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N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus. / Dong, Y; Kalueff, AV; Song, C.

In: Journal of Neuroimmunology, Vol. 307, 2017, p. 7-13.

Research output: Contribution to journal › Article

Harvard

Dong, Y, Kalueff, AV & Song, C 2017, 'N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus', Journal of Neuroimmunology, vol. 307, pp. 7-13. https://doi.org/0.1016/j.jneuroim.2017.03.005

APA

Dong, Y., Kalueff, AV., & Song, C. (2017). N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus. Journal of Neuroimmunology, 307, 7-13. https://doi.org/0.1016/j.jneuroim.2017.03.005

Vancouver

Dong Y, Kalueff AV, Song C. N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus. Journal of Neuroimmunology. 2017;307:7-13. https://doi.org/0.1016/j.jneuroim.2017.03.005

Author

Dong, Y ; Kalueff, AV ; Song, C. / N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus. In: Journal of Neuroimmunology. 2017 ; Vol. 307. pp. 7-13.

BibTeX

@article{2ebf2fff838f46118c1c14a9070e9160,
title = "N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus",
abstract = "Increased levels of interleukin (IL)-1β and its gene expression are implicated in the etiology of Alzheimer{\textquoteright}s disease (AD). IL-1β activates microglia and stimulates glutamatergic N-methyl-D-aspartate receptor NMDA receptor expression, thereby disturbing intracellular Ca2+ homeostasis. Ca2+ disequilibrium, in turn, may trigger endoplasmic reticulum (ER) stress, contributing to overall excitotoxicity and neuronal death that evoke AD. However, it is unclear whether IL-1β-induced neuronal apoptosis is mediated by the glutamatergic system, ER stress and/or Ca2+ dysfunction. The present study investigated the role of NMDA receptor (NMDAR) in ER stress and IL-1β-evoked neuronal death by assessing NMDAR-induced Ca2+ overload and NMDA-mediated ER stress. Male Long Evans rats were treated with IL-1β (with or without NMDAR antagonist MK801) injected intracerebroventricularly for 8 days. Glutamate concentration was measured by HPLC, and mRNA and protein expression of microglial biomarkers and NMDAR, as well as markers of",
keywords = "interleukin-1beta, microglia, NMDA receptor, endoplasmic reticulum stress, neurotoxicity",
author = "Y Dong and AV Kalueff and C. Song",
year = "2017",
doi = "0.1016/j.jneuroim.2017.03.005",
language = "не определен",
volume = "307",
pages = "7--13",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - N-methyl-D-aspartate receptor-mediated calcium overload and endoplasmic reticulum stress are involved in interleukin-1beta-induced neuronal apoptosis in rat hippocampus

AU - Dong, Y

AU - Kalueff, AV

AU - Song, C.

PY - 2017

Y1 - 2017

N2 - Increased levels of interleukin (IL)-1β and its gene expression are implicated in the etiology of Alzheimer’s disease (AD). IL-1β activates microglia and stimulates glutamatergic N-methyl-D-aspartate receptor NMDA receptor expression, thereby disturbing intracellular Ca2+ homeostasis. Ca2+ disequilibrium, in turn, may trigger endoplasmic reticulum (ER) stress, contributing to overall excitotoxicity and neuronal death that evoke AD. However, it is unclear whether IL-1β-induced neuronal apoptosis is mediated by the glutamatergic system, ER stress and/or Ca2+ dysfunction. The present study investigated the role of NMDA receptor (NMDAR) in ER stress and IL-1β-evoked neuronal death by assessing NMDAR-induced Ca2+ overload and NMDA-mediated ER stress. Male Long Evans rats were treated with IL-1β (with or without NMDAR antagonist MK801) injected intracerebroventricularly for 8 days. Glutamate concentration was measured by HPLC, and mRNA and protein expression of microglial biomarkers and NMDAR, as well as markers of

AB - Increased levels of interleukin (IL)-1β and its gene expression are implicated in the etiology of Alzheimer’s disease (AD). IL-1β activates microglia and stimulates glutamatergic N-methyl-D-aspartate receptor NMDA receptor expression, thereby disturbing intracellular Ca2+ homeostasis. Ca2+ disequilibrium, in turn, may trigger endoplasmic reticulum (ER) stress, contributing to overall excitotoxicity and neuronal death that evoke AD. However, it is unclear whether IL-1β-induced neuronal apoptosis is mediated by the glutamatergic system, ER stress and/or Ca2+ dysfunction. The present study investigated the role of NMDA receptor (NMDAR) in ER stress and IL-1β-evoked neuronal death by assessing NMDAR-induced Ca2+ overload and NMDA-mediated ER stress. Male Long Evans rats were treated with IL-1β (with or without NMDAR antagonist MK801) injected intracerebroventricularly for 8 days. Glutamate concentration was measured by HPLC, and mRNA and protein expression of microglial biomarkers and NMDAR, as well as markers of

KW - interleukin-1beta

KW - microglia

KW - NMDA receptor

KW - endoplasmic reticulum stress

KW - neurotoxicity

U2 - 0.1016/j.jneuroim.2017.03.005

DO - 0.1016/j.jneuroim.2017.03.005

M3 - статья

VL - 307

SP - 7

EP - 13

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

ER -

ID: 7738187