Effects of transient cerebral ischemia on glial fibrillary acidic protein phosphorylation and immunocontent in rat hippocampus

Transient global cerebral ischemia induced in rats by four-vessel occlusion for 20 min produced an increase in the immunocontent of glial fibrillary a cidic protein and a protein phosphorylation response that was different in the CA1 and dentate gyrus areas of the hippocampus. We studied different ti mes of reperfusion (one, four, seven, 14 and 30 days) and observed that the immunocontent and in vitro rate of phosphorylation of glial fibrillary aci dic protein in the CA1 region was significantly increased at all intervals after the ischemic insult, indicating that the astrocytic response was main tained for at least 30 days. After reperfusion for 14 days a significant in crease in the ratio "in vitro phosphorylation rate/ immunocontent" in the C A1 region was observed when compared to control values, to other intervals and to the dentate gyrus, suggesting a hyperphosphorylation of this interme diate filament protein at this interval. In the dentate gyrus, an area less vulnerable to the insult, labelling and immunocontent of glial fibrillary acidic protein were equally increased from four days of reperfusion and the increase remained significant until 30 days, confirming that neuronal deat h is not the only determining factor for gliosis to occur. In control sham- operated animals, neither the CA1 region nor the dentate gyrus showed signi ficant increases in labelling or immunocontent. Changes in the phosphorylation of glial fibrillary acidic protein may be es sential for the plastic response of astrocytes to neuronal damage, as neuro ns and astrocytes can act as functional units involved in homeostasis, plas ticity and neurotransmission. (C) 1999 IBRO. Published by Elsevier Science Ltd.