Today in class we learned about the functioning of olfactory nerves. It was really quite interesting, especially to find out how the olfactory system is organized. Let’s begin in the nasal cavity. Here, present in the mucus layer, are projections of the olfactory receptor cells. Each receptor cell is only capable of binding to one specific type of odorant molecule. These receptor cells travel through the porous bone separating the skull from the nasal cavity, and feed into a specific glomerulus. Glomeruli are located in the olfactory bulb, and have multiple receptors feeding into them. However, each glomerulus receives input from only one receptor type. In the glomerulus, the receptor neurons make excitatory connections with other cells, whose own axons project into the olfactory cortex in the brain. What is cool here is that there are about 1000 different types of olfactory receptor neurons, which each have their own proteins. This means that there are most likely 1000-2000 genes encoding for olfaction. It has been shown that this is not a combinatorial system like that developed for immunity.

Another cool thing I learned was that every time someone blows their nose, they are losing part of their brain. Seriously though, it’s not quite as bad as it sounds. What is really happening is that you are losing the olfactory receptor cells that protrude out into the mucus layer inside the nasal cavity. The neat thing is that these cells are able to regenerate, which is unusual for other human neural cells. I was wondering, if perhaps, due to the organization of the olfactory nerves, regeneration is able to happen because of the interaction between the olfactory receptor neurons and the glomeruli. Perhaps the protruding parts of the cells are able to be regenerated because they are actually only part of the cell, not the entire cell. If this is true, then if the glomerulus were destroyed, would that permanently destroy the sense of smell? Or would the glomerulus be capable of regeneration, like the olfactory receptor cells that feed into it?

I was happily absorbed in my slightly vegetative stupor on the couch when my roommate walked into the room and starting talking about physics. Ugh, physics, I thought, but I politely listened as she began talking about lenses, specifically how they are related to sight. It is common knowledge that the images we see are inverted on the retina, and then further processed. However, my roommate was discussing experiments done on humans that inverted their vision by 180 degrees and found that, though at first they could not function normally, eventually they adapted. I thought this was fascinating, and wondered what the brain had to do with this process. Unfortunately my roommate’s knowledge was pretty limited, so I decided to do some research of my own.

Research on visual distortion of the retina has been going on for quite some time. Devices have been used that invert the retinal image, so that everything is seen upside down. At first subjects wearing this device will reach for things and miss, or will bump into things as they travel about a space. Eventually, they adapt. What I wanted to know is how do they adapt? What changes take place in the brain that allow them to do so? Is it just simply learning to reach a little farther to grab something, or walk a bit differently to avoid bumping into something? What is happening at the neural level?

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I found an article about new brain cells that I thought was really interesting. Researchers at the Yale School of Medicine discovered the mechanism behind how new neural cells are integrated into the adult brain. It turns out that new neural cells take a while to mature and fully integrate themselves into existing neural networks in the brain. While they are maturing, they rely on signals from other brain regions so that they do not disturb ongoing functions of the brain. They can receive input from these other regions for up to 10 days before they are ready to make any of their own outputs. So how long does it take to fully develop their synaptic connections so that they can talk to one another? Up to 3 weeks.

So why do we care; what is significant about this discovery? This mechanism sheds light on how neural cells integrate themselves into existing networks, which will impact how stem cells are used to replace neurons lost to injury or disease. The main concern is about neurons firing inappropriately, which could cause seizures or cognitive dysfunction.

The full article can be found in the Journal of Neuroscience, Vol. 27

So one of the questions on our Neurobiology test due today was to see if there were any heritable diseases in humans that are caused by defects in ion channel genes. I discovered that mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene have been linked to Cystic Fibrosis (CF).

CF is a genetic disease that affects the lungs and digestive system of its victims. The defective CFTR gene produces a thick, sticky mucus that provides an environment for life-threatening pathogens to establish an infection, and can clog the lungs. This unusually thick mucus also interferes with the pancreas, and impairs the enzymes that help to break down food and allow the body to absorb it. The symptoms of CF include frequent lung infections; persistent coughing, oftentimes accompanied by phlegm; wheezing or shortness of breath; poor growth or weight gain, despite a healthy diet and appetite; salty tasting skin; and difficulty in bowel movements or greasy, bulky stools. The incidence is about one thousand new cases a year.

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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?

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.

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