Nicotine withdrawal

ABSTRACT: g-Aminobutyric acid subtype B (GABA-B) receptors play an important role in regulating brain reward function. Accumulating evidence suggests that chronic exposure to drugs of abuse may alter GABA-B receptor function. The present studies investigated whether chronic nicotine administration, using a regimen that induces nicotine dependence, increased inhibitory regulation of brain reward function by GABA-B receptors, as measured by intracranial self-stimulation (ICSS) thresholds in rats. Such an action of nicotine may contribute to the reward deficit observed during nicotine withdrawal. Nicotine-dependent and control rats received the GABA transaminase inhibitor g-vinyl-GABA or the GABA-B receptor agonist CGP44532 according to a within-subjects Latin square design, and ICSS thresholds were assessed post-injection. Systemic administration of the lowest doses of GVG or CGP44532 did not alter reward thresholds in control or nicotine-treated rats, whereas the highest doses of each drug elevated thresholds similarly in both groups. Further, micro-infusion of CGP44532 directly into the ventral tegmental area elevated ICSS thresholds similarly in saline- and nicotine-treated rats. Overall, these data demonstrate that prolonged nicotine exposure did not alter GABA-B receptor-mediated regulation of brain reward function, and suggest that alterations in GABA-B receptor activity are unlikely to play a role in the brain reward deficits associated with spontaneous nicotine withdrawal.

Certain chronic conditions are becoming increasingly ignored due to the magnitude of COVID-19. However, continued research on these conditions, such as nicotine addiction and heart disease, and how they relate to COVID-19 will help researchers assess case severity more adequately. It has been commonly asserted that smoking cessation will reduce COVID-19 mortality rates for smokers due to how it damages the lungs. However, smoking cessation results in nicotine withdrawal , which is proven to cause side effects that could conversely increase the severity of COVID-19. This study aims to determine how nicotine withdrawal increases the probability of developing cardiac arrhythmia, and how that relationship increases COVID-19 mortality rates. To conduct our study, we compiled datasets from various health organizations, including the CDC and WHO, to find correlations between these three conditions. We first investigated the complications that result from nicotine withdrawal and how they may develop into cardiac arrhythmia. Following initial inquiries, we then calculated how cardiac arrhythmia increases COVID-19 mortality rates. To validate our conclusions, we compared smoking cessation rates with COVID-19 mortality rates in different states to isolate direct correlation between the two conditions. We determined that nicotine withdrawal has a 32.7% probability of causing cardiac arrhythmia, and that cardiac arrhythmia increases the chance of death from COVID-19 by 14.7%. Ultimately, we found that nicotine withdrawal increases the COVID-19 mortality rate by 4.8% compared to the general population, a significant and concerning finding.