Peculiarities of neurodegeneration of hippocampus fields after the action of kainic acid in rats

Abstract

The prolonged effect of excitotoxin (kainic acid, KA) on the morphological state of different dorsal hippocampus fields during its one-time introduction in different regions of the brain (intrahippocampal (0.2 μg/μL) and intraventricular (0.6 μg/μL)) was compared. The studies were carried out on light (cresyl violet dye) and fluorescent (fluorojade B) levels. The results showed that KA introduced intrahippocampally at a dose that does not result in animal epileptization caused clearly pronounced degenerative effects in hippocampus. It was found that layers of pyramidal cells in the CA3 and CA4 fields were absent 2 weeks after KA introduction and degenerative changes and cell lysis also applied to the CA1 field by the fourth week. Different level of impairments in hippocampus (from particular impairment of pyramidal neurons of the CA3 and CA4 fields to complete loss of pyramidal layers in the CA1, CA3, and CA4 fields) was observed during intra-ventricular introduction of KA into rats with epileptic status 4 weeks later. The layer of cells in the CA2 field was mainly maintained under both means of KA introduction, indicating the special role of this field. During one-time KA introduction, both methods of introduction resulted in long-term impairment of the nervous tissue (which probably have a common character, but different speeds of neuronal reaction from its field to the impairing factor). Activation of GluR6-containing kainate receptors on pyramidal neurons of the CA3 field is one explanation for the prolonged effect of the KA excitotoxicity; it introduces a chronic character to the single effect of KA and favors the death of the remaining neurons in a necrotic fashion while neurons die by apoptosis at the initial stage of the KA effect.