Enhanced NMDAR-dependent epileptiform activity is controlled by oxidizing agents in a chronic model of temporal lobe epilepsy

Journal of Neurophysiology

Volumn 76, Issue 6, 1996, Pages 4185-4189

  Hirsch, J C ^a   Quesada, O ^a   Esclapez, M ^a   Gozlan, H ^a   Ben Ari, Y ^a   Bernard, C L ^a  

^a Hôpital de Port Royal ^*  (France)

Author keywords

[No Author keywords available]

Indexed keywords

5,5' DITHIOBIS(2 NITROBENZOIC ACID); AMINO ACID RECEPTOR BLOCKING AGENT; AMINO ACID RECEPTOR STIMULATING AGENT; KAINIC ACID; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; OXIDIZING AGENT; 2 AMINO 5 PHOSPHONOVALERIC ACID; AMPA RECEPTOR; REDUCING AGENT;

ANIMAL; ARTICLE; CHRONIC DISEASE; DISEASE MODEL; DRUG ANTAGONISM; DRUG EFFECT; ELECTROSTIMULATION; EVOKED RESPONSE; IN VITRO STUDY; MALE; OXIDATION REDUCTION REACTION; RAT; SYNAPTIC TRANSMISSION; TEMPORAL LOBE EPILEPSY; WISTAR RAT; ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; CONTROLLED STUDY; EPILEPTIC DISCHARGE; EPILEPTOGENESIS; EXCITATORY POSTSYNAPTIC POTENTIAL; NONHUMAN; PRIORITY JOURNAL; PYRAMIDAL NERVE CELL;

ANIMALS; CHRONIC DISEASE; DISEASE MODELS, ANIMAL; DITHIONITROBENZOIC ACID; ELECTRIC STIMULATION; EPILEPSY, TEMPORAL LOBE; EVOKED POTENTIALS; EXCITATORY AMINO ACID AGONISTS; EXCITATORY AMINO ACID ANTAGONISTS; KAINIC ACID; MALE; OXIDANTS; OXIDATION-REDUCTION; RATS; RATS, WISTAR; RECEPTORS, N-METHYL-D-ASPARTATE; SYNAPTIC TRANSMISSION;

EID: 0030300126     PISSN: 00223077     EISSN: None     Source Type: Journal    
DOI: 10.1152/jn.1996.76.6.4185     Document Type: Article

References (31)

