Synaptic desensitization of NMDA receptors by calcineurin

Science

Volumn 267, Issue 5203, 1995, Pages 1510-1512

  Tong, Gang ^a,b   Shepherd, Dawn ^a   Jahr, Craig E ^a  

^a OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE 5' O (3 THIOTRIPHOSPHATE); CALCINEURIN; CALCIUM; ENZYME INHIBITOR; ETHYLENE GLYCOL 1,2 BIS(2 AMINOPHENYL) ETHER N,N,N',N' TETRAACETIC ACID; GLUTAMATE RECEPTOR; ION CHANNEL; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; PHOSPHATASE; RECEPTOR SUBTYPE;

ANIMAL CELL; ARTICLE; CALCIUM TRANSPORT; CONTROLLED STUDY; DEPHOSPHORYLATION; HIPPOCAMPUS; NONHUMAN; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RAT; SYNAPSE;

ANIMALIA;

EID: 0028929331     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.7878472     Document Type: Article

References (30)

1. S. M. Dudek and M. F. Bear, Proc. Natl. Acad. Sci. U.S.A. 89, 4363 (1992).
2. R. M. Mulkey et al., Nature 369, 486 (1994).
3. M. F. Bear and R. C. Malenka, Curr. Opin. Neurobiol. 4, 389 (1994).
4. L.-Y. Wang et al., Nature 369, 230 (1994).
5. D. N. Lieberman and I. Mody, ibid., p. 235.
6. Y. T. Wang and M. W. Salter, ibid., p. 233.
7. G. Tong and C. E. Jahr, J. Neurophysiol. 72. 754 (1994).
8. W. Sather et al., Neuron 4, 725 (1990); I. V. Chizhmakov et al., J. Physiol. (London) 448, 453 (1992).
9. W. Sather et al., Neuron 4, 725 (1990); I. V. Chizhmakov et al., J. Physiol. (London) 448, 453 (1992).
10. R. A. J. Lester and C. E. Jahr, J. Neurosci. 12, 635 (1992).
11. M. L. Mayer et al., ibid. 7, 3230 (1987); P. Ascher and L. Nowak, J. Physiol. (London) 399, 247 (1988); C. E. Jahr and C. F. Stevens, Nature 325, 522 (1987); C. Rosenmund et al., J. Neurophysiol. 73, 427 (1995).
12. M. L. Mayer et al., ibid. 7, 3230 (1987); P. Ascher and L. Nowak, J. Physiol. (London) 399, 247 (1988); C. E. Jahr and C. F. Stevens, Nature 325, 522 (1987); C. Rosenmund et al., J. Neurophysiol. 73, 427 (1995).
13. M. L. Mayer et al., ibid. 7, 3230 (1987); P. Ascher and L. Nowak, J. Physiol. (London) 399, 247 (1988); C. E. Jahr and C. F. Stevens, Nature 325, 522 (1987); C. Rosenmund et al., J. Neurophysiol. 73, 427 (1995).
14. M. L. Mayer et al., ibid. 7, 3230 (1987); P. Ascher and L. Nowak, J. Physiol. (London) 399, 247 (1988); C. E. Jahr and C. F. Stevens, Nature 325, 522 (1987); C. Rosenmund et al., J. Neurophysiol. 73, 427 (1995).
15. 2, 20 μM glycine, 5 μM 2,3-dihydroxy-6-nitro-7-sulfa-moyl-benzo(F)quinoxaline (NBQX), and 50 to 100 μM picrotoxin, adjusted to pH 7.4 with NaOH. Autaptic EPSCs were evoked with voltage jumps to -20 or 0 mV from a holding potential of -60 to -90 mV (durations of 0.3 to 2 ms). Currents were sent through a low-pass filter at 0.5 to 10 kHz and were digitally sampled at 1 to 50 kHz. Series resistance compensation (80 to 100%) was used in all experiments. All experiments were performed at 22° to 24°C. Data are expressed as mean ±SEM.
16. The first two stimuli of the conditioning train were delivered 35 ms apart to allow for accurate measurement of the amplitude of the first EPSC. The second to fourth stimuli were delivered 20 ms apart.
17. Solution changes were made with gravity-fed flow tubes (7, 9).
18. N. A. Hessler et al., Nature 366, 569 (1993); C. Rosenmund et al.. Science 262, 754 (1993).
19. N. A. Hessler et al., Nature 366, 569 (1993); C. Rosenmund et al., Science 262, 754 (1993).
20. C. E. Jahr and C. F. Stevens, J. Neurosci. 10, 3178 (1990).
21. J.Kunz and N. N. Hall, Trends Biochem. Sci. 18, 334 (1993); Y. Hashimoto, B. A. Perrino, T. R. Soderling, J. Biol. Chem. 265, 1924 (1990). FK506 was added to the external solution, calcineurin inhibitory peptide was added to the internal solution, and cyclosporin A was added to both solutions.
22. J.Kunz and N. N. Hall, Trends Biochem. Sci. 18, 334 (1993); Y. Hashimoto, B. A. Perrino, T. R. Soderling, J. Biol. Chem. 265, 1924 (1990). FK506 was added to the external solution, calcineurin inhibitory peptide was added to the internal solution, and cyclosporin A was added to both solutions.
23. H. Ishihara et al., Biochem. Biophys. Res. Commun. 159, 871 (1989). Calyculin A was added to the external solution.
24. G. Swarup et al., ibid. 107, 1104 (1982).
25. J. A. Cooper, J. Cell Biol. 105, 1473 (1987).
26. C. Rosenmund and G. L. Westbrook, Neuron 10, 805 (1993).
27. R. Pethig et al., Cell Calcium 10, 491 (1989).
28. S. Goto et al., Brain Res. 397, 161 (1986).
29. 2+) recorded after the four-pulse conditioning stimulus was delivered were two and four times, respectively, the unstimulated frequency. In an additional cell, the frequency increased to a point where spontaneous events summated and could not be counted. It is unlikely that free glutamate remained in the cleft after delivery of the conditioning stimulus because the D-AP5 was washed out in this interval; this result suggests that the synaptic clefts were well perfused.
30. Supported by NIH grant NS21419.