Journal of Neurophysiology, Vol 66, Issue 1 103-111, Copyright © 1991 by APS

ARTICLES

Effect of anoxia on intracellular and extracellular potassium activity in hypoglossal neurons in vitro

C. Jiang and G. G. Haddad
Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06510.

1. A brain slice preparation was used to study the hypoglossal (XII) neuronal response to anoxia. Both intra- and extracellular potassium activities (K+i,K+o) were measured by the use of ion-selective microelectrodes, and K+ flux was assessed by the use of pharmacologic blockers. 2. Extracellular recordings showed that a short period of anoxia (4 min) induced an increase in K+o of 26.4 +/- 7.5 mM (mean +/- SD, n = 20) in the XII nucleus of adult rats. 3. Intracellular recordings (n = 31) in XII neurons showed a substantial decrease in K+i during anoxia. Fourteen neurons were analyzed in detail and these showed that XII neurons depolarized to -25.3 +/- 7.7 mV, whereas K+i dropped from 93.6 +/- 14.9 to 32 +/- 9.0 mM. These results strongly suggested that K+ is lost from XII neurons during anoxia. 4. Although the extracellular space (ECS) shrank by approximately 50% during anoxia, the possibility that the increase in K+o and decrease in K+i were mainly caused by shrinkage of the ECS and swelling of intraneuronal space was excluded to a great degree because the changes in K+i and K+o during anoxia were relatively very large. 5. To study the mechanisms by which K+ is lost from XII neurons, we used several pharmacologic blockers. High concentration of ouabain (10 mM) and strophanthidin (80 microM) increased K+o from baseline (3-4 mM) to 40.9 +/- 2.5 mM (n = 6) but did not abolish an additional anoxia-induced increase in K+o, suggesting that mechanisms other than Na(+)-K(+)-adenosine triphosphatase inhibition were also responsible for the anoxia-induced K+ leakage.(ABSTRACT TRUNCATED AT 250 WORDS)

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