Postischemic Neuronal Damage Causes Astroglial Activation and Increase in Local Cerebral Glucose Utilization of Rat Hippocampus

Abstract

Summary:The purpose of the present study was to de termine the consequences of postischemic neuronal dam age on CMRglc. Forebrain ischemia of \0 min duration was induced in male Wi star rats. The extent of neuronal damage and the numbers of immunocytochemically de tected astrocytes in the hippocampal CAl subfield as well as CMRglc were determined 2, 5, 7, and 14 days after ischemia. CBF was additionally measured 7 days post ischemia. CMRglc was decreased in cortical and thalamic structures up to 5 days postischemia, and was normalized again on day 7 after ischemia. In the hippocampal areas, CMRglc was decreased only on day 2 after ischemia, was normalized after 5 days, and increased in the stratum

Time Course of Hippocampal Glucose Utilization and Persistence of Parvalbumin Immunoreactive Neurons after Ibotenic Acid—Induced Lesions of the Rat Dentate Area

“…, 1987;Kozuka et a\. , 1989;Beck et a\., 1990aBeck et a\., , 1990bRischke and Krieglstein, 1991). The conclusion to be drawn is that removing a sin gle functional excitatory link in the interconnected chain of the hippocampal circuit does not only af fect the neuronal activity in the immediate vicinity of that lesioned structure, in the sense of a mono synaptically occurring response, but also has a pro found effect on the hippocampal circuitry as a whole.…”

Glial Fibrillary Acidic Protein in the Cerebrospinal Fluid: A Possible Indicator of Prognosis in Full-Term Asphyxiated Newborn Infants?

“…The gliotic reaction, beginning after 1-2 d in response to the injury, may contribute to, but can hardly explain, more than a part of the GFAP increase observed, at least in the severely affected cases. Furthermore, a rapid rise of GFAP synthesis has been shown in response to hypoxic damage that may relate to activation of glial cells with release of GFAP into the extracellular space and CSF (36).…”

Predictive Value of Brain-Specific Proteins in Serum for Neurodevelopmental Outcome after Birth Asphyxia

“…In asphyxiated newborns, serum protein S-100␤ peaked within 2-6 h after birth, presumably due to transitory increased permeability of the blood-brain barrier and decreased renal excretion as part of the asphyxial event (10). An experimental study demonstrated an early increase in the synthesis of intermediary filaments after hypoxic-ischemic events (31). After severe hypoxic-ischemic insult, cell death and disruption of cell membranes might increase the extracellular concentrations, which could further be transferred to the cerebrospinal fluid and explains the correlation to high concentrations of protein S-100␤ in the cerebrospinal fluid (27).…”