Influence Social Judgments


LTD, but rather its persistent impairment, that is associated with the transition to addiction. This persistent impairment in LTD could explain the loss of control on drug intake observed in Addict rats. LTD in the NAC is considered important in rescaling synapses that were enhanced during acquisition of motor responses and cuereward associations (31, 32), allowing those synapses to encode future associations and restore flexibility to neuronal circuits. The persistent inability to rescale synapses in Addict animals may render drug-seeking behavior consistently resistant to modulation by environmental contingencies, finally resulting in loss of control over drug intake. Thus, the major behavioral difference between Addict and Non-Addict animals, similar to that in humans (1), is their capacity to adjust their drug intake as a function of environmental contingencies. Non-Addicts can stop seeking drugs if they know that the drug is not available, if it requires an excessively high workload, or if taking the drug acquires negative consequences. Addicts have lost this ability and continue to seek drugs independently of environmental conditions. Our results also provide unanticipated insight into the type of homeostatic alterations that characterize Addicts. We expected, as largely assumed in the field, to discover a specific pathological adaptation—a particular phenotype— characterizing synaptic plasticity in Addicts. In contrast, the transition to addiction was associated, at least in the NAC, with a form of anaplasticity, i.e., the incapacity of Addicts to counteract initial drug-induced impairments. The anaplasticity of Addict rats is relevant to revising conceptualizations of the transition to addiction, currently seen as the progressive development of specific brain adaptations that lead to loss of control over drug intake. Our data sugges

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