Citation

Fineman I, Hovda DA, Smith M, Yoshino A, Becker DP. Brain Res. 1993; 624(1-2): 94-102.

Affiliation

Division of Neurosurgery, UCLA School of Medicine 90024-6901.

Copyright

(Copyright © 1993, International Brain Research Organization, Publisher Elsevier Publishing)

DOI

unavailable

PMID

8252419

Abstract

In order to determine the extent and duration of calcium (Ca2+) flux following a lateral fluid percussion brain injury in the rat, 45Ca autoradiography was used to study animals immediately, 6, 24 and 96 h after the insult. In addition, cell suspension studies were conducted to determine the extent of cellular flux of 45Ca. Optical density and/or scintillation counting was utilized to provide a relative measure of 45Ca accumulation within 20 different structures. The results indicated that in animals who exhibited no gross morphological damage, 45Ca accumulation following injury was exhibited primarily within the ipsilateral cerebral cortex, dorsal hippocampus and striatum. This accumulation continued for several days returning to control levels by the 4th day after injury. In animals who sustained morphological damage, the contusion site exhibited a marked accumulation of 45Ca which did not resolve spontaneously over the course of 4 days. We conclude from this work that Ca2+ flux is a major component of this experimental model of traumatic injury. Furthermore, that depending on the extent of cell damage, the accumulation of Ca2+ is regionally different. Finally, that even in an injury which by itself does not produce gross morphological tissue damage, accumulation of Ca2+ can continue for at least 48 h.

Language: en