Astrocytic Involvement in the Maturation Phenomenon After Temporary Cerebral Ischemia

Abstract

Astrocytes support neuronal functions by regulating the extracellular ion homeostasis and levels of neurotransmitters, and by providing fuel such as lactate to the neurons via their processes (APs). After two 10-min unilateral carotid occlusions with a 5-h interval in gerbils, we investigated maturing disseminated selective neuronal necrosis (DSNN) on the coronal surface sectioned at the infundibular level. We chronologically counted the normal appearing, degenerated, and dead neurons and astrocytes in the cerebral cortex; observed the ultrastructure of APs, and counted the number of their cut-ends and mitochondria in the neuropil; determined the percentage volume of APs according to Weibel’s point-counting method; compared the number of cut-ends and mitochondria and percentage volume of APs around the astrocytes and around the normal-appearing, degenerated, and dead ­neurons. Heterogeneous degeneration of APs was concluded to be closely associated with the maturation of DSNN.

Using the same model, at the coronally sectioned surface on the chiasmatic level, we investigated the mechanism of development of focal infarction in the maturing DSNN. Same as in the above study, we chronologically counted various neurons and astrocytes; observed and measured the area of the ultrastructure of astrocytic end-feet; counted the number of carbon-black-suspension-perfused microvessels. We concluded that after temporary cerebral ischemia, secondary focal ischemia was induced by microvascular obstruction compressed by swollen astrocytic end-feet, resulting in delayed focal infarction.