What type of nerve fibers are myelinated

Separating adjacent lengths of myelin are the nodes of Ranvier, where the axons are bare. Transverse sections through nodes of Ranvier can be identified by the electron dense undercoating of the axolemma and a cytoplasm that commonly shows an increase in the frequency of profiles of microtubules Figs. It is at nodes of Ranvier that myelinated nerve fibers branch Fig. Adjacent to the nodes of Ranvier are the paranodes, where the spiraled lamellae of myelin gradually terminate Fig.

Between the paranodes is the extensive intersegmental myelin sheath. The myelin sheaths in the central nervous system are formed by a pair of layers of the plasma membrane of the myelin- forming oligodendrocyte. The paired plasma membranes wrap around a length of the enclosed axon in a spiral fashion, with the outer surfaces of the paired plasma membrane being apposed to each other to form the intraperiod line of the mature sheath. During development the cytoplasmic surfaces of the paired plasma membrane are separated by oligodendrocyte cytoplasm, but as the sheath matures the cytoplasm is lost and the cytoplasmic surfaces of the plasma membrane become apposed to form the major dense line of the sheath.

However, in the mature sheath some cytoplasm is retained in the inner and outer ends of the spiraled plasma membranes and in transverse sections of mature myelinated nerve fibers this cytoplasm is seen to be contained in the inner and outer tongue processes of cytoplasm Fig.

Obviously these tongues of cytoplasm are sections through ridges of cytoplasm that extend along the length of the segment of myelin and at some point the outer tongue is in continuity with a cell processes that connects the segmental length of myelin to the cell body of the parent oligodendrocyte. At the ends of the myelin segments are the paranodes, where the myelin sheath gradually becomes thinner as it approaches the node of Ranvier and the spiraled turns of myelin terminate.

However, breakdown products of myelin constituents, as well as exotic high molecular substances, not present in conventional myelin, can also be found. In addition, the myelinoid body fraction contains proteolytic activity. Studies using isotope labelling of myelin proteins show a source-product relation between myelin and myelinoid bodies. Altogether these data strongly support the hypothesis that myelinoid bodies reflect the catabolic side of myelin turnover.

These axons exhibit focally differentiated axolemmal areas. Nodes of Ranvier arrows are stained in green by an antibody to nodal molecule beta-IV spectrin. This image is linked to the following Scitable pages:. How does our nervous system operate so quickly and efficiently? The answer lies in a membranous structure called myelin.

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Where the plasma membrane on the inner faces of these pockets meet the axolemma, the two membranes, become very close to each other and form a junctional complex. There could be two reasons for these age-related increases in paranodal profiles. One is an increase in the lengths of the paranodes with age. The second is an overall increase in the numbers of paranodes. Consequently, the increase in frequency has to be due to an increase in the overall numbers of internodal lengths of myelin.

This would occur if remyelination were taking place, such that some of the original internodal lengths of myelin degenerate and are replaced by shorter internodes. The accepted hallmarks of remyelination are the presence of short internodes and of sheaths that are inappropriately thin for the size of the enclosed axons e.

Such internodes have been found in the aging central nervous system. We have not been able to identify demyelinated nerve fibers in the monkey brain, but this should not be a surprise, since such demyelinated nerve fibers would be expected to resemble unmyelinated nerve fibers.

However, in support of the fact that demyelination is taking place, we have seen fragments of degenerating myelin within the cytoplasm of both microglia, and more commonly within astrocytes in the brains of aging monkeys. Also some of the amorphous phagocytosed material within the cytoplasm of astrocytes in the cerebral cortex of old monkeys labels for antibodies to myelin basic protein Peters and Sethares, A recent article on the remyelination of rubrospinal nerve fibers that remyelinate after a contusion lesion of the spinal cords of mice serves to shed some light on what is happening during aging.

Lasiene et al. There is also evidence that there are reductions in conduction velocity in the nerve fibers of aging cats Morales et al. A reduction in conduction velocity also occurs in demyelinating diseases e.

Felts et al. Consequently, it can be assumed that remyelinated nerve fibers with shorter internodes in the aging monkey also have a slower conduction rate than the nerve fibers that remain unaffected by age, and that this would affect the timing in neuronal circuits e.

The reason for this correlation between CII and paranodal frequency may have to do with the unique role of prefrontal cortex in cognition. Similar dense inclusions also occur in the perikarya of old oligodendrocytes Peters, ; Peters and Sethares, ; Peters et al.

Similar swellings along oligodendrocyte processes have been reported in twitcher mice, which are a model for globoid leukodystrophy, and Levine and Torres suggest that the material in the swellings comes from components of myelin sheaths that are being renewed.

