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

Miguel Perez-Pinzon, L. Tao, C. Nicholson

Research output: Contribution to journalArticle

124 Citations (Scopus)

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
Pages (from-to)565-573
Number of pages9
JournalJournal of Neurophysiology
Volume74
Issue number2
StatePublished - Jan 1 1995
Externally publishedYes

Fingerprint

Potassium
Ischemia
Microelectrodes
Hippocampal CA3 Region
Ions
Valinomycin
Hippocampal CA1 Region
Extracellular Space
Cerebrospinal Fluid
Cations
Hippocampus
Oxygen
Glucose
In Vitro Techniques

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Extracellular potassium, volume fraction, and tortuosity in rat hippocampal CA1, CA3, and cortical slices during ischemia. / Perez-Pinzon, Miguel; Tao, L.; Nicholson, C.

In: Journal of Neurophysiology, Vol. 74, No. 2, 01.01.1995, p. 565-573.

Research output: Contribution to journalArticle

@article{5ca05eeb77e54bea82621040a7011533,
title = "Extracellular potassium, volume fraction, and tortuosity in rat hippocampal CA1, CA3, and cortical slices during ischemia",
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.",
author = "Miguel Perez-Pinzon and L. Tao and C. Nicholson",
year = "1995",
month = "1",
day = "1",
language = "English",
volume = "74",
pages = "565--573",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Extracellular potassium, volume fraction, and tortuosity in rat hippocampal CA1, CA3, and cortical slices during ischemia

AU - Perez-Pinzon, Miguel

AU - Tao, L.

AU - Nicholson, C.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0029093894&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029093894&partnerID=8YFLogxK

M3 - Article

C2 - 7472364

AN - SCOPUS:0029093894

VL - 74

SP - 565

EP - 573

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 2

ER -