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WIREs Cogn Sci
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Biological substrates of addiction

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This review is an introduction to addiction, the reward circuitry, and laboratory addiction models. Addiction is a chronic disease hallmarked by a state of compulsive drug seeking that persists despite negative consequences. Most of the advances in addiction research have centered on the canonical and contemporary drugs of abuse; however, addictions to other activities and stimuli also exist. Substances of abuse have the potential to induce long‐lasting changes in the brain at the behavioral, circuit, and synaptic levels. Addiction‐related behavioral changes involve initiation, escalation, and obsession to drug seeking and much of the current research is focused on mapping these manifestations to specific neural pathways. Drug abuse is well known to recruit components of the mesolimbic dopamine system, including the nucleus accumbens and ventral tegmental area. In addition, altered function of a wide variety of brain regions is tightly associated with specific manifestations of drug abuse. These regions peripheral to the mesolimbic pathway likely play a role in specific observed comorbidities and endophenotypes that can facilitate, or be caused by, substance abuse. Alterations in synaptic structure, function, and connectivity, as well as epigenetic and genetic mechanisms are thought to underlie the pathologies of addiction. In preclinical models, these persistent changes are studied at the levels of molecular pharmacology and biochemistry, ex vivo and in vivo electrophysiology, radiography, and behavior. Coordinating research efforts across these disciplines and examining cell type‐ and circuit‐specific phenomena are crucial components for translating preclinical findings to viable medical interventions that effectively treat addiction and related disorders. WIREs Cogn Sci 2014, 5:151–171. doi: 10.1002/wcs.1273 Conflict of interest: The authors have declared no conflicts of interest for this article. This article is categorized under: Neuroscience > Behavior Neuroscience > Physiology Neuroscience > Plasticity
Simplified schematic of the reward circuitry in the rodent brain emphasizing signaling to and from the nucleus accumbens (NAc) and ventral tegmental area (VTA). Glutamatergic transmission drives information through the reward and reward‐related circuitry (blue arrows). GABAergic transmission from NAc and other regions dampens target neuronal activity (red arrows). Dopamine release from the VTA and substantia nigra (SN) modulates synaptic transmission in target regions (green arrows). These regions are recruited and undergo synaptic, circuit, and genetic adaptations in response to drug experience. AMY, amygdala; BNST, bed nucleus of the stria terminalis; CeA, central nucleus of the amygdala; DS, dorsal striatum; LDTg, laterodorsal tegmentum; LHb, lateral habenula; LH, lateral hypothalamus; PFC, prefrontal cortex; SN, substantia nigra; VP, ventral pallidum.
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From circuits to synapses, addiction alters the brain. This schematic suggests cellular changes in second messenger signaling and transcription in response to drugs of abuse. Simplified tripartite synapse illustrating molecules known to be affected at different synapses within the reward circuits. Note: addiction‐related changes are most often region, cell type, and synapse specific. iGluR, ionotropic glutamate receptors (AMPA and NMDA receptors).
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Simplified schematic depicting proposed brain regions involved in disease states exhibiting comorbidities with addiction.
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Neuroscience > Plasticity
Neuroscience > Physiology
Neuroscience > Behavior

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