The Neurobiology of Nicotine and Opioid Comorbidity
Approximately 85% of individuals currently seeking treatment for an opioid use disorder are habitual users of nicotine-containing products. In preclinical rodent models, nicotine administration substantially augments the self-administration of opioids. Moreover, concurrent nicotine administration engenders a punishment-resistant phenotype in animals responding for intravenous opioids. We have recently demonstrated that nicotine administration directly within the insular cortex is sufficient to interfere with learning about the adverse consequences of acute opioid intoxication. As such, we are currently investigating the role of insular cortical nicotinic signaling on the development of compulsive-like opioid consumption. To this end we employ site-specific behavioral pharmacology and chemogenetic circuit dissection in rodent models. Current funding DA048336.
Neural and Behavioral Parameters Influencing the Escalation of Alcohol Intake
Alcohol use disorder is characterized, in part, by an escalation in alcohol intake and a desire to continue to consume alcohol despite the threat of harmful or adverse repercussions. One adaptation associated with escalation of alcohol intake is an insensitivity, or attentional blindness, to the aversive properties of alcohol. We are particularly interested in elucidating the neural and behavioral adaptations that are driving this decrease in salience. Currently we are exploring the role played by dopaminergic innervation of the insular cortex and how alcohol exposure across the lifespan may alter insular dopaminergic signaling. Current funding AA017823.