I like that Angel brought up the fact of outputs that appear to have no input, because I too was on the side that believed that it was there, just separated in time. The fact that random motion in ions can cause depolarization which causes action potentials is interesting, but I have to stick by my gut which tells me that there has been previous input which has modified a structure so that it has a tendency to fire an AP.

While not doubting that at times there is random movement that may cause an AP, I think that it is regulated (although I'm not sure how) so that the action potentials that are "supposed to happen" actually propagate.

This leads me to the place where I am confused. Action potentials have a purpose. No one would doubt that. Yet, we have also seen that they can be/are purposeless, merely obeying the laws of physics. The line between the two, where intent emerges is what I'd like to understand more of.

I just can't get my head around the fact that...I'm sitting here, thinking this...causing action potentials to occur, but...without directing those action potentials. How does the first neuron know to depolarize and send its message?

I agree with Evan's point that it is difficult to communicate what we know and have seen as a battery to what we know and have seen (under a microscope of course) of axons. For me it has been difficult to transform a battery from a small piece of metal, that DIES, to a more abstract definition of positive and negative fields, permeability, concentration gradients, random movement, and CONSTANT movement. Margaux's questions are similar to those that am still puzzling over. How do we recharge our batteries, and why does it seem that there are so many possibilities (myelin) for damage to our action potentials? What, if any, is the influence of excercise on action potentials and recharging?

I do not think that I can say I agree or disagree with the battery metphor, but more that I understand it more or less as we move through the reasoning. I have come to understand it more, but now I find myself forgetting what an action potential is doing. I've become lost in trying to understand the metaphor and have lost sight of the "bigger picture." Therefore, on the one hand the battery analogy has helped me understand an action potential, but my understanding of the system, that is our family of input output boxes, has not progressed.

After class on Thursday and reading some of the above posts, I realize how infinitely precious having a complete, working system/battery really is. If, as mcrepeau ponders,something as seemingly insignificant as a leaky cable really is a potential source of circuitry failures, it amazes me that so many batteries function without malfunctioning. Thinking about the complexity of the nervous system in such a way is a little bit daunting. In some ways, the more observations that are presented in class and through the thoughts of others on the forum, the more I am amazed that things manage to function constantly at all or conversely, the less confident I feel that that the system will continue to function as it has in the past.

On another note, the conclusion we came to at the end of class on Thursday concerning outputs without input finally makes sense to me. When we imagined this scenario a couple of weeks ago, I was on the side of those who believed that perhaps no input really is an input which would mean that its corresponding output was an output with an input (sorry for that garbled mess...I hope this makes sense!) However, we only considered this situation in respect to leaky regions of the membrane (which would cause the membrane to generate an action potential in the absence of input.) I wonder if there are other possibilities that could point to output without input!

Like epilepsy, Tourette Syndrome is another interesting phenomenon that involves the random generation of outputs from the nervous system without any understandable input to the nervous system and thus would seem to fit our model of the internal generation of action potentials and through them visible behavior. Tourette syndrome involves the production of both physical (motor) and verbal (phonic) "tics" that occur intermittently and unpredictably out of a background of normal motor activity" 1 having the appearance of "normal behaviors gone wrong."2 However, the cause for Tourette syndrome is largely unknown (i.e. the exact gene that pertains to the susceptibility of the phenomenon has still yet to be identified), although it does tend to be an inheritable trait. The cause of the "tics" themselves (excessive blinking, twitching, bodily jerking, coprolalia--the utterance of social unacceptable words or comments---etc.) are believed to be related to particular cable dysfunctions (i.e. axonal operations) in the thalamus, basal ganglia and the frontal cortex of the brain, in which "models implicate failures in circuits connecting the brain's cortex and subcortex"3. Could these circuit failures possibly be related to leaky circuits i.e. leaky cables?

What's more is that the state of these circuitry failures, these potentially leaky cables, are very plastic and mercurial. The very nature of Tourette’s is that the symptoms are almost always entirely sporadic and unpredictable, often occurring in irregular bouts with great stretches of time taking place in between episodes. Also, in most cases, Tourette’s is a phenomenon that tends to decrease in both number and severity of episodic occurrence as a person ages and often almost disappears entirely by the time a patient reaches adulthood. If we are to suggest that the circuitry failures underlining the visible symptoms of Tourette’s (i.e. the tics) is related to sodium leaky axons than what accounts for the change in the relative leakiness of these cables (i.e. how can they change their state of leakiness and if relative leakiness is plastic is leakiness then not part of the overall design of the nervous system...is Tourette’s just some kind of unregulated phenomenon of inappropriate leakiness?).

