Abstract:
:Cultures of chicken day 8 embryo retinal cells, essentially free of contaminating non-neuronal elements, were used to examine the neurotoxicity of various excitatory amino acid transmitter receptor agonists. At 7 days in vitro, N-methyl-D-aspartate (NMDA), following 24 hr exposure to 0.1-1.0 mM, destroyed 60-70% of the multipolar neurons, but apparently spared photoreceptors. The cytotoxic effect of NMDA was prevented by extracellular Mg2+ or phencyclidine, suggesting a role for the NMDA ion channel; competitive NMDA antagonists were also neuroprotective. The mixed excitatory amino acid receptor agonist glutamate (0.1-1.0 mM) was also neurotoxic (approximately 70% loss of multipolar neurons) and strongly blocked by NMDA (but weakly by non-NMDA) antagonists and Mg2+, indicating a major action at NMDA receptors. As with NMDA, glutamate did not appear to affect photoreceptors. The neurotoxic action of kainate against multipolar retinal neurons, as reported by others, was confirmed here. Kainate neuronal injury was sensitive to the quinoxalinedione non-NMDA antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and 6-cyanoquinoxaline-2,3-dione (CNQX), but not to Mg2+ or phencyclidine. Ibotenate and quisqualate, even at millimolar concentrations, were not neurotoxic. The monosialoganglioside GM1 was also effective in reducing NMDA and non-NMDA agonist neurotoxicity to retinal neurons. Maximal ganglioside benefit required 1-2 hr of pretreatment with 100-200 microM GM1. The percentage of multipolar neurons remaining after the neurotoxin insult approximately doubled with GM1 treatment. Gangliosides may thus have a therapeutic potential in excitatory amino acid-initiated neuropathologies.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Facci L,Leon A,Skaper SDdoi
10.1002/jnr.490270210subject
Has Abstractpub_date
1990-10-01 00:00:00pages
202-10issue
2eissn
0360-4012issn
1097-4547journal_volume
27pub_type
杂志文章abstract::There are two types of calcium-activated neutral protease (CANP), m-CANP and mu-CANP, following the nomenclature of Suzuki et al to show that each requires mM and microM Ca2+, respectively, for its activation. We found mu-CANP activity in a crude CANP fraction extracted from the peripheral nerve, which degraded the ne...
journal_title:Journal of neuroscience research
pub_type: 杂志文章
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of neuroscience research
pub_type: 杂志文章
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journal_title:Journal of neuroscience research
pub_type: 杂志文章
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journal_title:Journal of neuroscience research
pub_type: 杂志文章
doi:10.1002/jnr.490220404
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journal_title:Journal of neuroscience research
pub_type: 杂志文章
doi:10.1002/jnr.490110103
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journal_title:Journal of neuroscience research
pub_type: 杂志文章,评审
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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journal_title:Journal of neuroscience research
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更新日期:2004-09-01 00:00:00
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journal_title:Journal of neuroscience research
pub_type: 杂志文章
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