Genetic association between sleep disorders and risk of epilepsy

Started Nov. 16, 2022

Abstract or project description

Rhea's project centers around three main questions: Are some genes directly or indirectly associated with epilepsy and sleep disorders (specifically sleep cycle data)? Can we predict the development of epilepsy given certain sleep cycle disorders? How does having these genes predict patterns in sleep? She will use specific search queries in genetic databases to return lists of genes associated with certain conditions such as epilepsy and sleep apnea. She will use MATLAB to find cross matches between lists and then further investigate these target genes to determine if there are common mutations or common effects of groups of mutations that cause sleep disturbances associated with an increased risk of developing epilepsy.

The Modulatory Effect of Neurotransmitters on Amygdala Dysfunction and Anxiety Disorders

Started June 25, 2021

Abstract or project description

Regulation of emotional states including anxiety is controlled through the amygdala and the effects that are seen are initiated by neurotransmitters. Although many endogenous neurotransmitters exist, specifically GABA, serotonin, dopamine, and synthetics including LSD are focused on in this review. Each one modulates the amygdala differently in order to instigate its respective effects. Dopamine and serotonin are well-known neurotransmitters that are a primary target for a number of drugs. These drugs can be used to treat or help with disorders relating to or of anxiety by imitatively controlling the levels of it within the body. Serotonin is a neurotransmitter that facilitates fear extinction. Increased levels of serotonin in the synapse cleft have been found effective in decreasing the prevalence of phobias. Increased dopamine metabolism in the amygdala contributes to decreased GABAergic inhibitory control thus, increasing neuronal firing within the amygdala. Therefore, impaired neuronal signaling within the amygdala can induce anxiety disorders. This review aims to discuss the effect of the mentioned neurotransmitters and how they affect amygdala projections and it’s dysfunction.

Anxiety disorders occur due to the malfunction of nerve signaling or control within the amygdala. These impairments, which may be induced by defective regulation of endogenous neurotransmitters and their receptors, may instigate anxiogenic symptoms. Previous research has shown that the GABAergic system has a pivotal role in the modulation of anxiety disorders [2]. Different neurotransmitters have different effects on the GABAergic system within the amygdala. Due to excessive firing of neurons within the amygdala, a promising approach towards reducing its anxiogenic effects is through the intervention of neurotransmitters by synthetic drugs. Dopamine and serotonin are well-known neurotransmitters that are incorporated into a number of drugs. An increase in dopamine metabolism in the amygdala contributes to decreased GABAergic inhibitory control, and therefore, increased neuronal firing within the amygdala [3][6]. Conversely, an increase of serotonin levels in the synapse cleft has been found effective in decreasing the prevalence of phobias and anxiety disorders [8]. Receptor regulation and synthetic drugs are built to mimic the action and ability of their respective neurotransmitter. LSD is a synthetic neurotransmitter that mimicks serotonergic activity by acting as a receptor agonist for both serotonin and dopamine receptors [9]. Although LSD is not directly related to anxiety and fear, it can regulate emotion, thinking processes, and other psychological effects by imitating other neurotransmitters. In this paper, we will discuss the different neurotransmitters, their effects on the signaling within the amygdala and observe their respective synthetic drugs’ ability to induce any change.