Excitotoxic cell death

Wiley - Tập 23 Số 9 - Trang 1261-1276 - 1992
Dennis W. Choi1
1Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110

Tóm tắt

AbstractExcitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states. Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload. It is possible that excitotoxic death may share some mechanisms with other forms of neuronal death. © 1992 John Wiley & Sons, Inc.

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Tài liệu tham khảo

10.1016/0006-8993(91)91141-M

10.1038/342918a0

10.1038/321168a0

10.1073/pnas.87.4.1620

10.1016/0306-4522(85)90299-4

10.1016/0304-3940(78)90140-4

10.1016/0891-5849(89)90056-7

10.1016/0896-6273(92)90104-L

10.1126/science.1317970

10.1016/S0079-6123(08)61986-X

10.1016/0304-3940(85)90069-2

10.1002/jnr.490350513

10.1016/0896-6273(88)90162-6

10.1016/0166-2236(88)90200-7

10.1016/0896-6273(88)90162-6

Choi D. W., 1991, Excitatory Amino Acid Antagonists, 216

10.1523/JNEUROSCI.08-01-00185.1988

Choi D. W., 1990, Methods for antagonizing glutamate neurotoxicity, Cerebrovasc. Brain Metab. Rev., 2, 105

Choi D. W., 1991, Neurodegenerative Disorders: Mechanisms and Prospects for Therapy, 233

10.1007/BF00174615

10.1126/science.2452481

10.1016/0166-2236(87)90172-X

Coyle J. T., 1981, Excitatory amino acid neurotoxins: selectively and mechanisms of action, Neurosci. Res. Prog. Bulletin, 19, 331

Coyle J. T., 1983, Neurotoxic action of kainic acid, J. Neurochem., 41, 1

Curtis D. R., 1974, Amino acid transmitters in the mammalian central nervous system, Ergebnisse Physiologie, 69, 98

10.1038/327326a0

10.1073/pnas.88.14.6368

10.1016/0165-6147(91)90602-O

10.1073/pnas.80.20.6361

10.1038/336068a0

10.1111/j.1471-4159.1987.tb10014.x

10.1146/annurev.cb.07.110191.003311

10.1016/0306-4522(89)90085-7

10.1111/j.1471-4159.1989.tb07327.x

10.1111/j.1471-4159.1991.tb02031.x

10.1016/0304-3940(86)90189-8

10.1016/0304-3940(86)90256-9

10.1038/336385a0

10.1016/0304-3940(87)90463-0

10.1073/pnas.85.17.6556

Hartley D. M., 1989, Delayed rescue of N‐methyl‐d‐aspartate receptor‐mediated neuronal injury in cortical culture, J. Pharmacol. Exp. Ther., 250, 752

10.1126/science.197604

Higgins D. S., 1989, A unique glutamate binding site in an autoradiographic assay, Soc. Neurosci. Abstr., 15, 1163

10.1016/0006-8993(85)90989-8

Horvitz H. R., 1991, Neurodegenerative Disorders: Mechanisms and Prospects for Therapy, 5

Huck S., 1984, The glutamate analogue alpha‐aminoadipic acid is taken up by astrocytes before exerting its gliotoxic effect in vitro, J. Neurosci., 4, 2650, 10.1523/JNEUROSCI.04-10-02650.1984

10.1126/science.1653450

10.1113/jphysiol.1990.sp018060

10.1016/0306-4522(83)90054-4

10.1016/0006-8993(87)91531-9

10.1126/science.2875522

Koh J., 1990, Non‐NMDA receptor‐mediated neurotoxicity in cortical culture, J. Neurosci., 10, 693, 10.1523/JNEUROSCI.10-02-00693.1990

10.1016/0006-8993(91)91140-V

10.1073/pnas.88.21.9431

10.1016/0306-4522(83)90013-1

10.1016/0006-291X(91)91330-F

Kurth M. C., 1989, Relationship between glutamate‐induced 45Ca influx and resultant neuronal injury in cultured cortical neurons, Neurology, 39, 217

10.1016/0014-4886(82)90106-6

10.1038/321519a0

Manev H., 1989, Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death, Mol. Pharmacol., 36, 106

10.1016/0896-6273(92)90087-T

Marcoux F. W., 1988, Sigma and phencyclidine‐like compounds as molecular probes in biology, 735

10.1038/349760a0

10.1002/jnr.490210236

Mattson M. P., 1989, Roles for mitotic history in the generation and degeneration of hippocampal neuroarchitecture, J. Neurosci., 9, 1223, 10.1523/JNEUROSCI.09-04-01223.1989

10.1523/JNEUROSCI.09-11-03728.1989

10.1016/0014-4886(87)90059-8

10.1038/263517a0

10.3109/10408448209033629

10.1042/cs0680113

10.1523/JNEUROSCI.10-01-00283.1990

10.1038/355722a0

10.1016/0896-6273(90)90302-V

10.1126/science.256.5060.1217

10.1038/354031a0

10.1126/science.2564700

10.1016/0304-3940(90)90405-X

10.1126/science.1317969

10.1523/JNEUROSCI.07-12-04145.1987

10.1016/0006-8993(88)90941-9

10.1038/271676a0

10.1523/JNEUROSCI.06-07-01905.1986

10.3109/03602538909103536

10.1007/BF00406601

10.1126/science.164.3880.719

10.1007/BF00234911

10.1097/00005072-197207000-00006

10.1016/0006-8993(74)90640-4

10.1016/0304-3940(80)90273-6

10.1007/978-1-4684-7971-3_48

10.1016/0304-3940(86)90121-7

10.1126/science.2185543

Pauwels P. J., 1989, Ca2+‐Mediated neuronal death in rat brain neuronal cultures by veratridine: protection by flunarizine, Mol. Pharmacol., 36, 525

10.1111/j.1471-4159.1988.tb01187.x

10.1523/JNEUROSCI.12-05-01882.1992

Rose K., 1990, Nordihydroguaiaretic acid (NDGA). attenuates slow excitatory amino acid‐induced neuronal degeneration in cortical cultures, Soc. Neurosci. Abstr., 16, 288

Rose K., 1992, Nitric oxide synthase activation, or cystine depletion, may not be critical to NMDA receptor‐mediated injury in murine cortical cultures, Soc. Neurosci. Abstr., 18, 645

10.1523/JNEUROSCI.05-06-01483.1985

10.1016/0166-2236(87)90177-9

10.1016/0306-4522(87)90347-2

Schwarcz R., 1977, Kainic acid: neurotoxic effects intraocular injection, Invest. Ophthal. Vis. Sci., 16, 141

Siesjö B. K., 1989, Free radicals and brain damage, Cerebrovasc. Brain Metab. Rev., 1, 165

10.1523/JNEUROSCI.09-05-01579.1989

10.1038/317717a0

10.1002/cne.902800203

10.1016/0896-6273(92)90118-W

10.1126/science.1710829

10.1017/S095252380001097X

10.1016/0166-2236(87)90171-8

10.1016/0165-6147(90)90038-A

10.1016/0006-8993(89)90970-0

10.1126/science.2157282

10.1212/WNL.40.8.1288

Weiss J. H., 1992, Non‐NMDA receptor‐mediated damage to NADPH‐D(+). neurons is Ca2+ dependent, Soc. Neurosci. Abstr., 18, 82

10.1038/341739a0

10.1016/S0074-7696(08)62312-8