Abstract：
:Evidence suggests that nitric oxide (NO) may mediate, at least in part, excitotoxic effects of excessive N-methyl-D-aspartate (NMDA) receptor activation both in vivo and in vitro. In the present experiments, NMDA-induced excitotoxicity has been studied in CHP100 neuroblastoma cell cultures. Application of NMDA (0.25-1.5 mM) produced concentration-dependent cell death. These effects were antagonized by co-application of dizocilpine (MK801), a selective and non-competitive NMDA receptor complex antagonist. Protection from NMDA-induced lethal effects was also afforded by N omega-nitro-L-arginine methyl ester, a potent NO-synthase inhibitor, and by hemoglobin, a NO-trapping agent. In addition, substitution of L-arginine, normally present in the exposure solution with its D-isomer, abolished the cell death induced by the excitotoxin. In conclusion, the present experiments support the suggestion that excitotoxic effects induced by NMDA receptor stimulation involve L-arginine-NO pathway activation.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Corasaniti MT,Tartaglia RL,Melino G,Nisticò G,Finazzi-Agrò Adoi
10.1016/0304-3940(92)90600-ckeywords:
subject
Has Abstractpub_date
1992-12-07 00:00:00pages
221-3issue
2eissn
0304-3940issn
1872-7972pii
0304-3940(92)90600-Cjournal_volume
147pub_type
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journal_title：Neuroscience letters
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