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Presynaptic Adrenoceptors.
Handb Exp Pharmacol
September 2024
Institut für Experimentelle und Klinische Pharmakologie und Toxikologie, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.
Presynaptic α-adrenoceptors are localized on axon terminals of many noradrenergic and non-noradrenergic neurons in the peripheral and central nervous systems. Their activation by exogenous agonists leads to inhibition of the exocytotic release of noradrenaline and other transmitters from the neurons. Most often, the α-receptor subtype is involved in this inhibition.
View Article and Find Full Text PDFAdrenergic mechanisms of absence status epilepticus.
Front Neurol
November 2023
Institute of Higher Nervous Activity and Neurophysiology of Russian Academy of Sciences, Moscow, Russia.
Absence status epilepticus is a prolonged, generalized absence seizure that lasts more than half an hour. The mechanisms underlying the absence of status epilepticus are still not entirely understood. In this study, the study concentrates on alpha2-adrenergic mechanisms of absence status using the WAG/Rij rat model.
View Article and Find Full Text PDFSerotonin Syndrome Associated With Vilazodone Overdose in a 22-Month-Old Treated With Dexmedetomidine.
J Emerg Med
February 2021
Department of Emergency Medicine, Maine Medical Center, Portland, Maine; Tufts University School of Medicine, Boston, Massachusetts.
Background: Vilazodone was approved by the U.S. Food and Drug Administration in 2011 as a treatment for major depression disorder.
View Article and Find Full Text PDFModulation of sympathetic preganglionic neuron activity via adrenergic receptors.
Hypertens Res
July 2018
Division of Cardiology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan.
The sympathetic preganglionic neurons (SPNs) play a key role in the sympathetic nervous system. Previous reports have suggested that norepinephrine (NE) directly affects SPNs via both inhibitory hyperpolarization interactions mediated by α2 receptors and excitatory depolarization interactions mediated by α1 receptors. It remains poorly understood, however, whether the excitability of SPNs can be inhibited indirectly (presynaptically) as well as directly (postsynaptically).
View Article and Find Full Text PDFChanges in brain activation during sedation induced by dexmedetomidine.
J Int Med Res
June 2017
4 Department of Pediatric Dentistry and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Korea.
Objective Dexmedetomidine (DEX) has been widely used as a sedative, acting as an α2-adrenergic agonist on autoreceptors, presynaptic receptors and postsynaptic receptors without risk of respiratory depression. Although consciousness impairment is closely related to disturbances of brain function in different frequency bands, the time-varying DEX effects on cortical activity in specific frequency bands has not yet been studied. Methods We used electroencephalography (EEG) to analyse differences in cerebral cortex activity between the awake and sedated states, using electromagnetic tomography (standardized low resolution electromagnetic tomography (sLORETA)) to localize multiple channel scalp recordings of cerebral electric activity to specific brain regions.
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