Ionic concomitants of astroglial transformation to reactive species.
Brain injury, including ischemia, changes normal astrocytes into reactive species that hypertrophy and begin to proliferate. Understanding the mechanisms that underlie these changes could lead to new abilities to promote regeneration and retard neural degeneration after ischemia. Because ionic changes occur after nonneural cells are exposed to mitogens, we have begun to examine the ionic changes that may trigger reactive gliosis. We showed that two changes thought to be important for mitogenesis, elevation of interstitial potassium or intracellular pH, are correlated with reactive gliosis as indicated by increased immunohistochemical staining for glial fibrillary acidic protein. This relation was seen after activation of cerebral cortex by recurrent spreading depression but not by physiologic stimulation. Deoxyribonucleic acid synthesis occurs in fibroblasts only when intracellular potassium exceeds 90 mM, a level seen in astrocytes only during spreading depression. Thus, our results support the contention that a threshold level of potassium (and pH) must be exceeded in eukaryotic cells before proliferation or anabolism will proceed.
Kraig
R P
RP
Department of Neurology, University of Chicago, Ill. 60637.
Jaeger
C B
CB
D000818:Animals; D001253:Astrocytes / Q000737:chemistry / Q000378:metabolism* / Q000502:physiology; D002455:Cell Division; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D006863:Hydrogen-Ion Concentration; D007150:Immunohistochemistry; D008564:Membrane Potentials / Q000502:physiology; D010775:Photic Stimulation; D011188:Potassium / Q000378:metabolism*; D051381:Rats
D005904:Glial Fibrillary Acidic Protein; D011188:Potassium