Nature Neuroscience 9, 605 - 607 (2006)
Published online: 23 April 2006; | doi:10.1038/nn1687
BDNF-dependent synaptic sensitization in midbrain dopamine neurons after cocaine withdrawalLu Pu, Qing-song Liu
& Mu-ming Poo
Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, USA.
Correspondence should be addressed to Mu-ming Poo mpoo@berkeley.edu 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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