While I was reading the assigned chapters of the book Soul Made Flesh (Zimmer, 2004) for class this past week, I came upon the story of the physician Thomas Sydenham. He was particularly good at making careful bedside observations while he was treating patients. In fact, he made the observation that diseases acted the same in everyone, and they were not unique to an individual. He made careful notes on disease symptoms, and even suggested that perhaps diseases should be treated as if they are individual species.

Sydenham’s work turned out to be controversial, because when prescribing a treatment, sometimes he would not use the traditional one, but instead would experiment with different treatments. Other physicians wanted to get his license revoked because his experimentation outraged them, even though Sydenham documented which treatments seemed to work better. We discussed this a bit in class, but I want to know why his new treatments were so controversial. If he devised his treatments in a manner that seemed logical, and he had experimental evidence to back it up, why was there such resistance? Is it perhaps that people could not accept that traditional treatments really did not work, and that they may now be responsible for the deaths of many people that could have been saved? Or is it simply a matter of people not being able to accept that things change?

I must be the last one to hop on this bandwagon — only because I had to give everyone else a chance first, you know, I wouldn’t want to drain all the donors^* — but now it’s about time I joined in. Scienceblogs is working to raise money for teachers, and we need you all to chip in and donate to DonorsChoose. Go ahead and donate to any of the projects on the Scienceblogs leaderboard, or you can donate to the
specific projects in the Pharyngula challenge. It’s all a good deal, because Seed will match funds, up to $15000.

So come on, dig into your pockets, and hand over a little cash to the deserving cause of science education.

^*Actual reason: because I suck. But you all knew that.

My students are getting their first take-home exam in neurobiology tomorrow, and I’m using this entry to give them a convenient link to a paper they’re expected to analyze. The rest of you people can just ignore this.

1. We’ve discussed the ionic basis of the action potential and had an overview of channel properties. I’d like you to read the following paper from a recent issue of Nature, which neatly combines several subjects we’ve discussed:

Binshtok AM, Bean BP, Woolf CJ (2007) Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers. Nature 449, 607-610.

There is also a News and Views summary in the same issue, A local route to pain relief, that will give you a digested version of the article.

It’s a clever experiment to generate a very specific analgesia. I want you to do two things in an essay:

1. Half the essay should be a short description of the TRPV1 ion channel: specificity, permeability, gating, pharmacology, and structure. You’ll need to do some research beyond this one paper to answer the question adequately.

2. The rest should be a critical analysis of the voltage-clamp method used in the Binshtok et al. paper. Don’t try to explain every result in the paper: focus on a key result and show me that you understand how to interpret the experiment and can explain the meaning of the data.

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Oh, also! Let’s plan on meeting in the Turtle Mountain Cafe tomorrow morning instead of the classroom, again — I’ll need my coffee while we discuss chapters 10 and 11 of Soul Made Flesh.

Jonah unkindly mentions that California will spend three times as much operating its prisons than running the UC system. Doesn’t that reassure you so much about America’s priorities?

Hello again! It’s been a little while since my last post and I need to post for this week or I’ll be docked points from Dr. Myers. I’ve been a little bit behind on things as I’ve been preparing for my upcoming senior seminar, but I did have time to check out at least one cool article I found on different energy systems used while running.

I had a race today and I noticed that every time I do an 8k (5 miles), about three miles in I hit a wall of fatigue. I get dizzy, it’s hard to focus on the guy in front of me, driving my knee up feels next to impossible, and the only thing I care about is eventually getting to the finish line. I know that much of this is probably because I’ve depleted a good portion of my glycogen stores and have worn out my muscles fairly well. But how does this tie in with my nervous system?

According to the article, a good portion of my glycogen stores are found in my liver. If too much of the glycogen is used hypoglycaemia can occur resulting in brain damage. Other bodily harm such as myocardial ischaemia, heat stroke, and severe ATP depletion from my muscles can occur too if my body is allowed to be pushed far enough.

Luckily for me, my muscles have a built in negative feedback to stop me from killing myself out there. My muscles somehow know to send a signal up to the brain for a release of serotonin and inhibition of dopamine secretion, which results in a further lack of ability to move, which results in a slower time, which puts Morris on the backburner in terms of our men’s cross country team. I’m still wondering though, how do my muscles know when to signal my brain to cut back on the neurotransmitters? And how much does mentality (a positive attitude towards the race, or the expectation of a good run) play a role in the regulation of my muscles (do I release more ACh and endorphins by simply having a good attitude, or is the causality the other way around?)? Either way, if you haven’t moved in a while, get out and enjoy this great October weather while it lasts. Or you can check out this pretty funny link of a band I found on youtube.

Adult neurogenesis

The creation of new neurons, known as neurogenesis, is an important process. It is by this process that the brain forms, and most of it occurs during pre-natal development. An early theory proposed by neuroanatomists that has recently been refuted by experimental evidence is that adult neurogenesis does not occur. In adult neurogenesis, it has been observed that most of the new neurons die shortly after their formation, while only a few become integrated into the functioning structure of the brain. So what is the significance of adult neurogenesis?

While the functioning of this process is not known, it has been speculated that it is important for memory and learning processes, and is linked to stress. Stress causes a lot of people a lot of harm, and has been linked to many disorders, such as depression. Depression is a condition that is regulated by antidepressants. Know what other activity is regulated by the activity of antidepressants? You guessed it, NEUROGENESIS! A recent study showed that the brain responds to stress-relieving situations, such as those that build learning and memory, with increased neurogenesis. Stressful situations, such as those that induce physiological or psychological stress, are marked by decreased neurogenesis. A decrease in neurogenesis has been indicated to be a key factor in the progression of depression.

[Read more…]