Search

Background: Economic stress can serve as a second hit for people who have already accumulated a history of adverse life experiences. How one recovers from a setback is a core feature of resilience but is seldom captured in animal studies., Methods: We challenged mice in a novel 2-hit stress model by first exposing them to chronic social defeat stress and then testing adaptations to increasing reward scarcity on a neuroeconomic task. Mice were tested across months on the Restaurant Row task, during which they foraged daily for their primary source of food while on a limited time budget in a closed-economy system. An abrupt transition into a reward-scarce environment elicits an economic challenge, precipitating a drop in food intake and body weight to which mice must respond to survive., Results: We found that mice with a history of social stress mounted a robust behavioral response to this economic challenge that was achieved through a complex redistribution of time allocation among competing opportunities. Interestingly, we found that mice with a history of social defeat displayed changes in the development of decision-making policies during the recovery process that are important not only for ensuring food security necessary for survival but also prioritizing subjective value and that these changes emerged only for certain types of choices., Conclusions: These findings indicate that an individual's capacity to recover from economic challenges depends on that person's prior history of stress and can affect multiple decision-making aspects of subjective well-being, thus highlighting a motivational balance that may be altered in stress-related disorders such as depression., (Copyright © 2023 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Adolescents and adults engage in anabolic-androgenic steroid (AAS) misuse seeking their anabolic effects, even though later on, many could develop neuropsychological dependence. Previously, we have shown that nandrolone induces conditioned place preference (CPP) in adult male mice. However, whether nandrolone induces CPP during adolescence remains unknown. In this study, the CPP test was used to determine the rewarding properties of nandrolone (7.5 mg/kg) in adolescent mice. In addition, since D1 dopamine receptors (D1DR) are critical for reward-related processes, the effect of nandrolone on the expression of D1DR in the nucleus accumbens (NAc) was investigated by Western blot analysis. Similar to our previous results, nandrolone induced CPP in adults. However, in adolescents, nandrolone failed to produce place preference. At the molecular level, nandrolone decreased D1DR expression in the NAc only in adult mice. Our data suggest that nandrolone may not be rewarding in adolescents at least during short-term use. The lack of nandrolone rewarding effects in adolescents may be due, in part to differences in D1DR expression during development. [ABSTRACT FROM AUTHOR]

• Extinction learning induced Bdnf upregulation in the ventral striatum. • Extinction resistance was associated with selective gene targets. • Extinction training counteracts the withdrawal-associated plasticity. • The lack of extinction training induced a widespread modulation of genes. Persistent drug-seeking behavior has been associated with deficits in neural circuits that regulate the extinction of addictive behaviors. Although there is extensive data that associates addiction phases with neuroplasticity changes in the reward circuit, little is known about the underlying mechanisms of extinction learning of opioid associated cues. Here, we combined morphine-conditioned place preference (CPP) with real-time polymerase chain reaction (RT-PCR) to identify the effects of extinction training on the expression of genes (mRNAs) associated with synaptic plasticity and opioid receptors in the ventral striatum/nucleus accumbens (VS/NAc). Following morphine extinction training, we identified two animal subgroups showing either extinction (low CPP) or extinction-resistance (high CPP). A third group were conditioned to morphine but did not receive extinction training (sham-extinction; high CPP). RT-PCR results showed that brain derived neurotrophic factor (Bdnf) was upregulated in rats showing successful extinction. Conversely, the lack of extinction training (sham-extinction) upregulated genes associated with kinases (Camk2g), neurotrophins (Ngfr), synaptic connectivity factors (Ephb2), glutamate neurotransmission (Grm8) and opioid receptors (μ1, Δ1). To further identify genes modulated by morphine itself, comparisons with their saline-counterparts were performed. Results revealed that Bdnf was consistently upregulated in the extinction group. Alternatively, widespread gene modulation was observed in the group with lack of extinction training (i.e. Drd2, Cnr1, Creb, μ1, Δ1) and the group showing extinction resistance (i.e. Crem, Rheb, Tnfa). Together, our study builds on the identification of putative genetic markers for the extinction learning of drug-associated cues. [ABSTRACT FROM AUTHOR]