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Pitock, J. R.

Publications and source records attributed to Pitock, J. R..

3 recordsLinked to original sources

Variables affecting acquisition and maintenance of operant ethanol self-administration in male and female Long-Evans rats

AimsThe goal of the present study was to determine the effect of prior experience with ethanol drinking and changes in session duration on the acquisition and maintenance of operant ethanol self-administration. MethodsAdult male and female Long-Evans rats were trained to operantly self-administer ethanol. A subset of male rats underwent intermittent-access two-bottle choice drinking in the home cage prior to operant training. Controls were given access to two bottles of water. Once fully trained in 30-min operant sessions, session duration was reduced to 15 min for all male and female rats. Differences between 30- and 15-min sessions were also assessed in a separate group of male and female rats trained to self-administer sucrose. ResultsNo differences were observed in acquisition rates, the magnitude of responding for ethanol, or total ethanol consumed between male rats allowed to drink ethanol in the home cage and those that remained ethanol naive prior to operant training. A significant decrease in appetitive and consummatory behaviors was observed in males trained to lever press for either ethanol or sucrose. Females exhibited a similar decrease in operant performance for sucrose, but their behavior was largely unchanged in response to changes in session duration when ethanol was the reinforcer. ConclusionsThese data suggest that the use of prior home cage ethanol drinking as an initiation procedure offers little advantage over no initiation procedure at all. Moreover, reducing operant session duration from 30-min to 15-min has the potential to decrease, rather than increase, levels of ethanol intake. Short summaryIntermittent-access two-bottle choice ethanol drinking offers no advantage as an initiation procedure for operant ethanol self-administration over animals that are ethanol-naive prior to training. In addition, shortening the operant session duration does not increase overall intake or promote binge-like patterns of intake for either ethanol or sucrose reinforcer.

neuroscience↗

Attenuated incubation of ethanol-induced conditioned taste aversion in a model of dependence

RationalePreclinical studies report attenuated ethanol-induced conditioned taste aversion (CTA) following chronic ethanol exposure, suggesting that tolerance develops to the aversive properties of ethanol. However, these studies are confounded by pre-exposure to the unconditioned stimulus (US; ethanol), which is well known to hinder conditioning. ObjectivesThis study was designed to determine whether chronic ethanol exposure produces tolerance to the aversive properties of ethanol in the absence of a US pre-exposure confound. MethodsCTA was performed in adult male and female Long-Evans rats by pairing 0.1% ingested saccharin with an intraperitoneal injection of ethanol (1.5 or 2.0 g/kg) or saline. Rats were then rendered ethanol dependent using chronic intermittent ethanol (CIE) vapor exposure. Controls were exposed to room air (AIR). The effect of chronic ethanol on CTA expression and reconditioning were examined following vapor exposure. ResultsPrior to vapor exposure, both sexes developed CTA to a comparable degree with 2.0 g/kg producing greater CTA than 1.5 g/kg ethanol. Following vapor exposure, AIR controls exhibited an increase in CTA magnitude compared to pre-vapor levels. This effect was absent in CIE-exposed rats. These group differences were eliminated upon re-conditioning after vapor exposure. ConclusionsThese data suggest that chronic ethanol does not facilitate tolerance to the aversive properties of ethanol but rather, attenuates incubation of ethanol-induced CTA. Loss of CTA incubation suggests that CIE exposure disrupts circuits encoding aversion.

neuroscience↗

A translational rodent model of individual differences in sensitivity to the aversive properties of ethanol

BackgroundA strong relationship exists between individual sensitivity to the aversive properties of ethanol and risk for alcohol use disorder (AUD). Despite this, our understanding of the neurobiological mechanisms underlying subjective response to ethanol is relatively poor. A major contributor to this is the absence of preclinical models that enable exploration of this individual variability similar to studies performed in humans. MethodsAdult male and female Long-Evans rats were trained to associate a novel tastant (saccharin) with acute exposure to either saline or ethanol (1.5 g/kg or 2.0 g/kg i.p.) over three conditioning days using a standard conditioned taste aversion (CTA) procedure. Variability in sensitivity to ethanol-induced CTA was phenotypically characterized using a median split across the populations studied. ResultsWhen examining group averages, both male and female rats that had saccharin paired with either dose of ethanol exhibited reduced saccharin intake relative to saline controls of ethanol-induced CTA. Examination of individual data revealed a bimodal distribution of responses uncovering two distinct phenotypes present in both sexes. CTA-sensitive rats exhibited a rapid and progressive reduction in saccharin intake with each successive ethanol pairing. In contrast, saccharin intake was unchanged or maintained after an initial decrease from baseline levels in CTA-resistant rats. While CTA magnitude was similar between male and female CTA-sensitive rats, CTA-resistant females were more resistant to the development of ethanol-induced CTA than their male counterparts. Phenotypic differences were not driven by differences in baseline saccharin intake. CTA sensitivity correlated with behavioral signs of intoxication in only a subset of rats. ConclusionsThese data parallel work in humans by revealing individual differences in sensitivity to the aversive properties of ethanol that emerge immediately after initial exposure to ethanol in both sexes. This model can be leveraged in future studies to investigate the neurobiological mechanisms that confer risk for AUD.

neuroscience↗