BDNF-dependent synaptic sensitization in midbrain dopamine neurons after cocaine withdrawal (original) (raw)
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- Published: 23 April 2006
Nature Neuroscience volume 9, pages 605–607 (2006)Cite this article
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Abstract
The neural mechanism underlying the relapse to drug use after drug withdrawal is largely unknown. We found that after withdrawal from repeated cocaine exposure, excitatory synapses onto dopamine neurons in the ventral tegmental area (VTA) of the rat midbrain became highly susceptible to potentiation by weak presynaptic stimuli, an effect requiring endogenous brain-derived neurotrophic factor–tyrosine kinase B (BDNF-TrkB) signaling. The elevated BDNF expression in the VTA after cocaine withdrawal may prime these synapses for potentiation by cue-associated activity, triggering drug craving and relapse.
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Acknowledgements
We thank C.C. Lien, J.L. Du, Z.R. Wang and L. Cancedda for critical comments and suggestions. This work was supported by grants from the US National Institutes of Health.
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Authors and Affiliations
- Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, 94720, California, USA
Lu Pu, Qing-song Liu & Mu-ming Poo
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- Lu Pu
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Correspondence toMu-ming Poo.
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Pu, L., Liu, Qs. & Poo, Mm. BDNF-dependent synaptic sensitization in midbrain dopamine neurons after cocaine withdrawal.Nat Neurosci 9, 605–607 (2006). https://doi.org/10.1038/nn1687
- Received: 21 February 2006
- Accepted: 23 March 2006
- Published: 23 April 2006
- Issue Date: May 2006
- DOI: https://doi.org/10.1038/nn1687