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Repeated cocaine exposure potentiates GABA transmission from D1R-MSNs in the nucleus accumbens to GABA neurons in the ventral tegmental area, disinhibiting dopamine neurons and driving drug-adaptive behavior. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.ESTABLISHES_NEW_DIRECTION.

September 26, 2013

Cocaine Disinhibits Dopamine Neurons by Potentiation of GABA Transmission in the Ventral Tegmental Area

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Abstract

Drug-evoked synaptic plasticity in the mesolimbic system reshapes circuit function and drives drug-adaptive behavior. Much research has focused on excitatory transmission in the ventral tegmental area (VTA) and the nucleus accumbens (NAc). How drug-evoked synaptic plasticity of inhibitory transmission affects circuit adaptations remains unknown. We found that medium spiny neurons expressing dopamine (DA) receptor type 1 (D1R-MSNs) of the NAc project to the VTA, strongly preferring the GABA neurons of the VTA. Repeated in vivo exposure to cocaine evoked synaptic potentiation at this synapse, occluding homosynaptic inhibitory long-term potentiation. The activity of the VTA GABA neurons was thus reduced and DA neurons were disinhibited. Cocaine-evoked potentiation of GABA release from D1R-MSNs affected drug-adaptive behavior, which identifies these neurons as a promising target for novel addiction treatments.

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Cite This Study

Bocklisch et al. (Thu,) studied this question.

synapsesocial.com/papers/6a23968e9c28b44ec7d330d3 https://doi.org/https://doi.org/10.1126/science.1237059

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