cocaine inhibition of nicotinic acetylcholine receptorsinfluences dopamine release

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ID: 251186
2014
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Abstract
Nicotinic acetylcholine receptors (nAChRs) potently regulate dopamine (DA) release in the striatum and alter cocaine’s ability to reinforce behaviors. Since cocaine is a weak nAChR inhibitor, we hypothesized that cocaine may alter DA release by inhibiting the nAChRs in DA terminals in the striatum and thus contribute to cocaine's reinforcing properties primarily associated with the inhibition of DA transporters. We found that biologically relevant concentrations of cocaine can mildly inhibit nAChR-mediated currents in midbrain DA neurons and consequently alter DA release in the dorsal and ventral striatum. At very high concentrations, cocaine also inhibits voltage-gated Na channels in DA neurons. Furthermore, our results show that partial inhibition of nAChRs by cocaine reduces evoked DA release. This diminution of DA release via nAChR inhibition more strongly influences release evoked at low or tonic stimulation frequencies than at higher (phasic) stimulation frequencies, particularly in the dorsolateral striatum. This cocaine-induced shift favoring phasic DA release may contribute to the enhanced saliency and motivational value of cocaine-associated memories and behaviors.
Reference Key
eacevedo-rodriguez2014frontierscocaine Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Alexandra eAcevedo-Rodriguez;Lifen eZhang;Fuwen eZhou;Suzhen eGong;Howard eGu;Mariella eDe Biasi;Fu-Ming eZhou;John A. Dani
Journal Diabetes
Year 2014
DOI
10.3389/fnsyn.2014.00019
URL
http://journal.frontiersin.org/Journal/10.3389/fnsyn.2014.00019/full
Keywords
voltammetry addiction striatum substantia nigra ventral tegmental area neuropsychiatry biological psychiatry mesolimbicneurosciences

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