Effects of adolescent alcohol exposure on stress-induced reward deficits, brain CRF, monoamines and glutamate in adult rats

Abstract

These results demonstrate increased risk of repeated stress-induced anhedonia after AIE exposure, an effect that may be due to alterations in brain CRF and dopamine systems. These results suggest that the increased rates of depression reported in people with a history of adolescent alcohol exposure may be related to alterations in brain reward and stress systems that may contribute to increased stress-induced anhedonia.

Role of NMDA and AMPA glutamatergic receptors in the effects of social defeat on the rewarding properties of MDMA in mice

“…defeat had elevated reward thresholds in the intracranial self-stimulation paradigm (Boutros et al, 2018;Gottschalk et al, 2018) and mice defeated for four consecutive days showed reduced sucrose preference (Yashiro & Seki, 2017). In previous works from our laboratory, we attempted to uncover the behavioural mechanisms underlying the impairment in the acquisition of MDMA CPP induced by social defeat, using the same strain of mice and schedule of social defeat as in the present study.…”

“…Recently, Boutros et al . () showed an increase in the glutamate levels in the caudate‐putamen of rats after chronic social defeat. Furthermore, Novick et al .…”

“…If this were the case, the stressed animals could need a greater quantity of the drug to feel rewarding effects. In support of this hypothesis, it has been demonstrated that social defeat exposure induces anhedonia; for example, rats that underwent chronic social defeat had elevated reward thresholds in the intracranial self‐stimulation paradigm (Boutros et al ., ; Gottschalk et al ., ) and mice defeated for four consecutive days showed reduced sucrose preference (Yashiro & Seki, ). In previous works from our laboratory, we attempted to uncover the behavioural mechanisms underlying the impairment in the acquisition of MDMA CPP induced by social defeat, using the same strain of mice and schedule of social defeat as in the present study.…”

“…Wang et al (2014) also reported an elevation of the AMPA receptor GluA1 subunit in the VTA 17 days after exposure to chronic (10 days) social defeat. Recently, Boutros et al (2018) showed an increase in the glutamate levels in the caudate-putamen of rats after chronic social defeat. Furthermore, Novick et al (2016) reported that repeated social defeat during adolescence produced long-term changes in the expression of NMDA receptors in several brain areas (increases in the CA3 and decreases in the infralimbic PFC and central amygdala) but not in others (CA1, nucleus accumbens, caudate-putamen, prelimbic and cingulate cortex, and basolateral amygdala).…”

Prefrontal cortex development and emergence of self‐regulatory competence: the two cardinal features of adolescence disrupted in context of alcohol abuse

“…This observation was associated with a loss of cholinergic neurons of up to 30–50% in the basal forebrain indicating that adolescent bingeing not only coincides with long‐lasting cholinergic deficits in the PFC but also with impaired cognitive flexibility (Fernandez et al ., ). In line with the former observation, adolescent rats injected twice a day with ethanol for three consecutive weeks preferred the risky option in a probability discounting task (Boutros et al ., ). This deficit was associated with decreased tyrosine hydroxylase and choline acetyltransferase in the prelimbic cortex.…”