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Increased cell fusion in cerebral cortex may contribute to poststroke regeneration.

Paltsyn A, Komissarova S, Dubrovin I, Kubatiev A.

Stroke Res Treat. 2013;2013:869327.

Institute of General Pathology and Pathophysiology of the Russian Academy of Medical Sciences, Baltiskaya Street 8, Moscow 125315, Russia ; Russian Medical Academy of Postgraduate Education, Moscow, Russia.

 

Abstract

 

In this study, we used a model of a hemorrhagic stroke in a motor zone of the cortex in rats at the age of 3 months The report shows that cortical neurons can fuse with oligodendrocytes. In formed binuclear cells, the nucleus of an oligodendrocyte undergoes neuron specific reprogramming. It can be confirmed by changes in chromatin structure and in size of the second nucleus, by expression of specific neuronal markers and increasing total transcription rate. The nucleus of an oligodendrocyte likely transforms into a second neuronal nucleus. The number of binuclear neurons was validated with quantitative analysis. Fusion of neurons with oligodendrocytes might be a regenerative process in general and specifically following a stroke. The appearance of additional neuronal nuclei increases the functional outcome of the population of neurons. Participation of a certain number of binuclear cells in neuronal function might compensate for a functional deficit that arises from the death of a subset of neurons. After a stroke, the number of binuclear neurons increased in cortex around the lesion zone. In this case, the rate of recovery of stroke-damaged locomotor behavior also increased, which indicates the regenerative role of fusion.

 

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Additional information:

Quantitative expression of any function is defined by number of  participating structures . There are structures among  intracellular ones  whose number doesn’t change. These are genes and their number defines quantity of all other structures responsible for any function. Therefore, functional loading which any population of neurons can carry out, is defined by the general genomic fund of this population, i.e. the amount  of all genes in all neurons. In case of  neurons’ death the fund of the  population is reduced, but it is not the main reason of age degradation of  brain. Now it is found out  that in normal life not  so many neurons are got lost. Another issue is  worse:  the number of synapses decrease with aging,  gets down synaptic tenacity and level of an expression of genes. These phenomenas without reducing the number of genes in fund make the  fund insufficient for performing  necessary volume of function. The influence  on brain function due to the  loss of synapses, weakening of synoptic connections and decrease in level of an expression of genes is equivalent to death of neurons. According to modern concepts these  age changes  are responsible for cognitive and physical decline in old age. Reduction of genomic fund of other organs is compensated by reproduction of cells providing function. But neurogenesis  was not discovered in many  brain’s parts. However it doesn’t mean that the brain doesn’t regenerate.  Fusion of neurons with oligodendrocytes and the subsequent neuron specific reprogramming of oligodendrocytic nuclei increases number of neuronal genomes in a brain, fills up the  fund. Second nucleus’ apperance  in neuron creates genomic provision for forming of many new sprouts and thousands new synapses. We suppose that is how the loss of the main property of nervous system –  connections – caused by age or some pathogenic factor is compensated.