Glutamate mediates cell death and increases the Bax to Bcl-2 ratio in a differentiated neuronal cell line

Schelman, William R.; Andres, Robert; Sipe, Kimberly J.; Kang, Evan; Weyhenmeyer, James A.

doi:10.1016/j.molbrainres.2004.06.011

Cited by 64 publications

(37 citation statements)

References 68 publications

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“…However, glutamatergic neurotransmission was blocked in those experiments (Marrazzo et al, 2005). Glutamatergic transmission is a factor in Ab 25-35 -induced cell death, and elevated glutamate levels have been shown to induce Bax upregulation in neurons (Schelman et al, 2004, Revett et al, 2013. Thus, our data suggest that s receptor activation by afobazole can reduce Bax expression and concomitant cell death in the presence of Ab 25-35 even when glutamatergic transmission is not blocked.…”

Section: Discussionmentioning

confidence: 60%

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Behensky

Yasny

Shuster

et al. 2013

J Pharmacol Exp Ther

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Section: Discussionmentioning

confidence: 60%

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Behensky

Yasny

Shuster

et al. 2013

J Pharmacol Exp Ther

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“…Chronic accumulation of MSG induced pyramidal neural loss in cortical organotypic culture (Young et al, 2007) and retinal ganglion cell death (Vorwerk et al, 2000). Twenty hours exposure increased cytotoxicity of 1mM or 10mM glutamate on differentiating N1E-115 neuronal cells; morphological changes observed as neuritis retraction and cell shrinkage leading to apoptosis (Schelman et al, 2004). Our data showed that prolonged exposure of MSG during early embryo development at dose 10µg/mL (50 µM) increased brain apoptosis.…”

Section: Msg Increased Circle Swimming Events and Decreased Locomotormentioning

confidence: 67%

Monosodium Glutamate Exposure at Early Developmental Stage Increases Apoptosis and Stereotypic Behavior Risks on Zebrafish (Danio Rerio) Larvae

Kurnianingsih

2016

Indonesian J. Pharm.

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Excessive glutamate may give neurotoxic effects and contribute to Autism spectrum disorder(ASD). In this study, we investigated prolonged exposure effects of 10 µg/mL Monosodium Glutamate (MSG) on intracellular calcium level, bax, bcl-2, ratio of bax/bcl-2 genes expression, caspase-3, apoptosis of brain cells and stereotypic behavior of Zebrafish (Danio rerio) larvae at early developmental stages. Genes expression were determined by real time PCR, caspase-3 using ELISA, intracellular Ca 2+ and apoptotic cells of brain using confocal microscopy, locomotor activity by using crossing lines assay whereas stereotypic behavior by circle swimming. The results indicated that MSG exposure increased brain bax and bcl-2; and caspase-3; intracellular Ca 2+ ; and apoptosis; stereotypic behavior; and decreased locomotor activity. Termination of MSG treatments resulted in recovery of bax, bcl-2, caspase-3 basal levels and stereotypic behavior. In conclusion, MSG exposure at early embryonic stage increased brain cell damage and risk of behavior changes.

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“…Furthermore, glutamate changes the localization of the apoptotic regulators, such as the antiapoptotic protein, Bcl-2 and proapoptotic protein, Bax [26]. Because excessive neuronal apoptosis can be harmful, the regulation of apoptosis in neuronal cells is important.…”

Section: Resultsmentioning

confidence: 99%

Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission

Chae¹,

Min²,

Leem³

et al. 2017

Pharmacology

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Chrysophanic acid, or chrysophanol, is an anthraquinone found in Rheum palmatum, which was used in the preparation of oriental medicine in ancient China. The hippocampus plays a major role in controlling the activities of the short- and long-term memory. It is one of the major regions affected by excessive cell death in Alzheimer's disease. Therefore, neuronal cell-death modulation in the hippocampus is important for maintaining neuronal function. We investigated chrysophanol's effects on glutamate-induced hippocampal neuronal cell death. Chrysophanol reduced glutamate-induced cell death via suppression of proapoptotic factors and reactive oxygen species generation. Furthermore, it downregulated glutamate-induced mitochondrial fission by inhibiting dynamin-related protein 1 (Drp1) dephosphorylation. Thus, chrysophanol suppressed hippocampal neuronal cell death via inhibition of Drp1-dependent mitochondrial fission, and can be used as a therapeutic agent for treating neuronal cell death-mediated neurodegenerative diseases.

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Glutamate mediates cell death and increases the Bax to Bcl-2 ratio in a differentiated neuronal cell line

Cited by 64 publications

References 68 publications

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Monosodium Glutamate Exposure at Early Developmental Stage Increases Apoptosis and Stereotypic Behavior Risks on Zebrafish (Danio Rerio) Larvae

Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission

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Glutamate mediates cell death and increases the Bax to Bcl-2 ratio in a differentiated neuronal cell line

Cited by 64 publications

References 68 publications

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β25–35

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β25–35

Monosodium Glutamate Exposure at Early Developmental Stage Increases Apoptosis and Stereotypic Behavior Risks on Zebrafish (Danio Rerio) Larvae

Chrysophanol Suppressed Glutamate-Induced Hippocampal Neuronal Cell Death via Regulation of Dynamin-Related Protein 1-Dependent Mitochondrial Fission

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Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35