Abstract：
: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)
journal_name
J Neurophysioljournal_title
Journal of neurophysiologyauthors
Jiang C,Haddad GGdoi
10.1152/jn.1991.66.1.103subject
Has Abstractpub_date
1991-07-01 00:00:00pages
103-11issue
1eissn
0022-3077issn
1522-1598journal_volume
66pub_type
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