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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2009; 55(3): 109-117


Morphological plasticity of hippocampal ca1 neurons in vitroafter short-term anoxia/hypoglycemia followed by reoxygenation

I.V.lushnikovA.

    O.O. Bogomoletz Institute of Physiology NationalAcademy Sciences of Ukraine, Kyiv


Abstract

Oxygen and glucose are known to modulate the neuronal plas­ticity. Their fluctuations have ability to induce cell damage, the degree of which is thought to depend on the intensity and dura­tion of pathological events. Experimental investigations have shown that a short-term anoxia-hypoglycemia results in delayed cell destruction through multiple cellular and molecular mecha­nisms and these processes are accompanied by certain morphological alterations. The aim of the present study was to evaluate the neuronal, synaptic and glial plasticity in hippocam-pal CA1 area after short-term (10 min) oxygen-glucose depri­vation (OGD) followed by reoxygenation during 1 h. The ex­periments were carried out on hippocampal slice cultures. We estimated the following parameters: viability and condensation of CA1 neurons, the number and volume of the simple and complex asymmetric synapses, postsynaptic density (PSD) thick­ness, total vesicle number and the state of vesicle pools, the glial volume contacted with CA1synapses. It is revealed that 10 min OGD has no influence on cell viability and condensation but the synapse number and volume have the tendency for reduction. Though, we found some changes in synaptic remodeling (an increase in PSD thickness, a decrease in the total vesicle number and the density of the active and reserve vesicle pools) and significant increase of the glial volume contacted with CA1synapses. Thus, it was assumed that the early structure changes could be the reason of the functional abnormality and tissue damage. Our data confirm also the glial ability to modu­late the neuronal function.

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