To Become New Again

To Become New Again

Neural plasticity is complex topic that deals with the brain's ability to shape and reorganize itself by forming new neuronal connections in response to new information or when learning new things. Typically neural plasticity is greater in younger organisms than old. There is a critical period in which organisms learn as much new information and the brain quickly forms neuronal connections
forming connections and bridges between concepts. 

The article, "Understanding the Brain's "Brake Pedal" in Neural Plasticity published January 2011 discussed new findings in the molecular mechanisms behind neural plasticity. I found this bit of information to be particularly exciting. A banded krait is a species of snake who's venomous bite can be lethal if not properly dealt with. The toxin affects the neurons and animates the muscles causing constant contraction. The interesting thing is that this toxin has a close molecular counterpart that is found in the human brain called Lynx1. The researcher responsible for this finding is professor Takao Hensch at Harvard lab. He believes this molecule serves as a "brake" in the brain that suppresses the ability of the neuron to grow and change with experience as seen in young organisms during their critical period. As the brain ages, it becomes much less receptive to learning new things. For example, as toddlers we picked up learning our native language without memorizing various rules because our neural plasticity was much more active. However as an adult it takes much longer to learn a new language because our brains are not as plastic and researchers believe that is a result of Lynx1 aggregates in the brain. 

To confirm these findings researchers conducted a few experiments to solidify their predictions. The first study looked to confirm if the levels of Lynx1 did in fact increase with age. They labeled and collected samples of labeled Lynx1 from mice of various ages and saw a general rise in Lynx1 concentration from young mice to old. The next experiment observed the effects of removing Lynx1 from mice completely. Researchers sutured on eye of the mouse shut. With only one eye open the brain would have to rewire to form stronger connections with the neurons associated with the eye that was not shut. Mice that did not have the Lynx1 molecule were observed to undergo this shift of dominance to the eye that was not sutured. Mice that still had the Lynx1 molecule were not observed to shift dominance to the unaffected eye. Lynx1 is found to block the receptor for acetylcholine an important neurotransmitter for the arousal of neurons throughout the brain. 

So far it has been shown that Lynx1 is an important inhibitor for neural plasticity. This inhibitor affects the arousal of neurons in the brain that are important for times of learning in the brain. This concept goes hand in hand with what Dr. Xiao-Wen Yu discussed in our neuroscience seminar. He discussed how a phenomenon, afterhyperpolarization (AHP), was associated with learning and aging. AHP was found at higher levels in aging subjects. The exact molecular mechanisms behind facilitating AHP is not exactly known. However what is known is the effects of a certain molecule PKC. This is a Ca2+ enzyme and in aging rabbits it was found that with less PKC in the hippocampus, learning impairments were observed in these rabbits. These learning impairments were clearly seen in the water maze test. This test looks at how quickly an animal will learn and traverse a maze. Calcium is just one of many molecules that contribute AHP. The bottom line is that lower AHP is required for learning and this is seen more in younger organisms.

Combining these two papers we start to get an idea of a possible association of membrane potentials and the molecule Lynx1. Since Lynx1 is an inhibitor for acetylcholine, which is an excitatory molecule, this could be correlated with reduced excitability of neurons in the hippocampus. The reduced excitability is a result of hyper polarization resulting in less action potentials. Less action potentials does not facilitate learning. Perhaps injecting higher levels of acetylcholine will reverse the effects of Lynx1 and could lead to more incidence of depolarization and neural plasticity. Another possibility is to reduce the levels of Lynx1 in the brain and free up more acetylcholine receptors and facilitate neural plasticity. Neural plasticity is an important process that keeps the mind malleable and more receptive to learning new things. These mechanisms are vital in our understanding of the process and providing potential for supplements in learning for future generations.

Works Cited:

Castro, Jason. "Understanding the Brain's "Brake Pedal" in Neural Plasticity." Scientific American. Scientific American. Web. 04 May 2016.

Disterhoft, John F., and M. Matthew Oh. "Learning, Aging and Intrinsic Neuronal Plasticity." Trends in Neurosciences 29.10 (2006): 587-99. Web.

Images:

http://www.collective-evolution.com/2012/11/26/neuroplasticity-brain-and-heart-interaction/

http://www.interactive-biology.com/3924/a-look-into-the-major-neurotransmitters-of-the-nervous-system/