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The conditioned taste aversion (CTA) induced by ethanol is a key factor limiting ethanol intake. Nicotine, a drug co-consumed with ethanol, may decrease this aversion by modulating the unconditioned effects of ethanol or by disrupting the association between ethanol and its associated cues. This study analyzed ethanol-induced CTA and conditioned place aversion (CPA) in Long-Evans rats with subchronic exposure to nicotine. The rats were treated with nicotine (0.0 or 0.4 mg/kg) three times before conditioning (on lickometer training sessions 3, 4, and 5) and across conditioning days. During the conditioning the rats were given ethanol (1.3 g/kg) preceded and followed by presentation of a taste (NaCl) and tactile (rod or hole floors) conditioned stimulus (CS+), respectively. On CS- conditioning days, the rats were given vehicle and exposed to alternative stimuli. Three CTA and CPA testing sessions were then conducted. It was found that nicotine reduced ethanol-induced CTA and enhanced locomotor activity, but did not significantly modify the magnitude of ethanol-induced CPA. The effects of nicotine on CTA were observed during both conditioning and testing sessions, and were specific to the NaCl CS+, having no effect on reactivity to water. The dissociation between the effect of nicotine on ethanol-induced CTA and CPA suggests that nicotine does not alter ethanol's motivational properties by generally increasing its positive rewarding effects, nor does it blunt all aversive-like responses to this drug. Instead, nicotine may impede ethanol-induced CTA induced by ethanol by disrupting the neural underpinnings of this specific form of associative learning.

Attention‐deficit/hyperactivity disorder (ADHD) is a persistent neurodevelopmental disorder characterized by inattention and/or hyperactivity‐impulsivity. Adolescents with ADHD commonly experience deficits in areas of executive function (EF). These deficits are associated with academic, social, and emotional impairments. Experimental research shows shortened sleep duration to cause poorer daily life EF in typically developing adolescents. However, no previous research has looked at the casual relationship between inadequate sleep and executive functioning deficits in teenagers with ADHD. The objective of this study was to investigate whether sleep duration impacted daily life executive functioning. The hypothesis was that restricted sleep would negatively impact daily life executive functioning in adolescents with ADHD. A three‐week at home sleep manipulation protocol was implemented, using an experimental crossover design. Participants completed a phase stabilization week, followed by a sleep restriction (SR) week (6.5 hours) and sleep extension (SE) week (9.5). SR and SE conditions were counterbalanced across participants. Each week, participants attended laboratory visits at the medical center where executive functioning was measured with a validated rating scale, the Behavior Rating Inventory of Executive Function, Second Edition (BRIEF2). The BRIEF2 measured different areas of EF domains such as working memory, inhibition, planning/organization, emotional control, and initiation. Sleep duration was monitored with actigraphy and sleep diaries. Analyses looked at 48 participants who successfully adhered to the study protocol and who had complete actigraphy data. The results of a paired sample t‐test showed significantly (ps <.05) more deficits in most daily life EF domains during the sleep restriction phase compared to the sleep extension phase. This study provides the first evidence for shortened sleep duration as a causal contributor to worsened executive functioning in adolescents with ADHD. Increased sleep may significantly impact academic, social, and emotional functioning in adolescents with ADHD, and sleep may be an important future target for future intervention.Support or Funding InformationThis research was supported by the National Institute of Mental Health (NIMH; grant R03MH109787; Dr. Becker). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIMH.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.