Topic: nicotine addiction

Nicotinic acetylcholine receptors (nAChRs) are pentameric ionotropic receptors composed of a combination of α and β subunits. Human genetic association and preclinical studies have shown a key role of α5 containing nAChRs (α5*nAChRs) in the risk to develop nicotine addiction. Tobacco smoking is highly comorbid with bulimia nervosa and binge eating disorders. Interestingly, genetic variation at CHRNA5 has also been associated with higher body mass index (BMI) in never smokers, but lower BMI in current smokers, and increased appetence for food in rodents. Here we sought to investigate the role o

Tobacco smoking is a major contributor to the burden of mental health disease worldwide. Nicotine is the primary reinforcing and main addictive component of tobacco. Nicotine addiction is a chronic relapsing disorder associated with multiple psychiatric comorbidities, and few effective interventions currently exist to curb addiction to nicotine. The neurocircuitry underlying nicotine addiction is broad, complex and depends on the stages of the disease process. It is well-acknowledged that nicotine impacts the reward system with prominent alterations of the firing properties of VTA DA neurons c

Nicotine use during adolescence (ADO) constitutes a risk factor to later develop mood disorders. Yet, the mechanisms underlying the enduring effects of adolescent nicotine exposure remain poorly elucidated. During ADO, the cognitive and goal-directed behaviors are refined in parallel to the development of dopamine (DA) circuitry, and both are uniquely sensitive to disruption by environmental influence during this time. Prolonged nicotine exposure in adult mice favors the appearance of depressive-like symptoms by altering the activity of ventral tegmental area (VTA) DA neurons and nicotinic pat

Prenatal pathologies like fetal hypoxia or prenatal stress are increasingly recognized contributors to later-life neuropsychiatric diseases. These pathologies often co-occur, making it challenging to distinguish their individual effects. To address this, we modeled prenatal severe hypoxia (PSH) associated with maternal stress, or prenatal intrauterine ischemia (PII). Both adult PSH and PII rats showed elevated HIF1α levels in the hippocampus (HPC), but only PSH rats exhibited an impaired circadian glucocorticoid rhythm, demonstrating the suitability of both models for the research objectives.C