Role of calcium channels in spreading depression in rat hippocampal slices.
In the CA1 region of rat hippocampal slices, spreading depression (SD) was provoked by a brief period of hypoxia or by localized application of high potassium solution. We measured extracellular DC voltage (Vo), extracellular potassium concentration ([K+]o) and/or extracellular Ca2+ concentration ([Ca2+]o). SD was provoked under control conditions and also when voltage-gated Ca2+ channels were blocked by application of 2 mM Ni2+ or Co2+. In some experiments, CPP, DNQX, or the two together were also applied to block glutamate receptor-coupled channels. When SD was provoked by hypoxia, these treatments significantly increased the latency of SD onset and decreased the amplitudes of the accompanying delta Vo, delta [Ca2+]o and delta [K+]o. Hypoxia-induced SD was never blocked completely, however and delta [Ca2+]o was reduced at most by 50%. When SD was provoked by application of high K+ solution near the recording site, Ni2+ or Co2+ partially suppressed the Vo and [Ca2+]o shifts but did not block SD altogether. When high K+ solution was applied at a distance, Ni2+ or Co2+ blocked the propagation of SD to the recording site. We conclude that during SD, a significant proportion of the calcium ions flowing into neurons does not pass through voltage-gated or glutamate receptor-linked channels.
Jing, J; Aitken, PG; Somjen, GG
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