Evening circadian preference is associated with sleep problems and daytime sleepiness in adolescents with ADHD.

Adolescence is a developmental period characterized by disruptions in sleep and changes in circadian preferences. Although adolescents with attention-deficit/hyperactivity disorder (ADHD) are at even higher risk of sleep disruption than their peers, no study has examined whether circadian preference is associated with sleep problems and daytime sleepiness in adolescents with ADHD. This study provides an initial test of the hypothesis that greater evening preference would be associated with more sleep problems and daytime sleepiness in adolescents diagnosed with ADHD. Participants were 80 adolescents (69% male), aged 13-17 years, with ADHD. Adolescents completed measures assessing circadian preference, pubertal development, anxiety/depressive symptoms and weeknight sleep duration. Both adolescents and parents completed measures of sleep problems and daytime sleepiness. In regression analyses controlling for a number of other variables (i.e., age, sex, pubertal development, ADHD medication use, and ADHD, oppositional defiant disorder and internalizing symptom severity), greater evening preference was associated with both adolescent- and parent-reported sleep problems and daytime sleepiness. Greater evening preference remained significantly associated with each of these sleep problems and daytime sleepiness when also controlling for weeknight sleep duration. This is the first study to demonstrate that evening circadian preference is associated with both sleep problems and daytime sleepiness in adolescents with ADHD. The results indicate that it is important to consider circadian function as research examining sleep in adolescents with ADHD continues to advance.

Nicotine affects ethanol-conditioned taste, but not place, aversion in a simultaneous conditioning procedure.

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.