Na+/Ca2+ exchanger activity induces a slow DC potential after in vitro ischemia in rat hippocampal CA1 region.
In rat hippocampal CA1 neurons recorded intracellularly from tissue slices, a rapid depolarization occurred approximately 5 min after application of ischemia-simulating medium. In extracellular recordings obtained from CA1 region, a rapid negative-going DC potential (rapid DC potential) was recorded, corresponding to a rapid depolarization. When oxygen and glucose were reintroduced after generating the rapid depolarization, the membrane further depolarized and the potential became 0 mV after 5 min. Contrary, the DC potential began to repolarize slowly and subsequently a slow negative-going DC potential (slow DC potential) occurred within 1 min. A prolonged application of ischemia-simulating medium suppressed the slow DC potential. Addition of a high concentration of ouabain in normoxic medium reproduced a rapid but not a slow DC potential. The slow DC potential was reduced in low Na+- or Co2+-containing medium, but was not affected in low Cl-, high K+ or K+-free medium, suggesting that the slow DC potential is Na+-and Ca2+-dependent. Ni2+ (Ca2+ channel blocker as well as the Na+/Ca2+ exchanger blocker) and benzamil hydrochloride (Na+/Ca2+ exchanger blocker) reduced the slow DC potential dose-dependently. These results suggest that the slow DC potential is mediated by forward mode operation of Na+/Ca2+ exchangers in non-neuronal cells, and that reactivation of Na+, K+-ATPase is necessary to the Na+/Ca2 +exchanger activity.
Uchikado
H
H
Department of Physiology, Kurume University School of Medicine, Fukuoka, Japan.
Tanaka
E
E
Yamamoto
S
S
Isagai
T
T
Shigemori
M
M
Higashi
H
H
D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology*; D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D015220:Calcium Channels / Q000187:drug effects; D002462:Cell Membrane / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology*; D007474:Ion Exchange; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000187:drug effects
D015220:Calcium Channels; D015222:Sodium Channels; D012964:Sodium; D011188:Potassium