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Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine
Journal article   Peer reviewed

Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine

Tanner Chase Francis, Stephanie C Gantz, Khaled Moussawi and Antonello Bonci
Current opinion in neurobiology, Vol.54, pp.66-72
02/2019
DOI: 10.1016/j.conb.2018.08.013
PMID: 30237117
url
https://pmc.ncbi.nlm.nih.gov/articles/PMC10131346/pdf/nihms-1890250.pdfView
Open Access

Abstract

•Cocaine drives plasticity to enhance excitation of VTA dopamine neurons.•Dopamine release is decreased after chronic cocaine.•Neuromodulation therapies show promise in treating cocaine addiction. Cocaine exposure induces persistent changes in synaptic transmission and intrinsic properties of ventral tegmental area (VTA) dopamine neurons. Despite significant progress in understanding cocaine-induced plasticity, an effective treatment of cocaine addiction is lacking. Chronic cocaine potentiates excitatory and alters inhibitory transmission to dopamine neurons, induces dopamine neuron hyperexcitability, and reduces dopamine release in projection areas. Understanding how intrinsic and synaptic plasticity interact to control dopamine neuron firing and dopamine release could prove useful in the development of new therapeutics. In this review, we examine recent literature discussing cocaine-induced plasticity in the VTA and highlight potential therapeutic interventions.

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