Insulin Protects Cortical Neurons Against Glutamate Excitotoxicity
Krasil’nikova I., Surin A., Sorokina E., Fisenko A., Boyarkin D., Balyasin M. V., Demchenko A. G., Pomy'tkin I. A., Pinelis V. G.
Frontiers in Neuroscience
Vol.13, Num.1027
Опубликовано: 2019
Тип ресурса: Статья
DOI:10.3389/fnins.2019.01027
Аннотация:
Glutamate excitotoxicity is implicated in the pathogenesis of numerous diseases, such as stroke, traumatic brain injury, and Alzheimer’s disease, for which insulin resistance is a concomitant condition, and intranasal insulin treatment is believed to be a promising therapy. Excitotoxicity is initiated primarily by the sustained stimulation of ionotropic glutamate receptors and leads to a rise in intracellular Ca2+ ([Ca2+]i), followed by a cascade of intracellular events, such as delayed calcium deregulation (DCD), mitochondrial depolarization, adenosine triphosphate (ATP) depletion that collectively end in cell death. Therefore, cross-talk between insulin and glutamate signaling in excitotoxicity is of particular interest for research. In the present study, we investigated the effects of short-term insulin exposure on the dynamics of [Ca2+]i and mitochondrial potential in cultured rat cortical neurons during glutamate excitotoxicity. We found that insulin ameliorated the glutamate-evok
Ключевые слова:
BDNF; cortical neuron; delayed calcium deregulation (DCD); glutamate excitotoxicity; insulin; mitochondrial depolarization; reactive oxygen species (ROS)
adenosine triphosphate; brain derived neurotrophic factor; calcium; glutamic acid; insulin; animal cell; Article; brain cell; cell function; cell respiration; cell survival; cell viability; controlled study; drug effect; drug exposure; excitotoxicity; mitochondrial membrane potential; MTT assay; nerve cell culture; neuroprotection; nonhuman; oxygen consumption; rat; signal transduction
Язык текста: Английский
ISSN: 1662-453X
Krasil’nikova I.
Surin A.
Sorokina E.
Fisenko A.
Boyarkin D.
Balyasin M. V. Maksim Vitalyevich 1996-
Demchenko A. G. Anna Gasy'movna 1996-
Pomy'tkin I. A. Igor` Anatolyevich 1957-
Pinelis V. G. Vsevolod Grigoryevich 0001-
Красил’никова И.
Сурин А.
Сорокина Е.
Фисенко А.
Бояркин Д.
Балясин М. В. Максим Витальевич 1996-
Демченко А. Г. Анна Гасымовна 1996-
Помыткин И. А. Игорь Анатольевич 1957-
Пинелис В. Г. Всеволод Григорьевич 0001-
Insulin Protects Cortical Neurons Against Glutamate Excitotoxicity
Текст визуальный непосредственный
Frontiers in Neuroscience
Frontiers Research Foundation
Vol.13 Num.1027
2019
Статья
BDNF cortical neuron delayed calcium deregulation (DCD) glutamate excitotoxicity insulin mitochondrial depolarization reactive oxygen species (ROS)
adenosine triphosphate brain derived neurotrophic factor calcium glutamic acid insulin animal cell Article brain cell cell function cell respiration cell survival cell viability controlled study drug effect drug exposure excitotoxicity mitochondrial membrane potential MTT assay nerve cell culture neuroprotection nonhuman oxygen consumption rat signal transduction
Glutamate excitotoxicity is implicated in the pathogenesis of numerous diseases, such as stroke, traumatic brain injury, and Alzheimer’s disease, for which insulin resistance is a concomitant condition, and intranasal insulin treatment is believed to be a promising therapy. Excitotoxicity is initiated primarily by the sustained stimulation of ionotropic glutamate receptors and leads to a rise in intracellular Ca2+ ([Ca2+]i), followed by a cascade of intracellular events, such as delayed calcium deregulation (DCD), mitochondrial depolarization, adenosine triphosphate (ATP) depletion that collectively end in cell death. Therefore, cross-talk between insulin and glutamate signaling in excitotoxicity is of particular interest for research. In the present study, we investigated the effects of short-term insulin exposure on the dynamics of [Ca2+]i and mitochondrial potential in cultured rat cortical neurons during glutamate excitotoxicity. We found that insulin ameliorated the glutamate-evok