Low sodium injury in the hippocampal slice is mediated through NMDA receptors.
Perfusion of hippocampal slices with normoxic medium containing no added sodium resulted in a rapid loss of the CA1 population spike, with only 35 +/- 10% (S.E.M.) (P < 0.001) recovery after a 15 min exposure. This injury was prevented by the non-competitive N-methyl-D-aspartate (NMDA) antagonist MK-801 (93 +/- 4% recovery, P < 0.001), suggesting that low sodium injury may be mediated by opening of the NMDA receptor-associated ionic channels, possibly secondary to the well known sodium dependency of transmitter uptake systems. By contrast, slice perfusion with a medium moderately low in sodium (26 mM) produced only slight injury to the CA1 population spike under normoxic conditions (76 +/- 8% recovery) and provided no protection against hypoxic injury. Low chloride medium also provided no protection against hypoxic injury.
Parsons
J E
JE
Epilepsy Research Laboratories VA Medical Center, Sepulveda, CA 91343.
Wallis
R A
RA
Panizzon
K L
KL
Wasterlain
C G
CG
D000818:Animals; D015687:Cell Hypoxia / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D002794:Choline / Q000494:pharmacology; D003470:Culture Media; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004566:Electrodes; D006624:Hippocampus / Q000473:pathology*; D066298:In Vitro Techniques; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology*; D012964:Sodium / Q000172:deficiency*
D002712:Chlorides; D003470:Culture Media; D016194:Receptors, N-Methyl-D-Aspartate; D016291:Dizocilpine Maleate; D012964:Sodium; D002794:Choline