Preliminary Investigation of Physiological and Neuronal Aging Effects of Nicotine on C. elegans
Start Date
April 2024
Location
2nd floor - Library
Abstract
Preliminary data of Caenorhabditis elegans treated acutely with 0 mM, 0.1 mM, 1mM, and 10mM concentrations of Nicotine during the early L1 developmental stage indicated differences in overall neuronal fluorescence at the early L4 stage. With rising nicotine use among youth, understanding these developmental impacts is crucial to anticipate health consequences. Nicotine acts as an agonist for nicotinic acetylcholine receptors (nAChR), which interact with the neurotransmitter acetylcholine (ACh), especially seen in neuro-muscular synaptic transmission, seen in both humans and C. elegans. The strain of C. elegans used in this investigation is BZ555, a strain that fluoresces where dopamine (DA) neuronal processes exist, and because DA and ACh have been found to modulate the effects of locomotion and behavior, this model gives strong insight into the effects on neuron integrity. The changes observed may indicate a loss of neuronal function due to varied chronic doses over the developmental stages, which are equivalent to childhood to early adulthood. Furthermore, differences in the pharyngeal pumping rate for the 0.1 mM dose suggests a change in coordinated muscle function as compared to no treatment. Preliminary data suggests a promising impact with a similar trend of initial impact at relevant lower doses, then oversaturation at higher doses. The future directions of this study include utilizing the neurotoxin hydroxydopamine to compare the fully inhibited neuronal fluorescence, as well as expand trials to include cotreatments of other common vape fluid components to examine the potential antagonistic or synergistic effects on nematode physiology.
Preliminary Investigation of Physiological and Neuronal Aging Effects of Nicotine on C. elegans
2nd floor - Library
Preliminary data of Caenorhabditis elegans treated acutely with 0 mM, 0.1 mM, 1mM, and 10mM concentrations of Nicotine during the early L1 developmental stage indicated differences in overall neuronal fluorescence at the early L4 stage. With rising nicotine use among youth, understanding these developmental impacts is crucial to anticipate health consequences. Nicotine acts as an agonist for nicotinic acetylcholine receptors (nAChR), which interact with the neurotransmitter acetylcholine (ACh), especially seen in neuro-muscular synaptic transmission, seen in both humans and C. elegans. The strain of C. elegans used in this investigation is BZ555, a strain that fluoresces where dopamine (DA) neuronal processes exist, and because DA and ACh have been found to modulate the effects of locomotion and behavior, this model gives strong insight into the effects on neuron integrity. The changes observed may indicate a loss of neuronal function due to varied chronic doses over the developmental stages, which are equivalent to childhood to early adulthood. Furthermore, differences in the pharyngeal pumping rate for the 0.1 mM dose suggests a change in coordinated muscle function as compared to no treatment. Preliminary data suggests a promising impact with a similar trend of initial impact at relevant lower doses, then oversaturation at higher doses. The future directions of this study include utilizing the neurotoxin hydroxydopamine to compare the fully inhibited neuronal fluorescence, as well as expand trials to include cotreatments of other common vape fluid components to examine the potential antagonistic or synergistic effects on nematode physiology.
