WE investigated the effect of nitric oxide (NO) upon CA1 neurons of th
e hippocampal slice. NO was given via perfusate without oxygen and wit
h glucose concentration increased to 10 mM to prevent hypoxic injury.
Exposure to NO for 10 min produced severe neuronal injury, with CA1 or
thodromic and antidromic population spike regaining only 3 +/- 3% and
9 +/- 3% of initial amplitude after 1 h recovery. Hypoxic controls in
contrast, showed orthodromic and antidromic recovery of 98 +/- 5% and
93 +/- 7%. Good protection from NO-induced injury was seen with 10 mM
nicotinamide, an inhibitor of poly-ADP-ribosylation, with CA1 PS recov
ering to 116 +/- 10% orthodromically, and 96 +/- 4% antidromically. Pr
otection was also seen with 3'-aminobenzamide, another poly-ADP-ribosy
lation inhibitor, suggesting that poly-ADP-ribosylation may play an im
portant role in NO-mediated neuronal injury.