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Redefinición de la Red Neuronal y la Sinapsis Inhibitoria en Interneuronas de Arranque Rápido por Exposición Crónica
Michael S Patton1, Samuel H Sheats1, Andreas B Wulff1
1Department of Pharmacology and Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Background:
Alcohol use disorder is characterized by persistent drinking in the face of negative consequences. Such inflexible drinking requires dorsolateral striatum fast-spiking interneurons, which comprise roughly 1% of all striatal neurons. How chronic ethanol exposure affects fast-spiking interneuron physiology is poorly understood.
Methods:
We exposed adult male and female mice to chronic intermittent ethanol and examined synaptic transmission onto dorsolateral striatum fast-spiking interneurons.
Results:
We discover that chronic ethanol exposure induced a dramatic loss of GABAergic, but not glutamatergic, synapses onto dorsolateral striatum fast-spiking interneuron somata and proximal dendrites where perineuronal nets, a subdivision of the extracellular matrix, are enriched. We found that chronic ethanol exposure degraded these perineuronal nets and that enzymatically degrading perineuronal nets similarly reduced GABAergic transmission onto dorsolateral striatum fast-spiking interneurons. Modeling the effect of alcohol, we find that silencing extrinsic GABAergic projections to the dorsolateral striatum increased voluntary ethanol consumption.
Conclusions:
These data suggest chronic alcohol exposure remodels perineuronal nets and inhibitory synapses on fast-spiking interneurons to facilitate alcohol drinking.
