Journal
JOURNAL OF NEUROSCIENCE
Volume 28, Issue 7, Pages 1672-1681Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4275-07.2008
Keywords
opiate; addiction; electrochemistry; voltammetry; acetylcholine; cholinergic
Categories
Funding
- NIDA NIH HHS [DA019695, F31DA023340, DA015918, P01 DA019695, F31 DA023340, R01 DA015918] Funding Source: Medline
- NIGMS NIH HHS [T32GM07839, T32 GM007839] Funding Source: Medline
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Behaviorally relevant stimuli prompt midbrain dopamine (DA) neurons to switch from tonic to burst firing patterns. Similar shifts to burst activity are thought to contribute to the addictive effects of opiates and nicotine. The nucleus accumbens DA overflow produced by these drugs is a key element in their pathological effects. Using electrochemical techniques in brain slices, we explored the effects of opioids on single-spike and burst stimuli-evoked DA overflow in the dorsal and ventral striatum. In specific subregions of the nucleus accumbens, mu-opioids inhibit DA overflow elicited with single-spike stimuli while leaving that produced by burst stimuli unaffected. This is similar to published effects of nicotinic receptor blockade or desensitization, and is mediated by opioid receptor-induced inhibition of cholinergic interneurons. Whereas delta-opioids have similar effects, kappa-opioids inhibit evoked DA overflow throughout the striatum in a manner that is not overcome with high-frequency stimuli.
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