|
|
||||||||
AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 2 277-R281, Copyright © 1993 by American Physiological Society
ARTICLES |
P. E. Bickler and S. M. Gallego
Department of Anesthesia, University of California at San Francisco 94143-0542.
Recent studies suggest that turtles avoid disturbances in brain ionic regulation during anoxia by reducing the activity of brain calcium and sodium channels. Because glutamate released during anoxia may cause cytotoxic elevations in intracellular calcium, blockade of glutamate-mediated calcium channels may be essential for cellular survival. Elevations in intracellular calcium, measured with the fluorescent dye fura 2, were used to assay glutamate-induced activation of calcium channels in cerebrocortical brain slices from rats and turtles. Fourteen hours of anoxia produced long-lasting reduction in glutamate-mediated calcium flux in the turtle brain. Furthermore, a plasma protein from turtles maintained under anoxic conditions produced blockade of glutamate-mediated calcium flux in cortical brain slices from both turtles and rats. These results suggest that long-lasting modulation of brain calcium channels as well as blockade of calcium channel activity by regulatory proteins may play important roles in reducing transcellular ion fluxes in turtles during anoxia.
This article has been cited by other articles:
![]() |
P. E. Bickler Reduction of NMDA receptor activity in cerebrocortex of turtles (Chrysemys picta) during 6 wk of anoxia Am J Physiol Regulatory Integrative Comp Physiol, July 1, 1998; 275(1): R86 - R91. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |