Behavioral and molecular approach to nicotine addiction in a genetically transmissible rodent model of psychosis
Abstract
Behavioral and molecular approach to nicotine addiction in a genetically transmissible rodent model of psychosis Henson, L. J., Cuozzo, A. M., Ahmed, C. D., Wills, L. J., Schmeichel B.E., Gass, J. T Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN People living with schizophrenia (SZ) consume nicotine at significantly higher rates than healthy populations. This is theorized to be an attempt to self-medicate SZ and is characterized by a dopamine dysregulation leading to heightened reward sensitivity and addiction vulnerability. The purpose of this study is to further understand the comorbidity of nicotine abuse within SZ to improve treatment and smoking cessation outcomes. This was done using the untreated offspring of both male and female parent rats neonatally treated with either quinpirole, a dopamine D2 receptor-like agonist (MQxFQ) or saline (MSxFS) in a nicotine vapor conditioned place preference (CPP) model. It was expected that MQxFQ rats would show higher preference to nicotine than MSxFS rats, as shown in our previous CPP studies. The nicotine vapor CPP paradigm used consists of two pre-conditioning tests followed by three conditioning trials and a final post-conditioning test. In each 10-minute conditioning session, rats were exposed to 10 three second puffs of vapor, which was either a control or nicotine vapor of different concentrations: 15mg/mL, 30mg/mL, or 60mg/mL. A subset of rats was administered 3mg/kg dihydro-β-erythroidine (DHβE) in the post-test to antagonize α4β2 nicotinic receptors, a significant mechanism in nicotine reinforcement. Additionally, the nucleus accumbens (NAc) and ventral tegmental area (VTA) were analyzed for brain derived neurotrophic factor (BDNF) via ELISA to see changes in plasticity relevant to addiction. Results have demonstrated a significant CPP dose-response across both MQxFQ and MSxFS groups. Administration of DHβE at the post-test blocked CPP of 60mg/mL nicotine, indicating that α4β2 is essential for recall and expression of nicotine-based reward. MQxFQ rats also showed enhanced BDNF expression across all vapor concentrations. These findings contribute to the understanding of mechanisms of nicotine vapor reward in the context of psychosis. Future studies will seek to elucidate specific neurocircuitry that induces nicotine use relapse.
Start Time
15-4-2026 9:00 AM
End Time
15-4-2026 12:00 PM
Room Number
Culp Ballroom 316
Poster Number
40
Presentation Type
Poster
Presentation Subtype
Posters - Competitive
Presentation Category
Health
Student Type
Undergraduate Student
Faculty Mentor
Justin Gass
Behavioral and molecular approach to nicotine addiction in a genetically transmissible rodent model of psychosis
Culp Ballroom 316
Behavioral and molecular approach to nicotine addiction in a genetically transmissible rodent model of psychosis Henson, L. J., Cuozzo, A. M., Ahmed, C. D., Wills, L. J., Schmeichel B.E., Gass, J. T Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN People living with schizophrenia (SZ) consume nicotine at significantly higher rates than healthy populations. This is theorized to be an attempt to self-medicate SZ and is characterized by a dopamine dysregulation leading to heightened reward sensitivity and addiction vulnerability. The purpose of this study is to further understand the comorbidity of nicotine abuse within SZ to improve treatment and smoking cessation outcomes. This was done using the untreated offspring of both male and female parent rats neonatally treated with either quinpirole, a dopamine D2 receptor-like agonist (MQxFQ) or saline (MSxFS) in a nicotine vapor conditioned place preference (CPP) model. It was expected that MQxFQ rats would show higher preference to nicotine than MSxFS rats, as shown in our previous CPP studies. The nicotine vapor CPP paradigm used consists of two pre-conditioning tests followed by three conditioning trials and a final post-conditioning test. In each 10-minute conditioning session, rats were exposed to 10 three second puffs of vapor, which was either a control or nicotine vapor of different concentrations: 15mg/mL, 30mg/mL, or 60mg/mL. A subset of rats was administered 3mg/kg dihydro-β-erythroidine (DHβE) in the post-test to antagonize α4β2 nicotinic receptors, a significant mechanism in nicotine reinforcement. Additionally, the nucleus accumbens (NAc) and ventral tegmental area (VTA) were analyzed for brain derived neurotrophic factor (BDNF) via ELISA to see changes in plasticity relevant to addiction. Results have demonstrated a significant CPP dose-response across both MQxFQ and MSxFS groups. Administration of DHβE at the post-test blocked CPP of 60mg/mL nicotine, indicating that α4β2 is essential for recall and expression of nicotine-based reward. MQxFQ rats also showed enhanced BDNF expression across all vapor concentrations. These findings contribute to the understanding of mechanisms of nicotine vapor reward in the context of psychosis. Future studies will seek to elucidate specific neurocircuitry that induces nicotine use relapse.
