With the rise in opioid use and opioid‐related death in modern society, it is imperative to understand how these drugs affect neural circuits, particularly those implicated in drug‐seeking and motivated behavior. Generally, all drugs of abuse are thought to increase mesolimbic dopamine concentrations through various mechanisms, and it is widely believed these fluctuations in dopamine concentrations (and subsequent hypodopaminergic states) are implicated in the acquisition, persistence, and maintenance of addiction. Here we sought to identify increases in phasic dopamine in the nucleus accumbens of rats after intravenous diacetylmorphine (heroin) administration. Then, we sought to identify the effects on phasic dopamine after buprenorphine administration, followed by subsequent heroin administration. Utilizing fast‐scan cyclic voltammetry in awake behaving animals, we administered cumulative animal‐equivalent doses based on clinical investigations that correlated subjective measures of the drug's effect to dosage in human subjects. Either heroin or buprenorphine administered alone causes large increases in dopamine transient amplitude and frequency, whereas heroin administration after buprenorphine causes a decrease in the amplitude and frequency of transients. These data suggest a modulatory effect of buprenorphine on opioid receptors in the presence of exogenous opiates.Support or Funding InformationFunding for the project was provided by NSF grant IOS‐1557755, NIH grant R03DA038734, Boettcher Young Investigator Award and NARSAD Young Investigator Award to EBO and an institutional UROP to KJP.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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