Spreading depression increases immunohistochemical staining of glial fibrillary acidic protein

• Published in: The Journal of neuroscience Vol. 11; no. 7; pp. 2187 - 2198
• Main Authors: Kraig, RP, Dong, LM, Thisted, R, Jaeger, CB
• Format: Journal Article
• Language: English
• Published: Washington, DC Soc Neuroscience 01.07.1991; Society for Neuroscience
• Subjects: Animals; Biological and medical sciences; Carbon Dioxide - pharmacology; Cortical Spreading Depression - physiology; Frontal Lobe - physiology; Fundamental and applied biological sciences. Psychology; Glial Fibrillary Acidic Protein - metabolism; Immunoenzyme Techniques; Isolated neuron and nerve. Neuroglia; Male; Oxygen - pharmacology; Parietal Lobe - drug effects; Parietal Lobe - physiology; Potassium Chloride - pharmacology; Rats; Rats, Inbred Strains; Vertebrates: nervous system and sense organs; Immunohistochemistry; Glial cell; Cerebral cortex; Rat; Rodentia; Central nervous system; Electrophysiology; Neuroglía; Astrocyte; Vertebrata; Glial fribrillary acidic protein; Mammalia; Spreading depression; Brain (vertebrata)
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/jneurosci.11-07-02187.1991

Reactive astrocytosis is a process by which astrocytes respond to brain injury by showing an increase in glial fibrillary acidic protein (GFAP) staining that is associated with hypertrophy and/or hyperplasia of these cells. Because spreading depression (SD) is a perturbation uncomplicated by neuronal necrosis and is seen in both in vivo and in vitro neural structures, we sought to determine whether SD was a sufficient stimulus to induce enhanced GFAP staining. SD was elicited in anesthetized rats by application of KCI to parietal cortex for 3 hr; equimolar NaCI was applied to contralateral cortex. SD was confirmed by monitoring DC potentials in frontal neocortices. Animals were allowed to recover for 48 hr, and their brains were processed for semiquantitative and computer-based analyses of GFAP staining intensity. Experimental GFAP staining was referenced to contralateral control levels. Neocortical SD (13-37 SDs) was associated with a significant (p less than 10(-4)), 43% increase in GFAP staining intensity, which remained statistically greater than normal for more than 2 weeks. If SD was inhibited by combined hyperoxia and hypercarbia, only a nonsignificant (p greater than 0.20), 7% increase in GFAP staining was seen. Thus, SD may be a useful physiologic process with which to begin to explore the cellular mechanisms that induce the transformation of normal astrocytes into reactive species.