AI Article Synopsis
- Cocaine exposure leads to long-lasting changes in how dopamine neurons in the ventral tegmental area (VTA) communicate and function.
- Despite advances in studying these changes, effective treatments for cocaine addiction are still unavailable.
- The review focuses on understanding the interaction between synaptic and intrinsic changes in neurons, which could aid in creating new therapies for addiction.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10131346 | PMC |
| http://dx.doi.org/10.1016/j.conb.2018.08.013 | DOI Listing |
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