1. AIZENMAN, E., LIPTON, S., AND LORING, R. Selective modulation of NMDA responses by reduction and oxidation. Neuron 2: 1257-1263, 1989.
2. ANDREASEN, M. AND LAMBERT, J. Regenerative properties of pyramidal cell dendrites in area CA1 of the rat hippocampus. J. Physiol. Lond. 483: 421-441, 1995.
3. ANDREASEN, M., LAMBERT, J., AND JENSEN, M. S. Effects of new non-N-methyl-D-aspartate antagonists on synaptic transmission in the in vitro rat hippocampus. J. Physiol. Lond. 414: 317-336, 1989.
4. ASHWOOD, T. J., LANCASTER, B., AND WHEAL, H. V. Intracellular electrophysiology of CA1 pyramidal neurones in slices of the kainic acid lesioned hippocampus. Exp. Brain Res. 62: 189-198, 1986.
5. ASHWOOD, T. J. AND WHEAL, H. V. The expression of N-methyl-D-aspartate-receptor mediated component during epileptiform synaptic activity in the hippocampus. Br. J. Pharmacol. 91: 815-822, 1987.
6. AVOLI, M. AND OLIVIER, A. Bursting in human epileptogenic neocortex is depressed by an N-methyl-D-aspartate antagonist. Neurosci. Lett. 76: 249-254, 1987.
7. BEN-ARI, Y. Limbic seizure and brain damage produced by kainic acid: mechanisms and relevance to human temporal lobe epilepsy. Neuroscience 14: 375-403, 1985.
8. BERNARD, C., HIRSCH, J. C., KHAZIPOV, R., BEN-ARI, Y., AND GOZLAN, H. Redox modulation of synaptic responses and plasticity in rat CA1 hippocampal neurons. Exp. Brain Res. In press.
9. BERNARD, C. AND WHEAL, H. V. A role for synaptic and network plasticity in controlling epileptiform activity in CA1 in the kainic acid-lesioned rat hippocampus in vitro. J. Physiol. Lond. 495: 127-142, 1996.
10. GOZLAN, H. AND BEN-ARI, Y. NMDA receptor redox sites: are they targets for selective neuronal protection? Trends Pharmacol. 16: 368-374, 1995.
11. GOZLAN, H., KHAZIPOV, R., DIABIRA, D., AND BEN-ARI, Y. In CA1 hippocampal neurons, the redox state of NMDA receptors determines LTP expressed by NMDA but not AMPA receptors. J. Neurophysiol. 73: 2612-2617, 1995.
12. ISOKAWA, M. AND LEVESQLIE, M. F. Increased NMDA responses and dendritic degeneration in human epileptic hippocampal neurons in slices. Neurosci. Lett. 132: 212-216, 1991.
13. ISOKAWA, M. AND MELLO, L. A. M. NMDA receptor-mediated excitability in dendritically deformed dentate granule cells in pilocarpine-treated rats. Neurosci. Lett. 129: 69-73, 1991.
14. 2+ entry into hippocampal neurons. Nature Lond. 357: 244-246, 1992.
15. KAPUR, J., STRINGER, J. L., AND LOTHMAN. E. W. Evidence that repetitive seizures in the hippocampus cause a lasting reduction of GABAergic inhibition. J. Neurophysiol. 61: 417-426, 1989.
16. LANCASTER, B. AND WHEAL, H. V. A comparative histological and electrophysiological study of some neurotoxins in the rat hippocampus. J. Comp. Neurol. 211: 105-114, 1982.
17. LOTHMAN, E. W., REMPE, D. A., AND MANGAN, P. S. Changes in excitatory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy. J. Neurophysiol. 74: 841-848, 1995.
18. MCDONALD, J. W., GAROFALO, E. A., HOOD, T., SACKELLARES, C., OILMAN, S., MCKEEVER, P., TRONCOSO, J., AND JOHNSTON, M. Altered excitatory and inhibitory amino acid receptor binding in hippocampus of patients with temporal lobe epilepsy. Ann. Neurol. 29: 529-541, 1991.
19. MODY, I. AND HEINEMANN, U. NMDA receptors of dentate gyrus granule cells participate in synaptic transmission following kindling. Nature Lond. 326: 701-704, 1987.
20. NADLER, J. V. Kainic acid as a tool for the study of temporal lobe epilepsy. Life Sci. 29: 2031-2042, 1981.
21. NADLER, J. V., PERRY, B., AND COTMAN, C. Selective reinnervation of hippocampal area CA1 and fascia dentate after destruction of CA3-CA4 afferents with kainic acid. Brain Res. 182: 1-9, 1980a.
22. NADLER, J. V., PERRY, B., GENTRY, C., AND COTMAN, C. Loss and reacquisition of hippocampal synapses after selective destruction of hippocampal synapses after selective destruction of CA3-CA4 afferents with kainic acid. Brain Res. 191: 387-403, 1980b.
23. PEREZ, Y., MORIN, F., JUTRAS, I., BEAULIEU, C., AND LACAILLE, J.-C. CA1 pyramidal cells in hyperexcitable slices of kainate-treated rats show sprouting of local axon collaterals. Eur. J. Neurosci. 8: 736-748, 1996.
24. PHELPS, S., MITCHELL, J., AND WHEAL, H. V. Changes to synaptic ultrastructure in field CA1 of the rat hippocampus following intracerebroventricular injection of kainic acid. Neuroscience 40: 687-699, 1991.
25. PYAPALI, G. K. AND TURNER, D. A. Denervation-induced dendritic alterations in CA1 pyramidal cells following kainic acid hippocampal lesions in rats. Brain Res. 652: 279-290, 1994.
26. SCHWARTZKROIN, P. A. AND KNOWLES, W. D. Intracellular study of human epileptic cortex: in vitro maintenance of epileptiform activity? Science Wash. DC 223: 709-712, 1984.
27. SPRUSTON, N., SCHILLER, Y., STUART, G., AND SAKMANN, B. Activity-dependent action potential invasion and calcium influx into hippocampal CA1 dendrites. Science Wash. DC 268: 297-300, 1995.
28. STROWBRIDGE, B. W., MASUKAWA, L. M., SPENCER, D. D., AND SHEPERD, G. Hyperexcitability associated with localizable lesions in epileptic patients. Brain Res. 587: 158-163, 1992.
29. TURNER, D. A. AND WHEAL, H. V. Excitatory synaptic potentials in kainic acid-denervated rat CA1 pyramidal neurons. J. Neurosci. 11:2786-2794, 1991.
30. WHEAL, H. V. Function of synapses in the CA1 region of the hippocampus: their contribution to the generation or control of epileptiform activity. Comp. Biochem. Physiol. C Comp. Pharmacol. 93A: 211-220, 1989.
31. WONG, R. K. S. AND STEWART, M. Different firing patterns generated in dendrites and somata of CA1 pyramidal neurones in guinea-pig hippocampus. J. Physiol. Lond. 457: 675-687, 1992.