{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:18:12Z","timestamp":1762100292003},"reference-count":36,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,10,11]],"date-time":"2004-10-11T00:00:00Z","timestamp":1097452800000},"content-version":"vor","delay-in-days":3406,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[1995,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Phosphoinositide\u2010specific phospholipase C (PLC) is a key enzyme in signal transduction. It was previously demonstrated that an antibody to an isozyme of PLC, PLC\u2010\u03b4, produces intense staining of neurofibrillary tangles (NFT), the neurites surrounding senile plaque (SP) cores and neuropil threads in the brains of patients with Alzheimer's disease (AD). Although the etiology of neuronal degeneration in AD is still to be defined, excitotoxic glutamate might be a candidate. In the present study, an anti\u2010PLC\u2010\u03b4 antibody was used to examine the influence of glutamate on PLC\u2010\u03b4 immunoreactivity in cultured rat cortical neurons. Exposure to glutamate caused the death of cultured cortical neurons and exhibited increased immunostaining with the anti\u2010PLC\u2010\u03b4 antibody. Subtoxic doses of glutamate also increased PLC\u2010\u03b4 immunoreactivity in a dose\u2010dependent manner. Both glutamateinduced neuronal degeneration and the increases in PLC\u2010\u03b4 immunoreactivity were prevented by removal of extracellular Ca2+ or the application of an N\u2010methyl\u2010D\u2010aspartate (NMDA) receptor antagonist, MK801. The glutamate\u2010induced increase in PLC\u2010\u03b4 immunoreactivity was also prevented by N<jats:sup>\u03c9<\/jats:sup>\u2010nitro\u2010Larginine, a nitric oxide (NO) synthase inhibitor. These results suggest that NO formation secondary to Ca<jats:sup>2+<\/jats:sup> influx by NMDA receptor activation leads to similar modifications of PLC\u2010\u03b4 to those seen in AD. \u00a9 1995 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.490410315","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T02:10:37Z","timestamp":1104545437000},"page":"418-426","source":"Crossref","is-referenced-by-count":13,"title":["Glutamate\u2010induced antigenic changes of phospholipase C\u2010\u03b4 in cultured cortical 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