Most probably the material is produced by degeneration of some components of the myelin sheaths that belong to the oligodendrocytes, and it is tempting to suggest that the material is related to the dense cytoplasm that accumulates between the lamellae of some sheaths in old monkeys. Figure 4. Electron micrograph of an oligodendrocyte in layer 6 of area 17 of a year-old rhesus monkey.

Three processes, p1—p3, extend from the cell body. One of the processes, p1, has a swelling that contains dense inclusions, which are similar to the dense inclusions in the cell body. Note the large swelling arrow on one of the processes. It is similar to the one seen on process p1 in the accompanying electron micrograph. Area 46 of a year-old monkey. It is also common in old monkeys to find oligodendrocytes in pairs, rows and groups, suggesting that oligodendrocytes may be proliferating with age Peters and Sethares, ; Peters et al.

In a more recent study an assessment was made of the effects of age on the populations of neuroglial cells throughout the depth of monkey primary visual cortex Peters et al. It was seen that the numbers of oligodendroglial cells in the various layers essentially reflects the frequency of myelinated nerve fibers within them, the greatest numbers of oligodendrocytes being in the deeper layers.

In contrast, there are no changes in the frequency of either astrocytes or microglial cells with age. There is also an increase in the frequency of oligodendrocytes in monkey optic nerve with age Sandell and Peters, , as well as in the fornix unpublished data , but not in the anterior commissure Sandell and Peters, The reason for this difference is not yet apparent.

What is the origin of the increased numbers of oligodendrocytes that are generated, and why are they necessary? The formation of groups and rows of oligodendrocytes during aging could be taken to suggest that oligodendrocytes are dividing, but the prevailing view is that mature oligodendrocytes do not divide see Keirstead and Blakemore, ; Ludwin, ; Norton, , and in a study of the generation of new cells in the adult dentate gyrus of the hippocampus in old monkeys using BrdU labeling no labeled oligodendrocytes were found Ngwenya et al.

Levine et al. Studies such as that by Cerghet et al. And interestingly, Cerghet et al. Moreover, Rivers et al. Unfortunately there is no information about the rate of turnover of oligodendrocytes in the adult monkey, but there is no reason to doubt that it is basically different from in rodents.

It is proposed that the following scenario can explain the available data on the effects of age on myelinated nerve fibers in the central nervous system of the monkey. During aging some neurons lose their long projecting myelinated axons that enter white matter, while retaining their local plexuses so that the parent neuron does not die.

The consequence of this is that, as has been demonstrated, some myelinated nerve fibers are lost from white matter, even though there is no significant loss of neurons from the cerebral cortex.

For other neurons the effects of aging are less severe see Figure 5 , since their axons remains intact, even though some of the internodal lengths of myelin that ensheath them degenerate Figure 5 B.

The process of demyelination probably begins as an oligodendrocyte shows stress and starts to accumulate dense inclusions in swellings of its processes and in its perikaryon, as well as in spaces between the lamellae of the myelin sheaths for which the oligodendrocyte is responsible. Ultimately the oligodendrocyte dies, which results in the degeneration and loss of the internodal lengths of myelin belonging to that oligodendrocyte Figure 5 C.

Oligodendrocyte precursor cells are then activated and generate new oligodendrocytes that repair the damage by remyelinating the bare lengths of axons. In the process of remyelination, several new oligodendrocytes are involved in the replacement of the original internode of myelin. These oligodendrocytes produce shorter internodal lengths than the original one, and the new sheaths are thinner Figure 5 D.

Thus, when profiles of sectioned myelin sheaths in older monkeys are examined, it is found there is an increase in the number of profiles of paranodes, and this is accompanied by an increase in the total number of oligodendrocytes. This breakdown of myelin sheaths, together with the formation of shorter internodal lengths of myelin and the consequent increase in the number of nodes of Ranvier, would result in a slowing down of the rate of conduction along affected myelinated nerve fibers.

Consequently the timing in neuronal circuits would be affected and contribute to cognitive impairment that occurs with increasing age. Figure 5. Diagrammatic representation of the degeneration of sheaths with age, and the subsequent remyelination of axons.

A Normal state. B Some sheaths become altered by the presence of dense cytoplasm and the formation of balloons. This is believed to occur when the oligodendrocyte accumulates dense inclusions within its cell body and within swellings along its processes.

C The degeneration of myelin sheaths leaves axons bare. D The bare axons are remyelinated by newly generated oligodendrocytes that form short internodal lengths with thin sheaths. The author declares that this research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author wishes to thank Claire Folger for her continued help and expert technical assistance during the performance of these studies on the aging brain.

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