Chronic Corticosterone Exposure during Adolescence Reduces Impulsive Action but Increases Impulsive Choice and Sensitivity to Yohimbine in Male Sprague-Dawley Rats

Abstract

Chronic stress during adolescence is associated with an increased risk for alcoholism and addictive disorders. Addiction is also associated with increased impulsivity, and stress during adolescence could alter cortical circuits responsible for response inhibition. Therefore, the present study determined the effect of chronic exposure to the stress hormone corticosterone (CORT) during adolescence on tests of impulsivity in adulthood and examined possible biochemical mechanisms. Male Sprague-Dawley rats were exposed to CORT by their drinking water during adolescence (post-natal day 30-50). The rats were then tested in adulthood to assess behavior on the 5-choice serial reaction time task (5CSRTT), stop-signal reaction time task (SSRTT), and the delay-discounting task, which differentially assess attention, impulsive action, and impulsive choice. Yohimbine-induced impulsivity on the 5CSRTT and biochemical analysis of the lateral orbital frontal cortex (lOFC) was also assessed owing to the ability of yohimbine to activate the hypothalamic-pituitary-adrenal axis and influence impulsivity. Adolescent CORT-treated rats were found to behave largely like controls on the 5CSRTT, but did show reduced premature responses when the intertrial interval was increased. Nevertheless, the CORT-treated rats tended to have more yohimbineinduced impulsive responses at low doses on this task, which was not found to be due to increased pCREB in the lOFC, but could be related to a higher expression/activity of the AMPA receptor subunit GluR1. Adolescent CORT-treated rats performed more accurately on the SSRTT, but showed greater impulsivity on the delay-discounting task, as indicated by steeper discounting functions. Therefore, adolescent CORT exposure reduced impulsive action but increased impulsive choice, indicating that chronic stress hormone exposure in adolescence can have long-term consequences on behavior.

The effects of lactation on impulsive behavior in vasopressin-deficient Brattleboro rats

“…Corticosterone levels were increased in control lactating rats twenty days after delivery, while AVP deficiency dampened this increase, a finding that is consistent with earlier reports (Fodor et al, 2013).These data might suggest that AVP contributes, in part, to maternal increases in impulsivity via the enhancement of HPA axis activity, as earlier reports showed that chronic corticosterone treatment leads to increased impulsivity (Torregrossa et al, 2012).…”

“…In addition to measurements of impulsive behavior, HPA axis activity (i.e. corticosterone levels) was also assessed, as the HPA axis has been reported to be altered by AVP deficiency (Fodor et al, 2013;Makara et al, 2012) and to play a role in impulsivity (Torregrossa et al, 2012).…”

The Behavioral Economics of Substance Use Disorders: Reinforcement Pathologies and Their Repair

“…With regard to impulsive discounting, the prefrontal and subcortical circuits are largely those that have been implicated with discounting decision making in fMRI research (Bickel et al 2009, McClure et al 2004), suggesting that commensurate impairment in discounting may be a behavioral manifestation of these neuroadaptive changes. With regard to the antireward system, the role of stress in discounting has been only modestly studied, and results are mixed (Diller et al 2011, Fields et al 2009, Torregrossa et al 2012, White et al 2008). However, purely from conjecture, given the laboratory evidence on withdrawal effects discussed above, the chronic augmentation of the antireward system may be a further plausible mechanism for increasing discounting.…”

Habitual alcohol seeking: Modeling the transition from casual drinking to addiction

“…Stress across the lifespan has been shown to increase the likelihood of alcohol use disorders (Enoch, 2011). In animal models, chronic activation of stress circuitry can promote the development of behaviors that are thought to phenotypes that are associated with early onset of drinking in humans (Hamilton, Ansell, Reynolds, Potenza, & Sinha, 2013; Torregrossa, Xie, & Taylor, 2012). In addition to driving behavioral inflexibility, prevailing theories suggest that alcohol use disorders represent reward surfeit disorders (Comings & Blum, 2000; Koob, 2013) in which an impaired ‘reward system’ promotes the development of addiction.…”