A Novel Role of Dexmedetomidine in the Modulation of Morphine Reward Memory via Gamma-Aminobutyric Acid Transporter-1 - PubMed
6 hours ago
- #GABA Transporter
- #Dexmedetomidine
- #Opioid Use Disorder
- Dexmedetomidine (Dex) facilitates the extinction of morphine-induced reward memory by inhibiting Gamma-Aminobutyric Acid Transporter-1 (GAT1).
- Dex increases extracellular GABA in the ventral tegmental area (VTA), reducing dopamine release and hyperactivity of D1-type medium spiny neurons (D1-MSNs) in the nucleus accumbens (NAc).
- The study used conditioned place preference (CPP) in mice, calcium imaging, and patch-clamp recordings to demonstrate Dex's effects on neuronal activity.
- Dex's pro-extinction effect is mediated via GABA receptors, not α₂-adrenergic receptors, indicating a novel GAT1-dependent mechanism.
- Findings suggest Dex could be a potential therapeutic agent for opioid use disorder (OUD).