Event‐Related Potential Responses to the Acute and Chronic Effects of Alcohol in Adolescent and Adult Wistar Rats

Abstract

Background The present study explored the hypothesis that adolescent ethanol exposure may cause long lasting changes in ethanol sensitivity by exploring the age-related effects of acute alcohol on intoxication and on event-related potential (ERP) responses to acoustic stimuli in ethanol naïve adolescent and adult male Wistar rats and in adult rats that were exposed to chronic ethanol/control conditions during adolescence. Methods Ethanol naïve adolescent (postnatal day 32 (PD32)) and adult male rats (PD99) were included in the first study. In a second study, rats were exposed to 5 weeks of ethanol vapor (Blood ethanol concentrations @ 175 mg%) or air from PD24 to PD59 and allowed to mature until PD90. In both studies rats were implanted with cortical recording electrodes, and the effects of acute ethanol (0.0, 1.5, and 3.0 g/kg) on behavioral and ERP responses were assessed. Results Adolescents were found to have higher amplitude and longer latency P3a and P3b components at baseline as compared to adult rats, and ethanol was found to produce a robust dose-dependent increase in the latency of the P3a and P3b components of the auditory ERP recorded in cortical sites in both adolescents and adults. However, ethanol produced significantly larger delays in P3a and P3b latencies in adults as compared to adolescents. Acute ethanol administration was also found to produce a robust dose dependent increase in the latency of the P3a and P3b components in adult animals exposed to ethanol vapor as adolescents and air exposed controls; however, larger acute ethanol-induced increases in P3a and P3b latencies were seen in controls as compared to adolescent vapor exposed rats. Conclusions Adolescent rats have a less intense P3 latency response to acute ethanol administration when compared to adult rats. Exposure to chronic ethanol during adolescence can cause “retention” of the adolescent phenotype of reduced P3 latency sensitivity to ethanol.

Role of the innate immune system in the neuropathological consequences induced by adolescent binge drinking

“…For instance, in rodents, the 2‐week period between postnatal days (P) 28–42 is the equivalent of the early to midadolescent period (∼12–18 years) in humans, while P43–55 is more comparable to the period of late adolescence/emerging adulthood in humans (∼18–25 years) (see Spear, ). To mimic binge drinking, alcohol was administered intraperitoneally, intragastrically (Vetreno & Crews, ), or using intermittent ethanol vapor exposure (e.g., Ehlers, Liu, Wills, & Crews, ; Ehlers, Desikan, & Wills, ) either intermittently or over several days to reach blood alcohol concentration (BAC) levels of 0.08 g/dl or higher (considered binge drinking levels, as defined by the National Institute on Alcohol Abuse and Alcoholism). For instance, one of the first adolescent models of binge drinking in rats (Pascual, Blanco, Cauli, Minarro, & Guerri, ) used an intraperitoneal injection of ethanol (3 g/kg) on 2 consecutive days at 48‐hr intervals over 14 days, and reached a BAC level of 0.16 g/dl.…”

Adolescent alcohol exposure and persistence of adolescent-typical phenotypes into adulthood: A mini-review

“…The same acute ethanol dose promoted 4–6 HZ power in the parietal cortex and hippocampus in adult Sprague-Dawley rats who had not received AIE exposure, whereas this ethanol effect was not evident in those exposed to AIE (Slawecki, 2002). Similarly, it is known that ethanol increases the latency of certain neocortical event-related potentials (ERPs), and does so less efficaciously in adolescent than adult rats (Ehlers et al, 2014). Interestingly, in the same study, when animals were exposed intermittently to ethanol vapor throughout adolescence and then tested in adulthood, their ERP latencies were less sensitive to acute ethanol than those of adult control animals.…”

“…on; 10 hr. off) ethanol vapor exposure with Wistar rats (e.g., Ehlers et al, 2013; 2014). Timing of the exposure has also varied across studies.…”

Ontogeny and adolescent alcohol exposure in Wistar rats: open field conflict, light/dark box and forced swim test

“…It has been demonstrated that chronic intermittent exposure to ethanol vapor during adolescence (14 hours exposure/10 hours no exposure, daily, over a 5-week period) can cause: increases in voluntary ethanol drinking, reductions in the size of the hippocampus as imaged by diffusion tensor imaging, reductions in measures of hippocampal neurogenesis, increases in the latency of the P300 component of the event-related potential, signs of behavioral disinhibition in the light/dark box and open field conflict test, immobility in the forced swim test, and reductions in cholinergic tone in the basal forebrain (see Criado and Ehlers, 2013; Ehlers et al, 2011, 2013a,b, 2014). …”

“…Adolescent rats display greater tolerance to the sedative effects of acute ethanol administration than adult rats, and regain consciousness at higher blood alcohol levels (Pian et al, 2008b; Silveri and Spear, 1998). For adult rats exposed to CIE during adolescence, the adolescent phenotype of reduced sensitivity to ethanol has been shown to be “retained” in behavioral measures (Slawecki, 2002; White et al, 2000 a,b), electrophysiological measures in the hippocampus (Fleming et al, 2012, 2013; Slawecki, 2002), and in the cortex (Ehlers et al, 2013c, 2014; Slawecki, 2002). Some authors have suggested that adolescent ethanol exposure may “lock-in” adolescent sensitivity to ethanol and then sustain it into adulthood (Fleming et al, 2012).…”