Structural features of ischemic damage in the hippocampus.
Cerebral ischemic injury resulting from either focal or global circulatory arrests in the brain is one of the major causes of death and disability in the adult population. The hippocampus, playing important roles in learning and memory, is selectively vulnerable to ischemic insults. Distinct populations of hippocampal neurons are targeted by ischemia and multiple factors, including excitotoxicity, oxidative stress, and inflammation, are responsible for their damage and death. Modifications of synapses occur very early after ischemia, reflecting related changes in synaptic transmission. These modifications structurally relate to spatial patterns formed by synaptic vesicles, geometry of postsynaptic density, and so forth. Ischemia-induced changes of synaptic contacts can be implicated in the mechanisms leading to delayed neuronal death. In this review, we summarize the available data on the structural aspects of ischemic injury of the hippocampus obtained in tissue culture and animal models and discuss pathways of neurodegeneration common for cerebral ischemia and various neurodegenerative disorders.
Nikonenko
Alexander G
AG
Bogomoletz Institute of Physiology, Bogomoletz street 4, Kiev, Ukraine.
Radenovic
Lidija
L
Andjus
Pavle R
PR
Skibo
Galyna G
GG
D000818:Animals; D020520:Brain Infarction / Q000473:pathology* / Q000503:physiopathology; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology; D013569:Synapses / Q000378:metabolism / Q000473:pathology