Biomedical subjects
Publications and source records attributed to A Goncerzewicz.
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Axon-myelin interrelationship was analysed morphometrically in developing optic nerves of Wistar rats maintained during the maturation on normal, lipid deficient and lipid enriched diets. The results obtained lead to the following conclusions: Myelinogenesis in the optic nerve of Wistar rats is severely retarded in animals maintained on a fatty acid deficient diet during the last period of intrauterine life and during their whole postnatal life. The axon diameter of the optic nerves in animals fed on a fatty acid deficient diet is normal in the first weeks of postnatal development, but it does not reach the values of normal ones in the young adult animals. The dietary deficit of fatty acids caused qualitative changes in the myelin-axon interrelationship in the course of myelinogenesis as indicated by an altered distribution of the ratios in the number of myelin lamellae to the axon diameter (the regression equation has changed from a linear to a parabolic one). Comparison of the morphometric and chemical studies of the developing myelin in the fatty acid deficiency experiments testify that the numerically normal myelin in young adult animals is still deficient in basic lipid classes.
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Wallerian degeneration of the rabbit optic nerve was produced by enucleation. The ultrastructure, enzyme histochemistry, myelin output as well as the lipid composition of degenerated nerve were studied. The obtained results lead to following conclusions: 1. Esterified cholesterol appeared in the lipid spectrum of myelin membranes undergoing Wallerian degeneration preceding a significant drop of myelin mass, without an involvement of lipomacrophages and without notable changes in the structure of myelin. 2. Esterification of cholesterol could function as a primary factor injuring the myelin membrane in central Wallerian degeneration, similarly as in other demyelinating processes. 3. Lipomacrophages occurring in the later stage of Wallerian degeneration of the optic nerve are of astroglial origin. 4. The slow progress of phagocytosis in the degenerating optic nerve might explain the almost unaffected pattern of myelin lipids in the course of Wallerian degeneration of this structure. 5. Lysocompounds play an important role in the pathomechanism of demyelination in the central nervous system including the optic nerve during further steps of myelin decay.
The investigations were performed on oligodendroglial cells isolated from the cerebral white matter of Wistar rats treated intravenously with a 3% solution of MNU at a dose of 60 mg/kg body weight. The oligodendroglial fraction showed a decrease of the sphingomyelin, phosphatidylserine and phosphoinositides content. The observed changes correlated with alterations of the lipid spectrum found in the myelin fraction of MNU intoxicated rats. This would indicate that MNU acting in the central nervous system affects in a similar way the lipid metabolism of both components of the oligodendroglia-myelin system.
In adult rabbits, unilateral enucleation was performed and morphological changes resulting from disconnection of the axons from their perikaryons of the optic nerve evaluated by means of light and electron microscopy. The morphological changes were compared with histochemically determined activities of several hydrolytic and oxidoreductive enzymes. The results obtained lead to the following conclusions: 1. Astroglial cells displaying increased enzymic activity of many hydrolases and oxidoreductases constitute the main cellular component of the mature optic nerve undergoing Wallerian degeneration. 2. Oligodendroglial cells of the degenerating optic nerve were found as well inside as in their usual position i.e. outside the axons. These cells displayed only slightly expressed morphological or histochemical signs of an increased biological activity. 3. In the mature optic nerve undergoing Wallerian degeneration some signs of remyelination i.e. formation of an aberrant myelin without proper connection to axons, were observed. 4. An intact functional connection between the perikaryons, the axons and myelin sheaths is in the mature optic nerve not indispensable for initiation of myelinogenesis during Wallerian degeneration.
Unilateral enucleation was performed in 8 days rabbits and morphological changes occurring in the degenerating immature optic nerve were evaluated by means of light and electron microscopy and correlated with histoenzymatic changes in the activity of various phosphatases, esterases and oxidoreductases. The results of these experiments have lead to the following conclusions: 1. In contrast to the marked hyperplasia of the astroglia, the cellularity of the neuroglia of the oligodendroglial line suffered a considerable decrease in the course of Wallerian degeneration of the immature optic nerve. 2. Disconnection of axons from their parental perikaryons caused a considerable delay and reduction of differentiation of the immature neuroglia cells into oligodendrocytes. 3. The histoenzymatic pattern of neuroglia in the immature degenerating optic nerve differs from and bears no relation to that of the normally developing nerve. 4. Cells of the oligodendroglia line, when maturing in contact with degenerating axons are incapable of promoting myelinogenesis. 5. The genetic information contained in both the immature and mature oligodendroglia cells is not the sole factor safeguarding the transformation of these cells into myelinating ones.
Wallerian degeneration of the rabbit optic nerve was produced by enucleation and the myelin output as well as its lipid composition were studied. In spite of the marked drop in the myelin mass, occurring very soon after enucleation the lipid composition of the corresponding myelin fractions did not change appreciably, phosphatidylcholine being the most resistant lipid species. However, from the very beginning of the degenerating process there appeared in the myelin lipid spectrum marked amounts of cholesteryl esters and phosphatidic acids and in the later period elevated amounts of lysophosphatidylcholine. Enhanced esterification of cholesterol could function as an early primary factor injuring the myelin membrane, the lysocompounds may be involved at a later stage in the pathomechanism of myelin decomposition in the central nervous system.
A histochemical study was performed on the activity of several phosphatases, esterases and oxidoreductases in the spinal cord of cat in the course of the myelinopathy provoked by the cerebrospinal fluid (CSF) exchange. The following results were obtained: 1. Neuroglial cells of the spinal cord react with a slight, focal increase of TPP-ase activity already during the early stage of myelinopathy evoked by repeated withdrawal and reinjecting of CSF into the Cisterna magna of experimental cats. 2. During the late stage of this experimental disease-- the oligo-and astroglia of the spinal cord dtsplay considerably increased activities of ATP-ase, acP, and of various oxidoreductases. 3. The observed morphological and functional (increased enzymic activity) changes of the oligodendroglia as well as the demonstrable damage of myelin sheath, seem to be the results of vasogenous edema. 4. The results of investigations performed did not yield any arguments, which would speak in favour of the assumption, that the changes of the oligodendroglia cells function as the primary cause in the myelinopathy provoked by the CSF exchange, affecting secondary the myelin sheaths. 5. The decissively increased lysosomal acP activity in oligodendroglial cells of the spinal cord investigated during the early stage of this myelinopathy, accompanied by an evidently damaged Golgi apparatus, may be explained when the Golgi zone is not necessarily the only cellular site where acid phosphatase may be performed.