The effects of non-competitive glutamate receptor antagonists on sleep-waking organization have been studied on Krushinskii-Molodkina rats having an inherited predisposition to audiogenic seizures and Wistar ones which are resistant to this action of sound. Two types of blockers of glutamate receptor open channels were used: selective blockers of NMDA receptors (memantine and IEM-1921) and blockers of mixed type, impacting both on the NMDA and Ca-permeable AMPA/ kainate receptors (IEM-1754 and IEM 1925). During the first 3 hours after administration of these glutamate antagonists the total or partial deprivation of fast-wave sleep was provoked. Additionally the selective NMDA receptor blocking drugs (memantine, IEM-1921) induced in the same period a significant increase of the representation of wakefulness at the cost of reducing of the total time of slow-wave sleep. These effects are most likely to be a consequence of the blockade of NMDA receptors responsible for the launch and maintenance of wakefulness, slow- and fast-wave sleep. In the same first 3 hours period after the administration of IEM-1754 and IEM-1925 the organization of sleep was not significantly affected. The evident reduction of wakefulness, total duration and increase of slow-wave sleep impact was observed, during the second three-hour period. It, apparently, can be caused by the blockade of AMPA/kainate receptors. The obtained results indicate the involvement of NMDA and AMPA/kainate receptors in the functioning of various parts of the sleep system of rats belonging to both lines.
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J Physiol Investig
January 2025
Department and Institute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates cell immune responses in a cell type-specific and ligand-dependent manner. In the central nervous system, astrocytic AhR plays important roles in regulating neuroinflammation by mediating responses to endogenous ligands generated from the inflammation-induced indoleamine 2,3-dioxygenase 1 (IDO1)/kynurenine (KYN) pathway. We previously demonstrated that reduction of AhR expression decreases lipopolysaccharide (LPS)-induced pro-inflammatory responses in microglia.
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Institute of Geriatrics, School of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, 430065, China.
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Adv Protein Chem Struct Biol
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Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences Hospital (NIMHANS), Institute of National Importance, Bangalore, Karnataka, India.
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Department of Molecular Oral Physiology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15 Kuramoto, 770-8504, Tokushima, Japan. Electronic address:
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January 2025
National Institute for Physiological Sciences (NIPS), 5-1 Higashiyama, Myodaiji, 444-8787, Okazaki, Aichi, Japan; Department of Integrative Physiology, Graduate School of Medicine, Akita University, Akita, Japan; Department of Physiology, School of Medicine, Aichi Medical University, Nagakute, Japan; Graduate University for Advanced Studies (SOKENDAI), Hayama, Kanagawa, Japan. Electronic address:
The volume-sensitive outwardly rectifying or volume-regulated anion channel, VSOR/VRAC, which was discovered in 1988, is expressed in most vertebrate cell types, and is essentially involved in cell volume regulation after swelling and in the induction of cell death. This series of review articles describes what is already known and what remains to be uncovered about the functional and molecular properties as well as the physiological and pathophysiological roles of VSOR/VRAC. This Part 2 review article describes, from the physiological and pathophysiological standpoints, first the pivotal roles of VSOR/VRAC in the release of autocrine/paracrine organic signal molecules, such as glutamate, ATP, glutathione, cGAMP, and itaconate, as well as second the swelling-independent and -dependent activation mechanisms of VSOR/VRAC.
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