Abstract
Reward-seeking behaviors depend critically on dopamine signaling—dopamine neurons encode reward-related information by switching from tonic to phasic (burst-like) activity. Using guinea pig brain slices, we show that nicotine, like cocaine and amphetamine, acts directly in striatum where it enhances dopamine release during phasic but not tonic activity. This amplification provides a mechanism for nicotine facilitation of reward-related dopamine signals, including responses to other primary reinforcers that govern nicotine dependence in smokers.
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Acknowledgements
Supported by a Beit Memorial Fellowship and the Michael J. Fox Foundation (S.J.C.), as well as the US/UK Fulbright Commission and the National Institutes of Health (M.E.R).
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Supplementary Fig. 1
Frequency sensitivity following nAChR desensitization by nicotine has upper limit. Nicotine increased paired-pulse ratios (P2/P1) (mean ± SEM) to values that depend inversely on pulse interval (high-pass filter) at intervals ≥ 10 ms (also Fig. 2). At shorter inter-pulse intervals, e.g. 5 ms, corresponding to 200 Hz, this trend failed and P2/P1 was depressed, consistent with a refractory period for release or action potential generation within 5 ms after P1 (n = 4-34) (JPG 35 kb)
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Rice, M., Cragg, S. Nicotine amplifies reward-related dopamine signals in striatum. Nat Neurosci 7, 583–584 (2004). https://doi.org/10.1038/nn1244
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DOI: https://doi.org/10.1038/nn1244
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