ArticleNeuroscience bulletin2026
The Central Medial Thalamus Serves as a Critical Hub for Preserved Arousability During Dexmedetomidine Sedation.
Article in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dexmedetomidine (DEX) induces a distinct state of "arousable sedation," yet the neural circuits that sustain arousal capacity remain unclear. Here, we identified that 40 μg/kg DEX produced sedation from which animals could be transiently aroused by tactile stimulation of the back, whereas 100 μg/kg induced deeper, unresponsive sedation. Functional mapping revealed selective activation of the central medial thalamus (CMT). Fiber photometry further confirmed that DEX dose-dependently and selectively activated glutamatergic neurons in the CMT while simultaneously suppressing activity in other thalamic regions. Chemogenetic inhibition of CMT glutamatergic neurons deepened DEX sedation and impaired tactile‑stimulation-induced arousal following administration of 40 μg/kg DEX, whereas activation of CMT glutamatergic neurons under a high-dose DEX (100 μg/kg) attenuated sedation and restored tactile responsiveness. Together, these results establish the CMT as a critical thalamic node for maintaining arousal capacity during DEX sedation.
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