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Articles

Calpain I activation is specifically related to excitatory amino acid induction of hippocampal damage

R Siman, JC Noszek and C Kegerise
Journal of Neuroscience 1 May 1989, 9 (5) 1579-1590; DOI: https://doi.org/10.1523/JNEUROSCI.09-05-01579.1989
R Siman
Neuroscience Group, DuPont Company, Wilmington, Delaware 19898.
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JC Noszek
Neuroscience Group, DuPont Company, Wilmington, Delaware 19898.
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C Kegerise
Neuroscience Group, DuPont Company, Wilmington, Delaware 19898.
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Abstract

Sustained stimulation of receptors for excitatory amino acids leads to both activation of the calcium-dependent cysteine protease calpain I and to the death of receptive neurons. Here, we have examined the relationship between the calpain I activation and neurodegeneration. Calpain I activation was manifested as increased levels of the major proteolytic fragments of the calpain substrate spectrin, detected and quantified by immunoblotting. Intraventricular administration of the excitatory amino acids kainate or N-methyl-D-aspartate (NMDA) produced calpain I-mediated spectrin degradation and hippocampal neuronal loss. The NMDA antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid selectively blocked NMDA- but not kainate-induced protease activation and hippocampal damage. Temporally, spectrin degradation preceded the onset of pyramidal cell degeneration monitored by silver- impregnation histochemistry. Only those doses of kainate (0.15–1 microgram) or NMDA (40–80 micrograms) sufficient to cause hippocampal damage markedly increased spectrin breakdown. Both the neuronal damage and calpain I activation induced by kainate occurred primarily in area CA3. Degeneration of hippocampal neurons evoked by colchicine was not accompanied by calpain activation, indicating that proteolysis is not stimulated simply as a secondary response to neuronal destruction. Thus, a close correspondence exists between excitatory amino acid induction of neuronal degeneration and of calpain I-mediated spectrin degradation. The results suggest that calpain I may be an intracellular mediator of excitatory amino acid action, and further, they support the hypothesis that calcium influx and calpain I activation are obligatory events in the initiation of excitatory amino acid neurotoxicity.

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The Journal of Neuroscience: 9 (5)
Journal of Neuroscience
Vol. 9, Issue 5
1 May 1989
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Calpain I activation is specifically related to excitatory amino acid induction of hippocampal damage
R Siman, JC Noszek, C Kegerise
Journal of Neuroscience 1 May 1989, 9 (5) 1579-1590; DOI: 10.1523/JNEUROSCI.09-05-01579.1989

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Calpain I activation is specifically related to excitatory amino acid induction of hippocampal damage
R Siman, JC Noszek, C Kegerise
Journal of Neuroscience 1 May 1989, 9 (5) 1579-1590; DOI: 10.1523/JNEUROSCI.09-05-01579.1989
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