Prenatal alcohol exposure and adolescent stress - unmasking persistent attentional deficits in rats

Prenatal alcohol exposure (PAE) can produce a myriad of deficits. Unfortunately, affected individuals may also be exposed to the stress of an adverse home environment, contributing to deficits of attentional processes that are the hallmark of optimal executive function. Male offspring of ad‐libitum‐fed Control (Con), Pairfed (PF), and PAE dams were randomly assigned to either a 5‐day period of variable chronic mild stress (CMS) or no CMS in adolescence. In adulthood, rats were trained in a non‐match to sample task (T‐maze), followed by extensive assessment in the five‐choice serial reaction time task. Once rats acquired the five‐choice serial reaction time task (stable accuracy), they were tested in three challenge conditions: (i) increased sustained attention, (ii) selective attention and, (iii) varying doses of d‐amphetamine, an indirect dopamine and norepinephrine agonist. At birth and throughout the study, PAE offspring showed reduced body weight. Moreover, although PAE animals were similar to Con animals in task acquisition, they were progressively less proficient with transitions to shorter stimulus durations (decreased accuracy and increased omissions). Five days of adolescent CMS increased basal corticosterone levels in adolescence and disrupted cognitive performance in adulthood. Further, CMS augmented PAE‐related disturbances in acquisition and, to a lesser extent, also disrupted attentional processes in Con and PF animals. Following task acquisition, challenges unmasked persistent attentional difficulties resulting from both PAE and adolescent CMS. In conclusion, PAE, adolescent CMS, and their interaction produced unique behavioural profiles that suggest vulnerability in select neurobiological processes at different stages of development. Interactions between prenatal alcohol exposure (PAE) and adolescent chronic mild stress (CMS) produce delays in acquisition of the 5‐CSRTT (A) in adulthood. Additionally (B), CMS augments (bottom) PAE‐related (top) attentional deficits (increased omissions). PAE and CMS interactions (C) dull later responses to a dopaminergic agonist, amphetamine, at doses that produce attentional deficits in PAE and Control counterparts, elucidating potential underlying mechanisms of developmental insults.