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Effects of kappa opioids on cocaine self-administration by rhesus monkeys. In addition, drug-induced emotional disruption may also possibly lead, in vulnerable individuals, to depressive disorders evolving independently from the initial substance abuse. In which brain regions? In this framework, available rodent evidence is inconsistent, and chronic stress-based models of depression have been associated with either increased effects of drugs of abuse a sensitization of reward pathways that would be consistent with the human comorbidity or decreased effects. Additional studies will be necessary to assess where KOR-positive amygdala neurons send projections, and whether dysregulation of nicotinic receptors, the direct nicotine targets, occurs in this or another brain region following stress exposure.

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Selective p38alpha MAPK deletion in serotonergic neurons produces stress resilience in models of depression and addiction.

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Paterson NE, Markou A. Neuroscience 96 1: Following repeated conditioning sessions, the animal subsequently exhibits preference or avoidance on re-exposure to the environmental stimuli in the absence of the druga behavior that depends on learning, motivational, and hedonic mechanisms. The attenuation of morphine-conditioned place preference following chronic mild stress is reversed by a CCKB receptor antagonist. The effect of this local manipulation on ultrasonic vocalizations was not assessed; however, it is likely that CeA KOR signaling may contribute to negative affect following chronic ethanol exposure. Endogenous kappa-opioid mediation of stress-induced potentiation of ethanol-conditioned place preference and self-administration. Prodynorphin gene disruption increases the sensitivity to nicotine self-administration in mice.

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