Ischemic damage in the hippocampus: a silver impregnation and immunocytochemical study in the rat.

Wistar rats were subjected to transient forebrain ischemia for 30 min. After a survival period of two to three days their brains were fixed and sections were processed for Nauta suppressive method (26) to study postischemic degenerative changes and for glial fibrillary acidic protein (GFAP) to study glial reaction. After two days somatodendritic argyrophilia was evident in the CA1a and CA4 areas. The somata and dendrites of CA1 a pyramidal neurons were intensely argyrophilic, and a clear border zone which separated these neurons from undamaged CA1b neurons was detected. In the CA4 area a few degenerating, probably mossy cells were found. Neuronal degeneration then proceeded rapidly during a 72 h survival period, when the somata and dendrites of complete CA1 and CA2 pyramidal cells became intensively argyrophilic. The area of CA4 was full of degenerated neurons, but the CA3 neurons remained intact. Postischemic glial changes were observed after 48h survival. The rostral part of CA1a area contained a higher concentration of astrocytes in the dendritic layer as well as in the pyramidal layer. These astrocytes revealed features of reactive astrocytes. An intense GFAP immunoreactivity with heavily stained astrocytic figures appeared in the CA2, CA3 dendritic layers, stratum molecular of the DG and hilus. The central region of CA4 area contained various vacuoles with clearly stained astrocytes. By 72 h after ischemia the tissue structure changed in all areas since the pyramidal layer contained shrunken neurons and large vacuoles. The GFAP immunoreactivity in the hippocampus was the same or even higher as observed after two days postischemia, but the astrocytes were seen more closely in the relation with the pyramidal cell layer.