The Effects of Chronic Nicotine Exposure on Skeletal Muscle Function in Lithobates pipiens
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Authors
Dunstan, Cormac
Karleskind, Maximillien
Date of Issue
2025-04-25
Type
Presentation
Language
en_US
Subject Keywords
Other Titles
Abstract
Nicotine influences skeletal muscle by binding to nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction. At these receptors, nicotine mimics the neurotransmitter acetylcholine, initiating depolarization of muscle fibers. This depolarization activates voltage-gated calcium channels, followed by the release of calcium ions from the sarcoplasmic reticulum. Once released, calcium binds to regulatory proteins and initiates the actin-myosin interactions that cause muscle contractions. Relaxation occurs when calcium pumps begin to move the ions back into the sarcoplasmic reticulum. Chronic exposure to nicotine has been shown to desensitize muscles by disrupting their baseline membrane potential. In this study, groups of leopard frogs will be separated into control (no nicotine), medium, and high nicotine exposure groups for 3 weeks. Dosages will be determined by percentage change in metabolic rate, with a 3-6% change for medium dose and a 6-12% change for high dose. To administer the nicotine, the leopard frogs will have 1 mL of control or nicotine solution applied to their seat patch daily. The seat patch is an area of highly vascularized skin that is particularly absorptive. Following exposure, direct muscle stimulation using a force transducer and BIOPAC software will be used to assess both the change between electrical threshold and maximal muscle response as well as the time taken to reach complete muscle fatigue. It is expected that the chronic exposure to nicotine will negatively affect threshold and maximal response, as well as decrease the time taken to reach muscle fatigue.