Also, in relation to Nelly's questions about voluntary behavior versus involuntary neurological phenomenon (the control of our own action potentials) Tourette syndrome also deals with "premonitory sensory phenomenon", in which Tourette's tics are understood as a semi-voluntary or "unvoluntary" (v. involuntary) 3 action, i.e. the "I-function" is conscious of the onset of their implementation and can suppress them to a certain degree the same way we anticipate a sneeze or an itch and, to a limited extent, can exercise some control over these actions. I am curious to known where this idea of the "unvoluntary" action, of the tic that is at once a seemingly random neurological generation beyond our perception, as well as, a semi-cognitive action, falls into our spectrum of "conscious v. unconscious" inputs and outputs, "random action potentials v. coordinated behavior".

1. The Tourette Syndrome Classification Study Group. "Definitions and classification of tic disorders". Arch Neurol. 1993 Oct;50(10):1013–16. PMID 8215958 Archived April 26, 2006.

2. Dure LS 4th, DeWolfe J. "Treatment of tics". Adv Neurol. 2006;99:191-96. PMID 16536366

3. "Tourette Syndrome". Wikipedia the Free Online Encyclopedia. Wikipedia Foundation. <http://en.wikipedia.org/wiki/Tourette_syndrome>.

Just some thoughts on the significance of perception...

In class on Tuesday, I was asked, as a dyslexic person "what does a page of text look like to you?" since then,I have been struggling to think of a way I could explain my experience as a dyslexic person to you non-dyslexics out there. This is made pretty difficult by the fact that I have nothing to compare by perceptions with- I have never not had dyslexia. That is the answer I gave in class, but looking back, I feel that it is a little bit of a cop-out to just revert to personal relativity. I might as well have answered Paul's question by asking "Well, what does a page of text look like to you?". If there were no way to convey personal perceptions, how would any sort of exchange ever take place between two individuals? It is in the name of this goal that I'm going to try, now, to explain to you what it's like for me to be dyslexic.

In first grade, I was told that in order to tell my left from my right, I could hold out my hands, palms away from me, fingers up and thumbs held horizontally. My forefinger and thumb of my left hand, my teacher told me, would make an L. From that day on until I was about 10 years old, I was convinced I had two left hands. (For the record, I have anatomically normal hands, I just couldn't see the difference between an 'L' and a backwards 'L'.) This story illustrates nicely the difficulty I have distinguishing left from right. It's not just that I don't know which hand is which, but I have a much deeper confusion about this sort of directionality. I really don't see a difference between letters written forwards or backwards, left to right or right to left. (this made b's and d's particularly difficult when I was younger.) I learned tricks to help me get by in elementary school. For instance, I now write with my paper held horizontally so that my actual notes are written in horizontal lines (relative to me)... apparently I don't have the same problem distinguishing up from down as I do with left and right (although, now p's and b's pose the same problem as b's and d's used to).

I read an article in the New York Times several years ago (“A Boy, a Mother, And a Rare Map of Autism’s World”; By Sandra Blakeslee; New York Times; 19 November, 2002... http://query.nytimes.com/gst/fullpage.html?sec=health&res=9404EFDA1130F93AA25752C1A9649C8B63 ) in which an autistic boy named Tito, who cannot speak or socially interacting with others by any normative standard, writes very eloquently about his experiencing of the world as an autistic individual. The article explains that when Tito was 4, he was looking at a cloud when he heard someone talking about bananas. It took him years to realize that bananas and clouds were different. Reading this, I recognize something of my own struggle to illuminate to you how I experience the world. I can give you anecdotes and specifics, but I cannot seem to find a way to impart to you a complete understanding of me reality as a dyslexic person any more than Tito can let me know, really know, what it's like to not be aware of my own body, or distinguish the difference between bananas and clouds. It seems that we are all ultimately mired in our own perceptions of the world, because outside of our perceptions, how are we to conceive of reality?

Okay... I think I've said more than I originally meant to. And I never worked in the subject line. It's referring to an essay by a philosopher named Thomas Nagel entitled "What is it like to be a Bat?". It's a pretty good piece- at least, I had fun reading it. If you would like to take a look, almost all of it is available on google-scholar (link below), the gist of his point is that even though he can imagine several possibilities of a bat's reality, at the end of the day he concludes that he's not a bat, so he doesn't know the answer to the question he has posed. I haven't read any counter-positions to this point, but if any body had any, I'd love to take a look at them...

((((What is it like to be a bat:

http://64.233.179.104/scholar?hl=en&lr=&client=firefox-a&q=cache:7sElIgW9i4QJ:www.clarku.edu/students/philosophyclub/docs/nagel.pdf+

It's a little easier to read if you download it as a pdf... click the link that will appear right at the top of the page in the little google-y box for the pdf version. ))))