Abstract：
: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.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Uchikado H,Tanaka E,Yamamoto S,Isagai T,Shigemori M,Higashi Hdoi
10.1016/s0168-0102(99)00119-4subject
Has Abstractpub_date
2000-02-01 00:00:00pages
129-40issue
2eissn
0168-0102issn
1872-8111pii
S0168-0102(99)00119-4journal_volume
36pub_type
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