Today I’m looking at synaesthesia, but more specifically lexical-gustatory synaesthesia in which certain phonemes (smallest unit of speech such as the /l/ sound in jelly) trigger specific tastes. For example, in Jamie Ward and Julia Simner’s (2003) report, Lexical-gustatory synaesthesia: linguistic and conceptual factors, a case study was done on a forty year old business man who reported tasting specific tastes in response to certain phonemes. In this case the man reported tasting cake when the phoneme /k/ was used in a word. Synaesthesia is thought to occur due to the crossing over or connection of neurons in certain areas of the brain that regulate and process senses. However, there are differing theories as to how this arises.

One idea is that certain neural connections linking sensory areas are not destroyed in infant stages of development as done in normal development. Synesthetes therefore link one sensation with another because connections are not destroyed. The second theory is that, rather than sensory areas in the brain being directly connected, they are connected through neural pathways in higher processing areas. For instance, instead of just hearing a phoneme and having just any taste sensation, it is the processing of the sequences of phoneme in the word used that links to specific learned schemas connected to the phonemes leading then toward a specific taste. Ward and Simner examined this in their case study.

Through documentation of tastes stimulated by specific words and phoneme triggers, Ward and Simner found that their data supported the latter of the two theories. The largest support comes from the idea that the subject’s tastes are specific for certain learned phoneme association rather than just random association of tastes to arbitrary phonemes. For example, as stated earlier, certain phonemes consistently trigger specific tastes such as the phoneme /k/ and the taste of cake. Also, the use of semantics in the sensory process is a strong argument for higher processing connections as food names exhibit their tastes (cabbage triggers the taste of cabbage). Much of this may be because certain patterns of phonemes can trigger specific tastes that have the same sequence of phonemes. So college, having the phoneme sequence /edg/ triggers the taste of sausage which also contains the phoneme sequence /edg/. These associations are done through higher processing which is learned throughout life, supporting a connection through higher processing areas of the brain rather than direct connection between sensory areas.

Although the idea of a direct connection between sensory areas from birth is not disproved by the study, it has supported that there is higher processing connections involved that have developed through learning. There is still much work in the field of synaesthesia, and with any luck, it will lead us to a better understanding of how our brains develop and process information. But despite all this, the best thing to do right now if you are not a lexical-gustatory synesthete is eat leftover turkey, potatoes (cheesy or mashed), and some pumpkin pie. Happy holidays.
~Bright Lights

This week I’ve been diving in a little more into doing some actual research myself. Nothing breakthrough mind you, just some simple experiment to sort of understand the world around and inside of me a little better. My partner and I are looking into how the optic nerve develops inside of zebra fish and how its development may be affected by developing the fish in total darkness. We are trying to stain 1-2 day old zebra fish with Dye-I by simply poking the dye into the retina with any sort of small sharp object we can find. We’ll then separate the groups of stained fish into those that develop in a small flask with normal exposure to light (about 10-15 hours a day of UV light) and those that develop in a tin-foil-wrapped flask with no UV exposure in which feeding will be done under red light.

Every few days, I hope to take some of the fish out and look at how their brains are developing using a fluorescent microscope that allows me to see how the dye is traveling. With any luck, I’ll see a decently clear pattern of paths of nerves from the retina to the lateral geniculate. I’m not sure where it leads from there as the zebra fish has mainly the midbrain rather than our large forebrain with a thalamus and cerebral cortex. More research on my fish is definitely needed before I can do any real analyzing of the staining technique, but my real problem right now is just getting some fish stained!

Using a pin head dipped in dye, I had been trying to poke the retinas of these fish. Once the retina ruptures, almost any amount of dye should stain the retina and lead to further staining of the optic nerve as development continues (from what I’ve read, usually the rods and cones develop about 4 days at the earliest). I ran into many problems with this of course and have been fishing (oh so hilarious, I know) for new solutions ever since.

The first problem I had is that the head of the pin is about the size of the fish’s eye itself, so trying to rupture the eye with it is like trying to shove a baseball bat through my own. Of course actually rupturing the retina with this gigantic tool will only happen if my mounted fish would stop moving every time I get close to it, which is the second problem. So far, I’ve created new tools by heating TLC spotters over a flame in the organic chemistry lab and then pulling it in half so that the glass is pulled into a tiny pipette with a head just smaller than the fish’s retina. This has been successful after coupling it with a technique for knocking out my fish to keep them still. I burst a small bubble of anesthetic (0.5 MESAB) over the water that I’m using to mount my fish before injecting the fish in augar onto the slide. This does a great job in keeping the fish still so I can do my dirty work of staining its eye, but sometimes the concentration of anesthetic is too strong and the fish will die. All in all, with much more research and some patience this may turn out to be a fun little project. If you have any ideas as to where I should be looking for research and anything else I could be doing with this experiment, let me know.
~Bright Lights

We’ve been talking quite a bit about how information is processed in our brains so that a specific reflexes and cognitive actions can be produced. It’s also the end of the cross country season and my mind has been mixing the two. Take Steve Prefontaine (one of the greatest American long distance runners of all time) for example. I was watching a video clip of Prefontaine running and paused it right as he was putting his foot down and picking his other leg up. He doesn’t extend his leg out very far. Instead, he lifts his knee up so that he can drive his pronated foot into the ground just under his hip. Since his foot is already pronated, he can further drive his leg behind him and use the ball of his foot as a launch pad to drive himself forward. This technique saves a lot of energy and keeps the runner mostly in the air, rather than on the ground (which is what you want).

