EXTRACELLULAR POTASSIUM, VOLUME FRACTION AND TORTUOSITY IN RAT HIPPOCAMPAL
CA1, CA3 AND CORTICAL SLICES DURING ISCHEMIA.
Perez-Pinzon, Miguel A., Lian Tao and Charles Nicholson.
Department of Physiology and Biophysics, New York University Medical
Center, 550 First Avenue, New York, NY 10016.
APStracts 2:0089N, 1995.
SUMMARY AND CONCLUSIONS
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 about
100 [mu]m 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 that initial volume fraction of a
region is a predictor of the rise of [K + ] o during ischemia though 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.
Received 22 March 1994; accepted in final form 26 January 1995.
APS Manuscript Number J57-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.