Extracellular potassium, volume fraction, and tortuosity in rat hippocampal CA1, CA3, and cortical slices during ischemia

M. A. Perez-Pinzon, L. Tao, C. Nicholson

Research output: Contribution to journalArticlepeer-review

129 Scopus citations

Abstract

1. An in vitro slice model of ischemia was used to study changes in extracellular potassium concentration and diffusion properties in the stratum pyramidale of CA1 and CA3 regions of the hippocampus and in the cortex of the rat. Slices were submerged in artificial cerebrospinal fluid, and ischemia was induced by removing oxygen and glucose until anoxic depolarization occurred. 2. Extracellular potassium concentration was measured with a valinomycin-based ion-selective microelectrode. The bathing medium contained 5 mM potassium, and in vitro ischemia caused the potassium concentration to rise to 45 mM in CA1, 12 mM in CA3, and 32 mM in cortex. 3. Extracellular volume fraction and tortuosity were determined during normoxic conditions and in vitro ischemia by measuring the diffusion of tetramethylammonium. This cation was iontophoretically released into the extracellular space and its concentration as a function of time determined with an ion-selective microelectrode ~100 μm away from the source. 4. During normoxia the volume fraction was 0.14, 0.20, and 0.18, and tortuosity was 1.50, 1.57, and 1.62 in CA1, CA3, and cortex, respectively. These data confirm that the volume fraction of CA1 is smaller than in the two other regions. 5. During ischemia the volume fraction decreased to 0.05, 0.17, and 0.09 in CA1, CA3, and cortex, respectively. Only in CA3 did the tortuosity change significantly by increasing to 1.75. Because of limitations in the time resolution of the diffusion method, the changes in volume fraction and tortuosity during the anoxic depolarization phase of ischemia may have been underestimated. 6. For both initial volume fraction and the change in this parameter during ischemia, the sequence CA1 < cortex < CA3 held, whereas the peak value of extracellular potassium attained during ischemia followed the opposite sequence: CA3 < cortex < CA1. These data are consistent with the idea that initial volume fraction of a region is a predictor of the rise of [K+](o) during ischemia, although other factors likely affect the magnitude of changes. 7. The merits of this in vitro model of ischemia and its fidelity to in vivo models are discussed.

Original languageEnglish (US)
Pages (from-to)565-573
Number of pages9
JournalJournal of neurophysiology
Volume74
Issue number2
DOIs
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

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