WPŁYW KRÓTKOTRWAŁEGO NIEDOKRWIENIA NA ULTRASTRUKTURĘ ZAKRĘTU HIPOKAMPA U CHOMIKÓW MONGOLSKICH CZĘŚĆ II. OBRAZ MIKROSKOPOWO-ELEKTRONOWY SYNAPS WE WCZESNYM OKRESIE PONIEDOKRWIENNYM

Ultrastructure of synaptic contacts, located in all cortical layers (stratum oriens, pyramidale, radiale, lacunosum-Moleculare and moleculare) of CA, hippocampal sector were studied in Mongolian gerbils, subjected to 7.5 min forebrain ischemia, resulting from bilateral ligation of common carotid arteries. Two experimental groups were used. Group I included animals with 12 h postischemic survival, group II consisted of those which survived 24 h after ischemic insult. CA, sector in animals from group I was characterized by cytoplasmic and mitochondrial swelling of hippocampal interneurons (both perikarya and cel processes and their endings) localized in stratum pyramidale. Additional abnormality consisted in remarkable swelling with vesicular disorganization of presynaptic bags situated mostly in stratum lacunosum-moleculare and to lesser degree in stratum moleculare. There was considerable swelling of astrocytic perikarya and processes, mostly perivascular ones in all Ammon's horn cortical layers. Pyramidal neurons and all other tissue elements remained ultrastructurally unchanged. In experimental group II ultrastructural abnormalities concerned CA, pyramidal neurons which showed either electron microscopic evidences of cel metabolic activation or features of early phase of the delayed neuronal death. On the contrary electron microscope picture of hippocampal interneurons was totally normalized. So was ultrastructure of great majority of presynaptic nerve endings visible in all cortical layers, However, great proportion of postsynaptic structures localized in stratum lacunosum-moleculare and partially in stratum moleculare revealed considerable swelling. This electron microscope picture was similar to thatd escribedasaxon-sparinglesions resulting from the action of excitotoxic substances.The authors conclude that the phenomenon known under the name of delayed neuronal death of CA, pyramidal cells may be initiated by imbalance between their excitatory and inhibitory innervation resulting from an early reversible insufficiency of GABA-ergic interneurons and excitatory action of glutaminergic synapses originating from Schaffer’ scollaterals.

Przedmiotem przedstawionej obecnie części pracy jest ultrastruktura synaps we wczesnym okresie poniedokrwiennym obejmującym fazę hiperaktywności bioelektrycznej komórek piramidowych.