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Science 11 June 1999:
Vol. 284. no. 5421, pp. 1845 - 1848
DOI: 10.1126/science.284.5421.1845
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Reports

Specific Coupling of NMDA Receptor Activation to Nitric Oxide Neurotoxicity by PSD-95 Protein

Rita Sattler, 1 Zhigang Xiong, 2 Wei-Yang Lu, 2 Mathias Hafner, 3 John F. MacDonald, 2 Michael Tymianski 1*

The efficiency with which N-methyl-D-aspartate receptors (NMDARs) trigger intracellular signaling pathways governs neuronal plasticity, development, senescence, and disease. In cultured cortical neurons, suppressing the expression of the NMDAR scaffolding protein PSD-95 (postsynaptic density-95) selectively attenuated excitotoxicity triggered via NMDARs, but not by other glutamate or calcium ion (Ca2+) channels. NMDAR function was unaffected, because receptor expression, NMDA currents, and 45Ca2+ loading were unchanged. Suppressing PSD-95 blocked Ca2+-activated nitric oxide production by NMDARs selectively, without affecting neuronal nitric oxide synthase expression or function. Thus, PSD-95 is required for efficient coupling of NMDAR activity to nitric oxide toxicity, and imparts specificity to excitotoxic Ca2+ signaling.

1 Toronto Western Hospital, University of Toronto, Lab 11-416, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada.
2 Department of Physiology, University of Toronto, Toronto, Ontario M5G 1X8, Canada.
3 Mannheim University of Applied Sciences, 68163 Mannheim, Germany.
*   To whom correspondence should be addressed. E-mail: mike_t{at}playfair.utoronto.ca

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