Sadly, no one brought the technique to my attention until about halfway through college. I’ve been overextending my legs without picking up my knees, landing on my heels, and rolling to the balls of my feet. This means I use more energy and a lot more time in projecting myself forward each stride. Ever since I learned of proper running techniques I’ve been trying to make them an automatic reflex in my strides, but this is incredibly hard to do.

For the past twenty two years, neurons in the motor cortex of my frontal cortex, cerebellum, Thalamus, and several other regions of my brain have been adapting to coordinate specific muscle actions to create my presently crappy running technique. This spider web of nervous tissue is constantly changing as neurons diverge and converge on each other, become more sensitive to or produce higher concentrations of specific neurotransmitters, and develop other specific interactions with other neurons that perfectly coordinate my behavior and actions. However, it has taken twenty two years to perfectly coordinate all this interaction so that I can run so terribly, meaning that learning to truly run could take a long time as I prune and pair more neurons to coordinate a totally different reflex.

So far I’ve been trying to reshape my neural network by doing one legged hang cleans. In the exercise I have to shrug a large amount of weight off one leg in a lunging position, get under the weight in mid air and catch it as it comes down in the same position. It is difficult to catch the weight without landing on the ball of my foot, which is pleasantly placed directly under my hips, making my body develop the correct foot placement as a reflex. This learning is actually the reshaping of the network of neurons inside my brain that deal with motor coordination as they make new interactions, destroy old ones, change their amplification of signals, or change their functions completely. At any rate, I haven’t even scratched the surface of how intertwined the processes are that go inside this skull of mine to create who I am and the things that I do. But I do find the little I know pretty amazing, and can only hope that my non-declarative memory will eventually kick in.
To see the proper running form, take a look at Michael Johnson in his world record 200m race.at the 1996 olympics.

Hello again, it’s been a while so I thought I’d drop in a comment or two about what I’ve found recently in the news about neurobio. I’ve lately been reading about neurotransmitters and how they bind to sites in specific neurons, instigating depolarization across the membrane of the neuron and allowing for an action potential to communicate to hundreds of thousands of other neurons. This communication between neurons in the central nervous system is relayed into actions in the peripheral nervous system resulting in behavior. But how is this synchronized? What neuron does what? What must be connected to what and why? These are all questions that may take a while to be answered, but we are finding new developments everyday.

In an article from Cornell News, I read about an experiment by James Goodson and Andrew Bass (2000) in which neurotransmitters’ role in the display of sex characteristics in plainfin midshipman fish were examined. In this particular fish, males will make vocal calls through the water that attract females who will come to the site to lay eggs for the vocalizing male to fertilize. However, a second type of male that is unable to make vocal calls waits nearby so that once the eggs are laid, he can get some free-fertilization-action.

Goodson and Bass anesthetized and stimulated the anterior portion of the hypothalamus in each fish to stimulate either a vocal call, or the female’s short grunt (a response to the male’s call). After stimulating normal calls in each fish, the neurotransmitters isotocin and vasotocin (identical to the mammalian oxytocin and vasopressin) were administered to the anterior hypothalamus of each fish. When administered, fish that normally could make calls lost the ability to do so and developed female like grunts, similar to the type II males that could not call but rather grunted like females. This meant that a trait that was typically thought to be controlled by sex (controlled or linked by the gonads) was actually independent, and regulated completely by the brain.

Who knows how many of our traits are linked to gonad development, probably much fewer than we might originally think. If I was given a good dose of estrogen would I not want to play football or wrestle with my best friends?…doubtful (it might just turn into flag football with the Vikes or a pillow fight). At any rate, we shouldn’t be so quick to make judgment calls on biology’s effects in gender behavior.

We are about to finish Soul Made Flesh by Carl Zimmer in class this week and I’ve been reflecting on how, despite science’s deep impact on how we think and act, we still have subconscious belief in superficial myths that slip out despite our common knowledge of biology and the world around us. For instance, Zimmer illustrates the battle that people like Thomas Willis went through in trying to draw attention to the superiority of the brain over the heart in its control over all our emotional and reasoning faculties. After dissecting thousands of brains, comparing and contrasting the anatomies of animals and humans, anatomies of past (Galen) and Willis’s present (Harvey), and pushing these ideas at just the right time over two decades and through two revolutions, Willis was finally able to solidify the brains mastery over the human body and personality rather than the heart.

Yet despite this great fight to make the brain’s superiority over the other organs common knowledge, we throw it all to the wind with sayings like “she broke my heart,” or, “he has a wicked heart.” Why have these sayings survived, and why do we still feel that emotions and our persons are derived from the heart? Can I say something like, “when she left it was like getting shot through the amagdyla,” or, “I’m so excited dopamine might spill out of my ears,” and not sound completely awkward?

Despite common knowledge about such happenings in the brain, we still communicate better with the myths of the past, such as the belief that the heart is the center for production of emotion and regulation of our actions and thoughts. I guess it really depends on how much we cling to these myths, and how far these myths go in messing true science. Most people know that emotional processes and personality are regulated by the brain, however, it is still easier to communicate our feelings and thoughts (which is essential to any culture) through common myths. Perhaps we’ll all use “scientifically correct” phrasing someday, but what has to happen to completely turn a culture to the truth?

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.