Dexmedetomidine Reduces Presynaptic γ-Aminobutyric Acid Release and Prolongs Postsynaptic Responses in Layer 5 Pyramidal Neurons in the Primary Somatosensory Cortex of <i>Mice</i>.
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ABSTRACT: Dexmedetomidine (DEX) exhibits notable sedative, analgesic, and anesthetic-sparing properties. While growing evidence suggests these effects are linked to the modulation of γ-aminobutyric acid (GABA) system, the precise pre- and postsynaptic mechanisms of DEX action on cortical GABAergic signaling remain unclear. In this study, we applied whole-cell patch-clamp recording to investigate the impact of DEX on GABAergic transmission in layer 5 pyramidal neurons of the mouse primary somatosensory cortex. We recorded spontaneous inhibitory postsynaptic currents (sIPSCs), miniature IPSCs (mIPSCs), and evoked inhibitory postsynaptic potentials (eIPSPs) before and during DEX application. Our findings demonstrated that DEX reduced activity-dependent spontaneous GABAergic transmission, as evid
SUBMITTER: Tang B
PROVIDER: S-EPMC11900034 | biostudies-literature | 2025 Feb
REPOSITORIES: biostudies-literature
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