BDNF-dependent synaptic sensitization in midbrain dopamine neurons after cocaine withdrawal. Nat Neurosci 2006 May;9(5):605-7
Date
04/25/2006Pubmed ID
16633344DOI
10.1038/nn1687Scopus ID
2-s2.0-33745740035 (requires institutional sign-in at Scopus site) 111 CitationsAbstract
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.
Author List
Pu L, Liu QS, Poo MMAuthor
Qing-song Liu PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAnimals, Newborn
Behavior, Animal
Brain-Derived Neurotrophic Factor
Cocaine
Dopamine
Dopamine Uptake Inhibitors
Electric Stimulation
Enzyme Inhibitors
Enzyme-Linked Immunosorbent Assay
Excitatory Postsynaptic Potentials
Gene Expression Regulation
In Vitro Techniques
Neurons
Patch-Clamp Techniques
Rats
Rats, Sprague-Dawley
Substance Withdrawal Syndrome
Synapses
Ventral Tegmental Area