Developmental differences in EEG and sleep responses to acute ethanol administration and its withdrawal (hangover) in adolescent and adult Wistar rats

Abstract

Age-related differences in sensitivity to the acute effects of alcohol may play an important role in the increased risk for the development of alcoholism seen in teens that begin drinking at an early age. The present study evaluated the acute and protracted (hangover) effects of ethanol in adolescent (P33–P40) and adult (P100–P107) Wistar rats, using the cortical electroencephalogram (EEG). Six minutes of EEG was recorded during waking, 15 min after administration of 0, 1.5, or 3.0 g/kg ethanol, and for 3 h at 20 h post ethanol, during the rats’ next sleep cycle. Significantly higher overall frontal and parietal cortical power was seen in a wide range of EEG frequencies in adolescent rats as compared to adult rats in their waking EEG. Acute administration of ethanol did not produce differences between adolescents and adults on behavioral measures of acute intoxication. However, it did produce a significantly less intense acute EEG response to ethanol in the theta frequencies in parietal cortex in the adolescents as compared to the adults. At 20 h following acute ethanol administration, during the rats’ next sleep cycle, a decrease in slow-wave frequencies (1–4 Hz) was seen and the adolescent rats were found to display more reduction in the slow-wave frequencies than the adults did. The present study found that adolescent rats, as compared to adults, demonstrate low sensitivity to acute ethanol administration in the theta frequencies and more susceptibility to disruption of slow-wave sleep during hangover. These studies may lend support to the idea that these traits may contribute to increased risk for alcohol use disorders seen in adults who begin drinking in their early teenage years.

Relationship between ethanol-induced activity and anxiolysis in the open field, elevated plus maze, light-dark box, and ethanol intake in adolescent rats

“…We cannot exclude the possibility, however, that enhanced ethanol drinking in the 3.25 g/kg group was driven by the negative effects of ethanol hangover. Following the administration of 3.0–4.0 g/kg ethanol, adult rats exhibit rebound hyperthermia [35], and adolescent but not adult rats exhibit alterations in slow-wave sleep [36]. Although we did not measure or observe overt signs of withdrawal, higher ethanol drinking in the present study may have been promoted by similar lingering aversive effects of high-ethanol dosing.…”

Differential Sensitivity to Ethanol‐Induced Circadian Rhythm Disruption in Adolescent and Adult Mice

“…This insensitivity is consistent with the only other study of which we are aware that examines the effect of developmental ethanol exposure on circadian endpoints, which reports changes in slow-wave sleep, but not circadian activity or temperature rhythms, in mice exposed to ethanol on postnatal day 7 (Wilson et al, 2016). It is also noteworthy that adolescent rats are initially less sensitive to ethanol-induced sleep disruption (Ehlers et al, 2013). Thus, it is conceivable that the initial lack of circadian- and sleep-related consequences adolescent rodents experience with acute ethanol may contribute to their higher alcohol consumption (Holstein et al, 2011, Melendez, 2011, Moore et al, 2010, Quoilin and Boehm, 2016).…”

“…Thus, it is conceivable that the initial lack of circadian- and sleep-related consequences adolescent rodents experience with acute ethanol may contribute to their higher alcohol consumption (Holstein et al, 2011, Melendez, 2011, Moore et al, 2010, Quoilin and Boehm, 2016). However, given that adolescent rats also show greater slow wave sleep suppression the day following acute ethanol compared to adults (Ehlers et al, 2013), it is also tempting to speculate that heavy drinking in adolescents may be reinforced during hangover to induce sleep.…”

Acute Binge Alcohol Administration Reverses Sleep-Wake Cycle in Sprague Dawley Rats

“…While alcohol hangover research is in its infancy, evidence exists to suggest that individuals experiencing hangover may consume (self-medicate) more alcohol to alleviate the symptoms of alcohol hangover resulting in the initiation of vicious cycle that may eventually culminate into the development of alcohol use disorder (Piasecki et al, 2010; Ehlers et al, 2013). In fact, heavy alcohol consumption, hangover resistance, and hangover frequency may each indicate low alcohol sensitivity which is an established risk factor for the development of alcohol dependence (Piasecki et al, 2012).…”