2026 ECNP Congress

S18.03

Improving translational impacts for understanding the psychiatric risks of adolescent nicotine and cannabis use with edible and vaping administration models

Steven Laviolette — University of Western Ontario, Anatomy & Cell Biology- Psychiatry, LONDON, Canada

Dr. Steven Laviolette will present recent advances in modelling the neurodevelopmental impacts of cannabis and nicotine exposure. His presentation will highlight the development of translationally relevant preclinical models that more closely reflect contemporary patterns of substance use, including pre-clinical cannabis edibles and nicotine vaping. Using these approaches in rodent models, Dr. Laviolette’s research demonstrates how adolescent exposure to Δ⁹-tetrahydrocannabinol (THC) and nicotine produces long-lasting alterations in corticolimbic circuitry, particularly within the prefrontal cortex and nucleus accumbens, leading to persistent changes in emotional regulation, reward processing, cognitive function and risk for neuropsychiatric disorders.

A key focus of the presentation will be the integration of these behavioural and circuit-level findings with emerging molecular and cellular data. Dr. Laviolette will discuss how these exposure paradigms induce disruptions in excitatory–inhibitory balance, synaptic plasticity, and intracellular signalling pathways linked to psychiatric vulnerability. Importantly, he will emphasize the growing role of human-derived cerebral organoids as a complementary translational platform. These three-dimensional neural models enable the investigation of human-specific developmental trajectories, gene expression profiles, and epigenetic modifications that cannot be fully captured in animal systems.

By aligning findings from rodent models with data derived from cerebral organoids, this work provides a powerful framework for bridging the gap between preclinical and human neuroscience discoveries. Dr. Laviolette will outline how this integrated strategy can accelerate the identification of molecular and genetic mechanisms underlying neurodevelopmental risk for mood, anxiety, schizophrenia and substance use disorders, ultimately informing more targeted and effective therapeutic interventions.