Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1

Science

Volumn 276, Issue 5319, 1997, Pages 1699-1702

  Tanaka, Kohichi ^a   Watase, Kei ^a   Manabe, Toshiya ^b   Yamada, Keiko ^c   Watanabe, Masahiko ^c   Takahashi, Katsunobu ^a   Iwama, Hisayuki ^a   Nishikawa, Toru ^a   Ichihara, Nobutsune ^a   Kikuchi, Tateki ^a   Okuyama, Shigeru ^d   Kawashima, Naoya ^d   Hori, Seiji ^e   Takimoto, Misato ^e   Wada, Keiji ^a  

^a NATIONAL INSTITUTE OF NEUROSCIENCE   (Japan)

^b UNIVERSITY OF TOKYO   (Japan)

^c HOKKAIDO UNIVERSITY   (Japan)

^d TAISHO PHARMACEUTICAL CO LTD   (Japan)

^e CIBA GEIGY LTD   (Switzerland)

Author keywords

[No Author keywords available]

Indexed keywords

GLUTAMIC ACID; N METHYL DEXTRO ASPARTIC ACID; N METHYL DEXTRO ASPARTIC ACID RECEPTOR;

AMINO ACID TRANSPORT; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; ASTROCYTE; BRAIN INJURY; CONTROLLED STUDY; ELECTROENCEPHALOGRAM; EPILEPSY; EXCITATORY POSTSYNAPTIC POTENTIAL; HETEROZYGOSITY; HIPPOCAMPUS; IMMUNOBLOTTING; MOUSE; NERVOUS SYSTEM; NONHUMAN; NORTHERN BLOTTING; PRIORITY JOURNAL; SEIZURE; SOUTHERN BLOTTING; SYNAPSE; SYNAPTIC TRANSMISSION;

AMINO ACID TRANSPORT SYSTEM X-AG; ANIMALS; ATP-BINDING CASSETTE TRANSPORTERS; BIOLOGICAL TRANSPORT; BRAIN; BRAIN INJURIES; ELECTROENCEPHALOGRAPHY; EPILEPSY; GENE TARGETING; GLUTAMIC ACID; HIPPOCAMPUS; MICE; MICE, INBRED C57BL; NERVE DEGENERATION; PYRAMIDAL CELLS; SYNAPSES; SYNAPTIC TRANSMISSION;

ANIMALIA;

EID: 0030812843     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.276.5319.1699     Document Type: Article

References (33)

