Neurobiology and Behavior, Week 8

One question that continues to perplex me from last week is the idea of the conductor-less corrolary discharge/efferent copy.  I understand that there seems to be no central organizer, but in fact several groups that coordinate the action of the whole (distributive organization). 

 

In thinking about how this system may work operationally, I began to wonder how well defined the small 'command centers' or pseudo-conductors were in relation to one another that were, in concert, coordinating the corrolary discharge.  In other words, we seemed to say that there was a distributive system, assuming that each node was of equal value to the system as a whole.  While Dr. Grobstein said this is true, that no one dominates another in terms of control of the system, couldn't it still be true that each node is entirely identical to each other one?  I suppose I am skeptical of the replicability of each node and want to believe that there exists some sort of variation (be it genetic or phenotypic) of each node that could provide variation over evolutionary time.  It might seem that the systems NEEDs to maintain this nodal identity if we are to assume that life ever achieved complexity in evolution.  From evolutionary theory, we think that variation in development (through phenotypic plasticity) could be exploited by natural selection to create adaptation, and ultimately speciation.  [See the work of Bryn Mawr's resident paleobiologist, Dr. Bruce Saunders on ammonoid suture complexity in evolution to learn about the evolution of complexity.]Assuming that each node is or could be unique, then it seems that some nodes would be inherently more valuable for the corrolary discharge than others.

Also, it seems that we assumed that the node (presumably at the level of a neuron or a few neurons) was defined.  This could explain why we would assume that each node could be equal to one another if they all exhibit many of the same properties as each other.  Nevertheless, I think it's important to question at what size level we define a 'command center' in the corrolary discharge so that we can better understand each node in they system.  Is the definition one of function (e.g. as soon as an area is able to stimulate an output it is a node)? or is the definition more arbitrary (e.g. a neuron or 3 neurons)?

Our interpretation of the world plays a great role in determining our behavior.  My experience in culture and education in South Korea where I was born and raised for about 15 years has deeply been stuck in my brain and it greatly affects my behavior even now.  For example, it feels rude for me to talk a lot in front of people who are older than me, and having lots of body gestures feel not ‘right’ to me sometimes based on my culture I grew up.  How I had been interacting with people in Korea greatly shapes my behavior even now in America. 

Central pattern generators have got me thinking about certain psychological disorders, such as Tourette Syndrome. The tics associated with Tourette Syndrome can be quite complex and involve multiple sets of motor neurons. For example, the shoulders of a person with Tourette Syndrome might jerk while their torso twists. Or the person might have vocalized tics, such as saying obscenities or repeated clearing of the throat. The movements and vocalizations are not voluntary, so their complexity points to the existence of "motor scores", and thus central pattern generators. Is Tourette Syndrome explained by the dysregulation of different sets of central pattern generators? If so, what is the regulation pathway for central pattern generators in a "normal" nervous system? And what is responsible for the dysregulation in people with Tourette Syndrome?

I think in some ways, learning about the reafferent loop, corollary discharge, and pattern generators are growing my understanding of some of the more basic aspects of psychology.  But I wonder how these components of the nervous system can connect to more multi-layered psychological occurrences, such as depression, the Oedipus complex, bipolar disorder, etc.

After our last class the thing that stuck with me is the idea of tricking the brain. When we were talking about phantom limbs, I started thinking about the way Dr. Ramachandran treat this problem. He would use a mirror box so that the patients could move the phantom limb. (http://endthepainproject.org/images/mirrorbox2.jpg) As seen in this picture the person can "see" the non existent limb and the brain receives this signal and is convinced that the limb exists. Then the person moves this limb by moving the actual arm. Moving the limb relaxes it and the pain is treated this way. 

After this I started thinking about the placebo effect. Though the placebo effect is not always existent, it is a true phenomenon. 

Both Dr. Ramachandran's treatment for phantom limbs and the placebo effect lead me to question Emily Dickinson's poem. If the brain is what creates everything and controls everything, then how is it that it can be tricked?  

After Thursday’s discussion on phantom limb pain I startedto think about other circumstances when there is loss of feeling in limbs. Themost common circumstance when this occurs in after a stroke when people maypermanently or temporarily loose feeling or control over certain limbs or bodyparts. I wanted to know if a temporary loss of sensation could lead to aphenomenon that has the same characteristics as phantom limb pain, even if theloss of limb was not permanent. I found a journal article that looked at theexperience of anosognosia and other disorders that involve abnormal attitudestowards or perceptions of the affected limb in patients that have recentlyexperienced strokes with damage to the right side of the brain. The researchersfound that about 92% of the stoke patients experienced some type of “disturbedsensation of limb ownership,” and that the patients that did have theseexperiences tended to have specific damage in the right posterior insula. Ihave been unable to determine what the role of this specific box is, but itseems that it is involved in own sense of limb ownership. It would make sensethat if this specific area were damaged, the individual would be more likely tohave a disorder such as anosognosia. I also looked at an article that looked atpatients with both right side and left side damage, and found that there was asignificant increase in anosognosia like symptoms in patients that had rightside brain damage. I was wondering if there was any correlation between theincidence of phantom limb pain and on which side the patient lost the limb. Iwould predict that because the part of the brain responsible for limb ownershipis located on the right side of the brain, patients that have lost a limb onthe left side of their body would experience more phantom pain. 

