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 -