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Previous Article | Next Article
The Journal of Neuroscience, September 1, 1998, 18(17):7033-7039
Increased Opioid Inhibition of GABA Release in Nucleus Accumbens during Morphine Withdrawal
Billy Chieng and John T. Williams The Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
The nucleus accumbens is a key component of the reward pathway that plays a role in addiction to many drugs of abuse, including psychostimulants and opioids. The effects of withdrawal from chronic morphine were examined in the nucleus accumbens using brain slices from morphine-treated animals. Recordings were made from interneurons in the shell of nucleus accumbens, and the presynaptic inhibition of GABA-A IPSCs by opioids was examined. In slices from control animals, opioids caused a maximal inhibition of 50%, forskolin increased the IPSC amplitude by less than twofold, and the maximal inhibition by opioids in the presence of forskolin was not changed. During withdrawal, however, forskolin caused approximately a fourfold increase in the amplitude of the IPSC, and the maximal inhibition by opioids was increased to 80%. The results indicate that transmitter release is increased during opioid withdrawal, particularly after the activation of adenylyl cyclase. The cAMP-dependent increase in transmitter release is potently inhibited by opioids, such that the overall effect of opioids is augmented during withdrawal. The induction of an opioid-sensitive cAMP-dependent mechanism that regulates transmitter release may be a critical component of acute opioid withdrawal.
Key words: µ-opioid; adenosine; cAMP; adenylyl cyclase; electrophysiology; A-kinase
Copyright © 1998 Society for Neuroscience 0270-6474/98/18177033-07$05.00/0
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