Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Science 23 March 1990:
Vol. 247. no. 4949, pp. 1474 - 1477
DOI: 10.1126/science.2157282
Prev | Table of Contents | Next

Articles

Science, Vol 247, Issue 4949, 1474-1477
Copyright © 1990 by American Association for the Advancement of Science

articles

The calcium channel blocker nifedipine attenuates slow excitatory amino acid neurotoxicity

JH Weiss, DM Hartley, J Koh, and DW Choi

Department of Neurology and Neurological Sciences, Stanford University Medical School, CA 94305.

High concentrations of potent N-methyl-D-aspartate (NMDA) agonists can trigger degeneration of cultured mouse cortical neurons after an exposure of only a few minutes; in contrast, selective non-NMDA agonists or low levels of NMDA agonists require exposures of several hours to induce comparable damage. The dihydropyridine calcium channel antagonist nifedipine was used to test whether this slow neurotoxicity is mediated by a calcium influx through voltage-gated channels. Nifedipine had little effect on the widespread neuronal degeneration induced by brief exposure to high concentrations of NMDA but substantially attenuated the neurotoxicity produced by 24-hour exposure to submaximal concentrations of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate, kainate, or quinolinate. Calcium ion influx through dihydropyridine-sensitive, voltage-dependent calcium channels may be an important step in the neuronal injury induced by the prolonged activation of NMDA or non-NMDA glutamate receptors.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Glutamate Transporter-Mediated Glutamate Secretion in the Mammalian Pineal Gland.
M.-H. Kim, S. Uehara, A. Muroyama, B. Hille, Y. Moriyama, and D.-S. Koh (2008)
J. Neurosci. 28, 10852-10863
   Abstract »    Full Text »    PDF »
17{beta}-Estradiol Protects Cortical Neurons Against Oxidative Stress-Induced Cell Death through Reduction in the Activity of Mitogen-Activated Protein Kinase and in the Accumulation of Intracellular Calcium.
Y. Numakawa, T. Matsumoto, D. Yokomaku, T. Taguchi, E. Niki, H. Hatanaka, H. Kunugi, and T. Numakawa (2007)
Endocrinology 148, 627-637
   Abstract »    Full Text »    PDF »
Vitamin D Hormone Confers Neuroprotection in Parallel with Downregulation of L-Type Calcium Channel Expression in Hippocampal Neurons.
L. D. Brewer, V. Thibault, K.-C. Chen, M. C. Langub, P. W. Landfield, and N. M. Porter (2001)
J. Neurosci. 21, 98-108
   Abstract »    Full Text »    PDF »
Decreased G-Protein-Mediated Regulation and Shift in Calcium Channel Types with Age in Hippocampal Cultures.
E. M. Blalock, N. M. Porter, and P. W. Landfield (1999)
J. Neurosci. 19, 8674-8684
   Abstract »    Full Text »    PDF »
L-Type Ca2+ Channels Are Essential for Glutamate-Mediated CREB Phosphorylation and c-fos Gene Expression in Striatal Neurons.
A. Rajadhyaksha, A. Barczak, W. Macias, J.-C. Leveque, S. E. Lewis, and C. Konradi (1999)
J. Neurosci. 19, 6348-6359
   Abstract »    Full Text »    PDF »
NMDA-Induced Intrinsic Voltage Oscillations Depend on L-Type Calcium Channels in Spinal Motoneurons of Adult Turtles.
P. A. Guertin and J. Hounsgaard (1998)
J Neurophysiol 80, 3380-3382
   Abstract »    Full Text »    PDF »
Neurotoxicity Mediated by Aberrant Patterns of Synaptic Activity Between Rat Hippocampal Neurons in Culture.
J. R. McLeod Jr., M. Shen, D. J. Kim, and S. A. Thayer (1998)
J Neurophysiol 80, 2688-2698
   Abstract »    Full Text »    PDF »
Rapid Ca2+ Entry through Ca2+-Permeable AMPA/Kainate Channels Triggers Marked Intracellular Ca2+ Rises and Consequent Oxygen Radical Production.
S. G. Carriedo, H. Z. Yin, S. L. Sensi, and J. H. Weiss (1998)
J. Neurosci. 18, 7727-7738
   Abstract »    Full Text »    PDF »
Neurotensin and Substance P Inhibit Low- and High-Voltage-Activated Ca2+ Channels in Cultured Newborn Rat Nucleus Basalis Neurons.
M. Margeta-Mitrovic, J. J. Grigg, K. Koyano, Y. Nakajima, and S. Nakajima (1997)
J Neurophysiol 78, 1341-1352
   Abstract »    Full Text »    PDF »
cAMP-Dependent Enhancement of Dihydropyridine-Sensitive Calcium Channel Availability in Hippocampal Neurons.
E. T. Kavalali, K. S. Hwang, and M. R. Plummer (1997)
J. Neurosci. 17, 5334-5348
   Abstract »    Full Text »    PDF »
Selective N-Type Calcium Channel Antagonist Omega Conotoxin MVIIA Is Neuroprotective Against Hypoxic Neurodegeneration in Organotypic Hippocampal-Slice Cultures.
A.K. Pringle, C.D. Benham, L. Sim, J. Kennedy, F. Iannotti, L.E. Sundstrom, and D. W. Choi (1996)
Stroke 27, 2124-2130
   Abstract »    Full Text »
Ca2+-Permeable AMPA/Kainate and NMDA Channels: High Rate of Ca2+ Influx Underlies Potent Induction of Injury.
Y. M. Lu, H. Z. Yin, J. Chiang, and J. H. Weiss (1996)
J. Neurosci. 16, 5457-5465
   Abstract »    Full Text »    PDF »
Expression of alpha 1D subunit mRNA is correlated with L-type Ca2+ channel activity in single neurons of hippocampal "zipper" slices.
K. C. Chen, E. M. Blalock, O. Thibault, P. Kaminker, and P. W. Landfield (2000)
PNAS 97, 4357-4362
   Abstract »    Full Text »    PDF »


To Advertise     Find Products

Science. ISSN 0036-8075 (print), 1095-9203 (online)