Efferent copy and corollary discharge do explain more in depth how the brain functions. Patterns of activity, actions and reactions, movement, behavior, it's all starting to become clear. However there is still something I do not understand. I still don't get how all this adds up to me, to us, to a thinking, individual person. Where does intelligence fit in? Or personality? Where am I in my own brain? I simply still do not understand how the interactions of chemicals and charges gives me the ability to think of a post or appreciate poetry. 

I understand it but I don't get it. Seeing, thinking, it should make sense, but I still feel like we are missing large pieces of the puzzle. I look forward to seeing if these pieces are all filled in by the end of this class.

At the beginning of this semester one of the questions I had regarding the brain was: how could an awareness of the self arise from chemicals and electric signals? I did not understand how psychological processes like consciousness and thought could arise from biological mechanisms. However, our discussion about efferent copies and corollary discharge has helped me to better understand this relationship between biology and psychology. It's fascinating that our brains are able to produce a copy of the efferent signals they send out and use this copy to determine if a signal is in reponse to an internal or external stimuli. And this ability to distinguish between self-produced signals and external signals is corollary discharge (I think..). This mechanism shows that these efferent signal copies help us to become aware of internal thoughts regarding self-awareness and how the self is separate from the external world. Moreover, efferent copies are used by our brains to predict the outcome or expected sensations of a given action that we engage in. This shows that these biological signals are also able trigger psychological processes such as the formulation of thoughts and expectations about the outcome of an action that the body engages in. Thus, while this mechanism does not directly answer how our brains produce internal thoughts, it shows that biology does play a big role in triggering and helping us become aware of these thoughts. And this gives us a greater understanding about how biology and psychology interact. 

I found out a little more about Dramamine... It is a salt of the active ingredient in benadryl (diphenylhydramine) and a mild stimulant (closely related to one of the molecules in coffee, chocolate, and tea).  Diphenylhydramine is an antihistamine; specifically an H1 histamine receptor antagonist.  Common side effects are mild sedation and drowsiness.  It is effective in treating motion sickness related nausea because it blocks certain signals to the nervous system and/or encourages the patient to relax, close their eyes, and sleep.  This is how the brain would like to handle the discrepancy in information it is receiving anyway.

Dramamine is not as effective in treating chemotherapy-induced nausea; there are better anti-emedics, such as Zofran and Kytril.  These drugs are 5-HT3 receptor antagonists blocking serotonin receptors in the central nervous system and gastrointestinal tract.  Other important classes of antiemetics used for treatment of chemotherapy-induced nausea are dopamine antagonists and cannabinoids.  Chemotherapy is thought to cause nausea and vomiting by releasing serotonin, dopamine, and histamine or by damage to stomach cells which also results in a release of serotonin. 

It is interesting to think about why Dramamine is used for motion sickness, but not other types of nausea.  I suspect it relates to a more general trend in medicine.  When nothing else can be done to alleviate the specific discomfort, doctors sedate the patient so that they are less aware of their discomfort.  

We were discussing the central process generators and I thought back to our Reeves discussion.  It is obvious that the central process generators of Reeve's extremities were not destroyed in any way, so I wonder if this lack of destruction of CPGs could lead to a more focused definition of what qualifies as paralysis.  Another interesting example I thought of was a friend of mine's sister -- at age 18, while diving, she broke her neck and became paralyzed from the neck down.  However, she began going to physical therapy (Operation Walk, Chicago) and learned how to walk again, despite not having any feeling in her legs.  She is also very mobile in her arms, despite having no feeling there.  Would this qualify as having damaged only her sensory neurons, while her motor neurons and CPGs remained intact?  This seems to justify another sort of definition/specification for paralysis (as doctors do still consider her to be a quadraplegic).

 I also have never thought of pain in the way of an 'out of the ordinary' response with which the brain does not know how to process.  In many ways, though, it makes sense.  On a personal level, I know that when I'm on an airplane in flight and I close my eyes, I get nauseated for a few seconds because my brain tells me that I'm flying a steady path but my perception feels a slight plummeting feeling.