Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

Autor: Alexander G. Nikonenko, Irina Nikonenko, Dominique Muller, Galina Skibo, T Kovalenko, I. V. Lushnikova, Kirill Voronin, Irina Osadchenko
Rok vydání: 2006
Předmět:
Dendritic spine
Cognitive Neuroscience
Excitatory Postsynaptic Potentials/physiology
Presynaptic Terminals
Synaptic Membranes
Presynaptic Terminals/pathology
Nonsynaptic plasticity
Hippocampus
Synaptic Transmission
Synaptic vesicle
Nerve Regeneration/physiology
Nerve Degeneration/etiology/ pathology/physiopathology
Organ Culture Techniques
Microscopy
Electron
Transmission
Synaptic augmentation
Neural Pathways
Animals
Pyramidal Cells/pathology
Synapses/ pathology
Neuronal Plasticity
Cell Death
Chemistry
Pyramidal Cells
Excitatory Postsynaptic Potentials
Cell Death/physiology
Synaptic Vesicles/pathology
Neuronal Plasticity/physiology
Nerve Regeneration
ddc:616.8
Rats
Disease Models
Animal
Synaptic fatigue
Animals
Newborn
Synaptic Transmission/physiology
Synaptic Membranes/pathology
Hypoxia-Ischemia
Brain
Nerve Degeneration
Synapses
Synaptic plasticity
Excitatory postsynaptic potential
Hippocampus/blood supply/ pathology/physiopathology
Hypoxia-Ischemia
Brain/ pathology/physiopathology
Synaptic Vesicles
Neural Pathways/blood supply/pathology/physiopathology
Postsynaptic density
Neuroscience
Zdroj: Hippocampus, Vol. 16, No 10 (2006) pp. 814-825
ISSN: 1098-1063
1050-9631
Popis: Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen-glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity.
Databáze: OpenAIRE
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