Abstract
Individuals who begin drinking during adolescence may be at a higher risk of developing an alcohol use disorder later in life, compared to those that refrain until adulthood. Adolescents and adults exhibit different sensitivities to ethanol, with adolescents typically displaying increased sensitivity to ethanol’s rewarding properties and reduced sensitivity to ethanol’s negative/aversive properties. These responses may promote elevated adolescent intake due in part to attenuated sensitivity to undesired ethanol effects that can curb intake. Although much work has characterized age-specific behavioral responses to the negative properties of ethanol, less is known about the neuronal substrates thought to drive those age differences. We hypothesized that neuronal ensembles implicated in aversive responding will be differentially activated in adolescents and adults following conditioned taste aversion (CTA), a classical conditioning behavioral paradigm that is used to study the extent of an adverse response. Using male cFos-lacz transgenic rats on a Sprague-Dawley outbred genetic background, we assessed neuronal activation using 5-bromo-4-chloro-3-indolyl β-D-Galactopyranoside (xGal) histochemistry immediately following behavioral CTA testing in adolescents [postnatal day (P)30] and adults (P70). A series of brain regions are set to be assessed, including the bed nucleus of the stria terminalis (BNST), interpeduncular nucleus, rostral medial tegmental nucleus (RMTg), ventral tegmental area (VTA), lateral habenula (LHb), dorsal hippocampus, and subnuclei within the hypothalamus will be stained and level of neural activation compared between age and exposure within each region due to their known involvement in aversive responding. In doing so, we hope to gain further insight into the regions that contribute to age-related differences in ethanol response.