Unmixing Memory and Desire

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Science  30 Sep 2005:
Vol. 309, Issue 5744, pp. 2139
DOI: 10.1126/science.309.5744.2139c

Recovering drug addicts often relapse after exposure to environmental or contextual cues that are associated with drugs. In a rat model system, the acquisition of cocaine-conditioned place preference (COC-CPP) depends on activation of the extracellular signaling-regulated kinase (ERK); it is blocked by inhibiting mitogen-activated protein kinase kinase (MEK), which normally phosphorylates and activates ERK. Miller and Marshall show increased phosphorylation of ERK in the nucleus accumbens core (AcbC, a midbrain region associated with cue-elicited drug seeking) in rats that had acquired COC-CPP. Infusion of a MEK inhibitor into the AcbC shortly before testing blocked COC-CCP-related behavior and the associated increase in ERK phosphorylation. Furthermore, rats that received a MEK inhibitor right after passing the test failed to exhibit COC-CCP when retested later and showed decreased activation of the AcbC ERK pathway. Thus, the authors conclude that disruption of memory reconsolidation blocks the expression of COC-CCP. Expression of the transcription factor Zif268 in the amygdala increases after reexposure to stimuli associated with self-administration of cocaine. In the study by Lee et al., rats learned to associate a light with a cocaine infusion; the association is so potent that the light acquires a reward value of its own and supports instrumental learning. When paired with a memory reactivation session, Zif268 antisense DNA infused into the basolateral amygdala eliminated the ability of light to promote acquisition of a new behavior. — EMA

Neuron 47, 873; 795 (2005).

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