Epileptiform activity but not synaptic plasticity is blocked by oxidation of NMDA receptors in a chronic model of temporal lobe epilepsy

References 

1. Andreasen, M., Lambert, J. and Jensen, M., Effects of the new non-N-methyl-d-aspartate antagonists on synaptic transmission in the in vitro rat hippocampus, J. Physiol. (Lond.), 414 (1989) 317–336. (Abstract)
2. Aniksztejn, L., Otani, S. and Ben-Ari, Y., Quisqualate metabotropic receptors modulate NMDA currents and facilitate induction of long-term potentiation through protein kinase C, Eur. J. Neurosci., 4 (1992) 500–505.
3. 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 (1987) 815–822.
4. Avoli, M. and Olivier, A., Bursting in human epileptogenic neocortex is depressed by an N-methyl-d-aspartate antagonist, Neurosci. Lett., 76 (1987) 249–254.
5. Bear, M.F. and Malenka, R.C., Synaptic plasticity, LTP and LTD, Curr. Opin. Neurobiol., 4 (1994) 389–399.
6. Ben-Ari, Y., Limbic seizure and brain damage produced by kainic acid: mechanisms and relevance to human temporal lobe epilepsy, Neuroscience, 14 (1985) 375–403.
7. Ben-Ari, Y., Aniksztejn, L. and Bregestovski, P., Protein kinase C modulation of NMDA currents: An important link for LTP induction, Trends Neurosci., 15 (1992) 333–339.
8. Bernard, C. and Wheal, H.V., Simultaneous expression of long-term depression of NMDA and long-term potentiation of AMPA receptor-mediated synaptic responses in the CA1 area of the kainic acid-lesioned hippocampus, Eur. J. Neurosci., 7 (1995) 1651–1655.
9. Bernard, C. and Wheal, H.V., Plasticity of AMPA and NMDA receptor-mediated epileptiform activity in a chronic model of temporal lobe epilepsy, Epilepsy Res., 21 (1995) 95–107.
10. Bernard, C. and Wheal, H.V., Simultaneous expression of EPSP/spike potentiation and EPSP/spike depression in the hippocampus, Neuroscience, 67 (1995) 73–82.
11. Bernard, C. and Wheal, H.V., Expression of EPSP/spike potentiation following low frequency and tetanic stimulation in the CA1 area of the rat hippocampus, J. Neurosci., 15 (1995) 6542–6551.
12. 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 (1996) 127–142.
13. 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 (1996).
14. Cornish, S. and Wheal, H.V., Long-term loss of paired pulse inhibition in the kainic acid-lesioned hippocampus of the rat, Neuroscience, 28 (1989) 563–571.
15. Crepel, V., Hammond, C., Krnjevic, K., Chinestra, P. and Ben-Ari, Y., Anoxia-induced LTP of isolated NMDA receptor-mediated synaptic responses, J. Neurophysiol., 69 (1993) 1774–1778.
16. Gozlan, H. and Ben-Ari, Y., NMDA receptor redox sites: are they targets for selective neuronal protection? Trends Pharmacol. Sci., 16 (1995) 368–374.
17. Gozlan, H., Diabira, D., Chinestra, P. and Ben-Ari, Y., Anoxic LTP is mediated by the redox modulatory site of the NMDA receptor, J. Neurophysiol., 72 (1994) 3017–3022.
18. 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 (1995) 2612–2617.
19. Hirsch, J.C., Quesada, O., Esclapez, H., Gozlan, H., Ben-Ari, Y. and Bernard, C., Enhanced NMDAR-dependent epileptiform activity is controlled by oxidizing agents in a chronic model of temporal lobe epilepsy, J. Neurophysiol, in press (1996).
20. Jensen, F., Gardner, G., Williams, P., Gallop, P., Aizenman, E. and Rosenberg, P., The putative essential nutrient pyrroloquinoline quinone is neuroprotective in a rodent model of hypoxic/ischemic brain injury, Neuroscience, 62 (1994) 399–406.
21. Lancaster, B. and Wheal, H.V., A comparative histological and electrophysiological study of some neurotoxins in the rat hippocampus, J. Comp. Neurol., 211 (1982) 105–114.
22. McBain, C.J. and Mayer, M.L., N-methyl-d-aspartic acid receptor structure and function, Physiol. Rev., 74 (1994) 723–760.
23. Mody, I. and Heinemann, U., NMDA receptors of dentate gyrus granule cells participate in synaptic transmission following kindling, Nature, 326 (1987) 701–704.
24. Nadler, J.V., Kainic acid as a tool for the study of temporal lobe epilepsy, Life Sci., 29 (1981) 2031–2042.
25. 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 (1980) 1–9.
26. 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 (1980) 387–403.
27. 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 (1996) 736–748.
28. 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 (1991) 687–699.
29. Quesada, O., Hirsch, J., Ben-Ari, Y. and Bernard, C., Redox sites of NMDA receptors can modulate epileptiform activity in hippocampal slices from kainic acid treated rats, Neurosci. Lett., 212 (1996) 171–174.
30. Turner, D.A. and Wheal, H.V., Excitatory synaptic potentials in kainic acid-denervated rat CA1 pyramidal neurons, J. Neurosci., 11 (1991) 2786–2794.
31. 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], 93A (1989) 211–220.