Chronic ethanol exposure in mice evokes pre- and postsynaptic deficits in GABAergic transmission in ventral tegmental area GABA neurons.

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Tác giả: Carolina Aguado, Rafael Luján, Ezequiel Marron Fernandez de Velasco, Eric H Mitten, Anna Souders, Kevin Wickman

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: England : British journal of pharmacology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 175483

BACKGROUND AND PURPOSE: GABAergic neurons in mouse ventral tegmental area (VTA) exhibit elevated activity during withdrawal following chronic ethanol exposure. While increased glutamatergic input and decreased GABA EXPERIMENTAL APPROACH: We used electrophysiological and ultrastructural approaches to assess the impact of chronic intermittent ethanol vapour exposure in mice on GABAergic transmission in VTA GABA neurons during withdrawal. We used CRISPR/Cas9 ablation to mimic a somatodendritic adaptation involving the GABA KEY RESULTS: The frequency of spontaneous inhibitory postsynaptic currents was reduced in VTA GABA neurons following chronic ethanol treatment and this was reversed by GABA CONCLUSIONS AND IMPLICATIONS: Chronic ethanol weakens the GABAergic regulation of VTA GABA neurons in mice via pre- and postsynaptic mechanisms, likely contributing to their elevated activity during withdrawal and expression of anxiety-related behaviour. As anxiety can promote relapse during abstinence, interventions targeting VTA GABA neuron excitability could represent new therapeutic strategies for treatment of alcohol use disorder.
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