1. D. W. Choi, Neuron 1, 623 (1988).
2. B. I. Kanner and S. Schuldiner, CRC Crit. Rev. Biochem. 22, 1 (1987).
3. M. Szatkowski and D. Attwell, Trends Neurosci. 17, 359 (1994); A. M. Palmer, A. W. Procter, G. C. Stratmann, D. M. Bowen, Neurosci. Lett. 66, 199 (1986); J. D. Rothstein, M. V. Kammen, A. I. Levey, L. J. Martin, R. W. Kuncl, Ann. Neurol. 38, 73 (1995); C. Portera-Cailliau, J. C. Hedreen, D. L. Price, V. E. Koliatsos, J. Neurosci. 15, 3775 (1995).
4. M. Szatkowski and D. Attwell, Trends Neurosci. 17, 359 (1994); A. M. Palmer, A. W. Procter, G. C. Stratmann, D. M. Bowen, Neurosci. Lett. 66, 199 (1986); J. D. Rothstein, M. V. Kammen, A. I. Levey, L. J. Martin, R. W. Kuncl, Ann. Neurol. 38, 73 (1995); C. Portera-Cailliau, J. C. Hedreen, D. L. Price, V. E. Koliatsos, J. Neurosci. 15, 3775 (1995).
5. M. Szatkowski and D. Attwell, Trends Neurosci. 17, 359 (1994); A. M. Palmer, A. W. Procter, G. C. Stratmann, D. M. Bowen, Neurosci. Lett. 66, 199 (1986); J. D. Rothstein, M. V. Kammen, A. I. Levey, L. J. Martin, R. W. Kuncl, Ann. Neurol. 38, 73 (1995); C. Portera-Cailliau, J. C. Hedreen, D. L. Price, V. E. Koliatsos, J. Neurosci. 15, 3775 (1995).
6. M. Szatkowski and D. Attwell, Trends Neurosci. 17, 359 (1994); A. M. Palmer, A. W. Procter, G. C. Stratmann, D. M. Bowen, Neurosci. Lett. 66, 199 (1986); J. D. Rothstein, M. V. Kammen, A. I. Levey, L. J. Martin, R. W. Kuncl, Ann. Neurol. 38, 73 (1995); C. Portera-Cailliau, J. C. Hedreen, D. L. Price, V. E. Koliatsos, J. Neurosci. 15, 3775 (1995).
7. T. Storck, S. Schulte, K. Hofmann, W. Stoffel, Proc. Natl. Acad. Sci. U.S.A. 89, 10,955 (1992); G. Pines et al., Nature 360, 464 (1992); Y. Kanai and M. A. Hediger, ibid., p. 467; K. Tanaka, Neurosci. Res. 16, 149 (1993); W. A. Fairman, R. J. Vandenberg, J. L. Arriza, M. P. Kavanaugh, S. G. Amara, Nature 375, 599 (1995).
8. T. Storck, S. Schulte, K. Hofmann, W. Stoffel, Proc. Natl. Acad. Sci. U.S.A. 89, 10,955 (1992); G. Pines et al., Nature 360, 464 (1992); Y. Kanai and M. A. Hediger, ibid., p. 467; K. Tanaka, Neurosci. Res. 16, 149 (1993); W. A. Fairman, R. J. Vandenberg, J. L. Arriza, M. P. Kavanaugh, S. G. Amara, Nature 375, 599 (1995).
9. T. Storck, S. Schulte, K. Hofmann, W. Stoffel, Proc. Natl. Acad. Sci. U.S.A. 89, 10,955 (1992); G. Pines et al., Nature 360, 464 (1992); Y. Kanai and M. A. Hediger, ibid., p. 467; K. Tanaka, Neurosci. Res. 16, 149 (1993); W. A. Fairman, R. J. Vandenberg, J. L. Arriza, M. P. Kavanaugh, S. G. Amara, Nature 375, 599 (1995).
10. T. Storck, S. Schulte, K. Hofmann, W. Stoffel, Proc. Natl. Acad. Sci. U.S.A. 89, 10,955 (1992); G. Pines et al., Nature 360, 464 (1992); Y. Kanai and M. A. Hediger, ibid., p. 467; K. Tanaka, Neurosci. Res. 16, 149 (1993); W. A. Fairman, R. J. Vandenberg, J. L. Arriza, M. P. Kavanaugh, S. G. Amara, Nature 375, 599 (1995).
11. T. Storck, S. Schulte, K. Hofmann, W. Stoffel, Proc. Natl. Acad. Sci. U.S.A. 89, 10,955 (1992); G. Pines et al., Nature 360, 464 (1992); Y. Kanai and M. A. Hediger, ibid., p. 467; K. Tanaka, Neurosci. Res. 16, 149 (1993); W. A. Fairman, R. J. Vandenberg, J. L. Arriza, M. P. Kavanaugh, S. G. Amara, Nature 375, 599 (1995).
12. J. D. Rothstein et al., Neuron 13, 713 (1994); K. Yamada et al., NeuroReport 7, 2013 (1996).
13. J. D. Rothstein et al., Neuron 13, 713 (1994); K. Yamada et al., NeuroReport 7, 2013 (1996).
14. K. Tanaka et al., data not shown.
15. 525).
16. 525).
17. In situ hybridization analysis was performed on the parasagittal brain sections as described [T. Shibata, M. Watanabe, K. Tanaka, K. Wada, Y. Inoue, NeuroReport 7, 705 (1996)]. Antisense oligonucleotide probes were as follows: for GLAST, CACATTATCACCGCGACCAATCGCATGATGGCTTCGTTAAGAGAA; for GLT-1, TCGTCGTTCTTCTTCCCGGGCCCTAGCTGCTTCTTGAGTTTGGGA; for EAAC1, ATCGCCCACAGGCTTCACCTCTTCCCGCTTGGTTTTGTACTGCTGA; and for EAAT4, GCCCCCAGCTCTGAACCATTGTCTGTCCTTACAATTGTCCTTGTCA.
18. + and the amount obtained in the choline-containing buffer. Experiments were done in triplicate for each concentration. The data were analyzed with a nonlinear least-squares curve-fitting technique.
19. M. A. Rogawski et al., J. Pharmacol. Exp. Ther. 249, 708 (1989).
20. To record EEGs, stainless steel flat electrodes were placed on the parietal and frontal portions of the dura mater. In GLT-1 mutant mice, the EEG recordings were normal in the absence of PTZ.
21. M. A. Kirschner, N. G. Copeland, D. J. Gilbert, N. A. Jenkins, S. G. Amara, Genomics 24, 218 (1994).
22. M. L. Rise, W. N. Frankel, J. M. Coffin, T. N. Seyfried, Science 253, 669 (1991).
23. 2+ block of the NMDA receptor. The values of the membrane potential were corrected for the liquid-junction potential at the electrode tip (-10 mV). Series and input resistances were monitored throughout the experiment. The time constant of the decaying phase of synaptic currents was calculated by fitting a single exponential curve. CNQX and L-AP5 were obtained from Tocris Cookson (Bristol, U.K.).
24. J. S. lsaacson and R. A. Nicoll, J. Neurophysiol. 70, 2187 (1993).
25. J. D. Clements, R. A. Lester, G. Tong, C. E. Jahr, G. L. Westbrook, Science 258, 1498 (1992).
26. J. I. Wadiche, J. L. Arriza, S. G. Amara, M. P. Kavanaugh, Neuron 14, 1019 (1995).
27. The wild-type and GLT-1 mutant mice were fixed transcardially with 4% paraformaldehycle in 0.1 M sodium phosphate buffer and embedded in paraffin wax. Five-micrometer paraffin sections were stained with toluidine blue for Nissl staining.
28. K. Tanaka et al., data not shown.
29. A. I. Faden, P. Demediuk, S. S. Painter, R. Vink, Science 244, 798 (1989); T. K. McIntosh, R. Vink, H. Soares, R. Hayes, R. Simon, J. Neurochem. 55, 1170 (1990).
30. A. I. Faden, P. Demediuk, S. S. Painter, R. Vink, Science 244, 798 (1989); T. K. McIntosh, R. Vink, H. Soares, R. Hayes, R. Simon, J. Neurochem. 55, 1170 (1990).
31. T. D. Oury, C. A. Piantadois, J. D. Crapo, J. Biol. Chem. 268, 15394 (1993).
32. R) × 100 (1) This calculation allowed the right hemisphere to serve as a control for the injured left hemisphere in the same mouse.
33. We thank S. Ogawa and Y. Imagawa for the analysis of edema development after cold injury and R. Kado, T. Takahashi, and T. Okada for critical comments on the manuscript. Supported in part by research grants from the Ministry of Education, Science and Culture of Japan; the Ministry of Health and Welfare of Japan; the Science and Technology Agency of Japan; and the Japan Foundation for Neuroscience and Mental Health.