Apoptosis of cerebellar granule cells induced by serum withdrawal, glutamate or β-amyloid, is independent of Jun kinase or p38 mitogen activated protein kinase activation

It has been reported that in differentiated PC12 cells and neurons from the superior cervical ganglion and hippocampus, that the activation of the stress-activated protein kinases jun-N-terminal kinase (JNK) and/or p38 mitogen-activated protein (p38MAP) kinase is central to the induction of apoptosi...

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Bibliographic Details
Published in:Neuroscience letters 1998-06, Vol.250 (1), p.53-56
Main Authors: GUNN-MOORE, F. J, TAVARE, J. M
Format: Article
Language:English
Subjects:
Ageing, cell death
Amyloid beta-Peptides - blood
Amyloid beta-Peptides - physiology
Animals
Apoptosis
Biological and medical sciences
Calcium-Calmodulin-Dependent Protein Kinases - physiology
Cell physiology
Cells, Cultured
Cerebellar granule cells
Cerebellum - cytology
Cerebellum - physiology
Enzyme Activation
Fundamental and applied biological sciences. Psychology
Glutamic Acid - blood
Glutamic Acid - physiology
JNK Mitogen-Activated Protein Kinases
jun-N-terminal kinase
Mitogen-Activated Protein Kinases
Molecular and cellular biology
Neurons - cytology
Neurons - physiology
p38 Mitogen-activated protein kinase
p38 Mitogen-Activated Protein Kinases
PC12 Cells - cytology
PC12 Cells - physiology
Rats
Survival
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Summary:It has been reported that in differentiated PC12 cells and neurons from the superior cervical ganglion and hippocampus, that the activation of the stress-activated protein kinases jun-N-terminal kinase (JNK) and/or p38 mitogen-activated protein (p38MAP) kinase is central to the induction of apoptosis by serum or neurotrophic factor withdrawal. Here we demonstrate that in cerebellar granule cells, withdrawal of serum does not result in the activation of JNK or p38MAP kinase, under conditions where profound apoptosis was observed. In addition, these protein kinases were not activated during the induction of apoptosis caused by addition of excitotoxic levels of glutamate or of β-amyloid (25–35) peptide. BDNF and insulin can prevent apoptosis induced by serum withdrawal or the addition of glutamate or β-amyloid peptide. EGF on the other can prevent apoptosis induced by glutamate and β-amyloid peptide, but not that caused by serum withdrawal. We conclude that the induction of apoptosis of cerebellar granule cells is independent of JNK or p38MAP kinase activation and that the mechanism by which serum withdrawal promotes apoptosis of these neurons may differ from that caused by glutamate and β-amyloid peptide.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(98)00438-8