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The α2-Adrenoceptor Agonist Dexmedetomidine Converges on an Endogenous Sleep-promoting Pathway to Exert Its Sedative Effects

Anesthesiology · 2003 · Vol. 98(2) · pp. 428–436
Laura E. NelsonJun LuTian‐Zhi GuoClifford B. SaperNicholas P. FranksMervyn Maze

Abstract

The authors propose that endogenous sleep pathways are causally involved in dexmedetomidine-induced sedation; dexmedetomidine's sedative mechanism involves inhibition of the LC, which disinhibits VLPO firing. The increased release of GABA at the terminals of the VLPO inhibits TMN firing, which is required for the sedative response.

Sleep and Wakefulness ResearchNeuroscience and Neuropharmacology ResearchMemory and Neural MechanismsDexmedetomidineAtipamezoleMedicineAgonistNon-rapid eye movement sleepPharmacologySedativeAlpha-2 adrenergic receptorAnesthesiaEndocrinology

MeSH terms

Adrenergic alpha-AgonistsAdrenergic alpha-AntagonistsAnimalsCell CountElectroencephalographyElectromyographyPostural BalanceGene Expression RegulationHypnotics and SedativesIbotenic AcidImidazolesImmunohistochemistryMice, Inbred C57BLNeural PathwaysPyridazines

Funding

  • Vanderbilt University
Citations
846
FWCI
7.79
field-weighted impact
References
1
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98%
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The α2-Adrenoceptor Agonist Dexmedetomidine Converges on an Endogenous Sleep-promoting Pathway to Exert Its Sedative Effects · Scinovex