Nicotine addiction leads to repeated exposure to electronic nicotine vapor, reinforcing cycles of intake and withdrawal symptoms. Understanding the systems-wide effects of nicotine, particularly on peripheral and central cellular functions, is crucial for addressing its role in addiction and its detrimental impacts on the lungs and brain.
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Addiction to nicotine drives the repeated exposure to electronic nicotine vapor in humans (Fig. 1). Indeed, exposure to nicotine is reinforcing and can lead to repeated cycles of intake culminating in the need for regular consumption and withdrawal symptoms during periods of abstinence (Markou, 2008). One of the primary goals of addiction research is to understand how nicotine or other drugs of abuse augment or impair cellular functions to produce long-lasting maladaptive changes to brain circuitry that promote addiction. However, nicotine passes through the lungs and cardiovascular system before it reaches the brain. Thus, it is important to understand the detrimental effects of nicotine from a systems perspective. The rest of the body, and the lungs in particular, is chronically exposed to nicotine, which leads to activation of peripheral nAChR. Thus, future studies will need to examine the interplay between peripheral and central effects of nicotine: for example, (1) how nicotine can directly alter cell signalling pathways both centrally and peripherally to change gene/protein expression, and (2) how peripheral alterations can trigger maladaptive changes in specific regions of the lungs and brain.
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