Journal
JOURNAL OF NEUROPHYSIOLOGY
Volume 111, Issue 1, Pages 103-111Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00269.2013
Keywords
chronic nicotine; beta 2 nicotinic subunit; dopamine release; in vivo cyclic voltammetry; dorsolateral striatum
Categories
Funding
- NIH [DA25875, R21 NS070269, DA025634]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS083383, R21NS070269] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [P30DA015663, R01DA025875] Funding Source: NIH RePORTER
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Nicotinic acetylcholine receptors (nAChRs) are expressed presynaptically on dopamine axon terminals, and their activation by endogenous acetylcholine from striatal cholinergic interneurons enhances dopamine release both independently of and in concert with dopamine neuron activity. Acute nAChR inactivation is believed to enhance the contrast between low-and high-frequency dopamine cell activity. Although these studies reveal a key role for acute activation and inactivation of nAChRs in striatal microcircuitry, it remains unknown if chronic inactivation/desensitization of nAChRs can alter dopamine release dynamics. Using in vivo cyclic voltammetry in anaesthetized mice, we examined whether chronic inactivation of nAChRs modulates dopamine release across a parametric range of stimulation, varying both frequency and pulse number. Deletion of beta 2*nAChRs and chronic nicotine exposure greatly diminished dopamine release across the entire range of stimulation parameters. In addition, we observed a facilitation of dopamine release at low frequency and pulse number in wild-type mice that is absent in the beta 2* knockout and chronic nicotine mice. These data suggest that deletion or chronic desensitization of nAChRs reduces the dynamic range of dopamine release in response to dopamine cell activity, decreasing rather than increasing contrast between high and low dopamine activity.
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