Long-term nicotine exposure depresses dopamine release in nonhuman primate nucleus accumbens.

The Journal of Pharmacology and Experimental Therapeutics
Xiomara A PerezMaryka Quik

Abstract

Tobacco use is a leading cause of preventable deaths worldwide. However, current smoking cessation therapies have very limited long-term success rates. Considerable research effort is therefore focused on identification of central nervous system changes with nicotine exposure because this may lead to more successful treatment options. Although recent work suggests that α6β2* nicotinic acetylcholine receptors (nAChRs) play a dominant role in dopaminergic function in rodent nucleus accumbens, the effects of long-term nicotine exposure remain to be determined. Here, we used cyclic voltammetry to investigate α6β2* nAChR-mediated release with long-term nicotine treatment in nonhuman primate nucleus accumbens shell. Control studies showed that nAChR-mediated dopamine release occurs predominantly through the α6β2* receptor subtype. Unexpectedly, there was a complete loss of α6β2* nAChR-mediated activity after several months of nicotine treatment. This decline in function was observed with both single- and multiple-pulse-stimulated dopamine release. Paired-pulse studies showed that the facilitation of dopamine release with multiple pulsing observed in controls in the presence of nAChR antagonist was lost with long-term nicotine treatme...Continue Reading

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Citations

Feb 25, 2014·Progress in Neuro-psychopharmacology & Biological Psychiatry·Scott H Kollins, R Alison Adcock
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May 3, 2012·The Journal of Pharmacology and Experimental Therapeutics·Tanuja BordiaMaryka Quik
Feb 11, 2021·Brain, Behavior and Evolution·Nabil Karnib, Moira J van Staaden

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