One month of cocaine abstinence potentiates rapid dopamine signaling in the nucleus accumbens core
Autor: | Regina M. Carelli, R. Mark Wightman, Courtney M. Cameron |
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Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
Male
0301 basic medicine Dopamine media_common.quotation_subject Fast-scan cyclic voltammetry Self Administration Pharmacology Nucleus accumbens Article Nucleus Accumbens Extinction Psychological Rats Sprague-Dawley Cocaine-Related Disorders 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Cocaine Neuroplasticity medicine Animals media_common Addiction Long-term potentiation Abstinence Rats 030104 developmental biology Psychology Self-administration 030217 neurology & neurosurgery medicine.drug |
DOI: | 10.17615/vq6w-9s30 |
Popis: | Cocaine addiction is a chronic relapsing disorder that is difficult to treat in part because addicts relapse even after extended periods of abstinence. Given the importance of the mesolimbic dopamine (DA) system in drug addiction, we sought to characterize cocaine abstinence induced changes in rapid DA signaling in the nucleus accumbens (NAc). Here, rats were trained to self-administer cocaine for 14 consecutive days, then divided into two groups. Day 1 rats (D1; n = 7) underwent 24 hours of abstinence; Day 30 rats (D30; n = 7) underwent one month of abstinence. After abstinence, all rats underwent a single extinction session. Immediately after, rats were deeply anesthetized and fast scan cyclic voltammetry (FSCV) was used to measure DA release and uptake dynamics in the NAc core before and following a single cocaine injection. We show that one month of cocaine abstinence potentiates the peak concentration of electrically evoked DA in the NAc core following an acute injection of cocaine. This potentiation is not related to alterations in DA uptake parameters, which are unchanged following abstinence, but may reflect alterations in release. These results further support the abundance of literature showing that cocaine abstinence induces neuroplasticity in brain areas implicated in drug reward and relapse. The present findings also demonstrate critical differences between abstinence-induced neuroadaptations in DA signaling and those caused by drug exposure itself. |
Databáze: | OpenAIRE |
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