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Relapse to Drug-Seeking and Drug Use Behaviors

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FIGURE 49–2. Models of neurobiological mechanisms of relapse to drug seeking and drug use.To elucidate the emerging neurobiology of mechanisms of relapse to drug-seeking and -use behaviors associated with drug addiction, we consider and compare three potential precipitants of relapse: conditioned drug-use reminders or cues (A, Cue-induced relapse model), stress (B, Stress-induced relapse model), and use/administration of the drug itself (C, Drug-induced relapse model). For each model presented, the neuroanatomical areas and neurotransmitter mechanisms involved (as defined by investigation of the reinstatement animal model of relapse) are shown on the right, and the distributed neural processing associated with experiencing the relapse precipitant (as defined by human in vivo functional neuroimaging studies in males) is shown on the left. It should be emphasized that these neurobiological mechanisms reflect major but not all research findings and represent an as-yet-incomplete characterization of the mechanisms of relapse. Therefore, strict comparisons of the underlying mechanisms between the three relapse precipitants should be done with caution.ACC = anterior cingulate cortex; Amyg = amygdala; BLA = basolateral amygdaloid nucleus; BNST = bed nucleus of the stria terminalis; CB = cerebellum; CE = central amygdaloid nucleus; CRF = corticotropin-releasing factor; CRF1R = corticotropin-releasing factor 1 receptor; CRF2R = corticotropin-releasing factor 2 receptor; D3R = D3 dopamine receptor; dACC = dorsal anterior cingulate cortex; dlPFC = dorsolateral prefrontal cortex; dStr = dorsal striatum; HC = hippocampus; Ins = insula; lOFC = left orbitofrontal cortex; mCC = middle cingulate cortex; MTG = medial temporal gyrus; Nac = nucleus accumbens; OFC = orbitofrontal cortex; pCC = posterior cingulate cortex; PFC = prefrontal cortex; VIS = visual cortex; VP = ventral pallidum; vStr = ventral striatum; VTM = ventral tegmentum.

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