PhD Scientific Days 2026

Poster Session 3.N - Neurosciences

Chronic Alcohol and Nicotine Exposure Effects on Caenorhabditis elegans Behavior

Name of the presenter

Brandl, Zsófia

Institute/workplace of the presenter

Institute of Biochemistry and Molecular Biology

Authors

Zsófia Brandl-Bodnár¹
1: Institute of Biochemistry and Molecular Biology

Text of the abstract

Addiction poses a great challenge to society with serious individual and economic consequences, highlighting the need to better understand the molecular background of long-term substance exposure. Dopamine and serotonin mediated reward related processes in humans, such as alcohol and nicotine dependence are caused by complex genetic and environmental factors, and the nematode Caenorhabditis elegans is a valuable model for studying these molecular mechanisms. In this study, we examined the effects of ethanol and nicotine exposure using thrashing and chemotaxis (diacetyl race) assays, as well as stress signaling and dopaminergic neuron integrity.
In the diacetyl race assay, chronic ethanol exposure caused significant slowing after a 1 h withdrawal period. Wild-type animals showed delayed goal-reaching after 24 h exposure to 400 mM ethanol, while tph-1 serotonin-deficient mutants were affected at both 200 and 400 mM (p < 0.05). Area under the curve (AUC) analysis confirmed reduced speed in alcohol-exposed animals; importantly, this decrease appeared only after withdrawal, indicating that the impairment is specifically withdrawal-induced.
Thrashing assays further demonstrated impaired motility. In wild-type animals, 800 mM ethanol significantly reduced performance (p < 0.001), while serotonin mutants showed a dose dependent trend of decreased swimming ability following both exposure and withdrawal.
Stress responses were assessed by HLH-30:GFP nuclear translocation, which was increased in a dose-dependent manner after ethanol treatment, indicating significant cellular stress. Neurotoxicity was evaluated with the DAT-1:GFP reporter strain, where ethanol and nicotine exposure caused damage to dopaminergic CEP and ADE neurons after 24 h treatment.
Together, these findings demonstrate that ethanol and nicotine induce behavioral impairment, stress activation, and dopaminergic neuron damage in C. elegans. Future studies will extend this approach to other addictive substances to further elucidate addiction-related mechanisms and potential therapeutic targets.