Astrocyte-neurone crosstalk mediates dexmedetomidine sedation.

As the clinical applications of dexmedetomidine expand, advances in neuroscientific research have provided further insights into its mechanisms of action. We provide a focused overview of the role that astrocytes play in the changes in neurotransmission that accompany the sedative action of dexmedetomidine. After activation of astrocytic α2A-adrenergic receptors, the subsequent rise in cytosolic calcium increases the permeability of bestrophin-1 channels, facilitating the release of γ-aminobutyric acid (GABA) that stimulates extrasynaptic GABAA receptors on glutamatergic neurones. This signalling cascade, involving multiple receptor systems, reduces neuronal excitability.