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PubMed1977

Glycoproteins are modified in the axon of R2, the giant neuron of Aplysia californica, after intra-axonal injection of [3H]N-acetylgalactosamine.

We have found evidence that mechanisms exist in the axon by which proteins, originally synthesized in the cell body, can be modified. Incorporation of [3H]N-acetyl-D-galactosamine into macromolecules was studied in the axon of R2, the giant identified neuron of the abdominal ganglion of Aplysia. The precursor sugar, injected directly into the major axon in the right connective, labeled both glycoproteins and glycolipids. These macromolecules were associated with membranes and at least 90% of the incorporated radioactivity could be sedimented by centrifugation at 105,000 X g. Radiocutography of injected axons with the light microscope showed that most of the silver grains were located over the axon rather than over other tissues in the right connective. Grains appeared over a variety of axonal components, but quantitative electron microscopic radioautography revealed that vesicles were the only organells significantly labeled. Disco polyacrylamide gel electrophoresis in sodium dodecyl sulfate (SDS) of the membrane fraction resolved [5-(3)H]glycoprotein components. These membrane glycoproteins ranged in apparent molecular weight from 20,000 to 160,000 daltons and could be digested by pronase. Only one component had a mobility similar to that of a glycoprotein found in the axon after injection of the cell body. Incorporation of [3H]N-acetylgalactosamine into axonal glycoprotein was unaffected by anisomycin, a potent inhibitor of protein synthesis in Aplysia, and therefore presumably occurred on already existing polypeptide chains. We conclude that these were synthesized in the cell body and exported into the axon where they were modified by the addition of sugar.

Acetylgalactosamine↗

PubMed1986

Axon development in mouse cerebellum: embryonic axon forms and expression of synapsin I.

A fundamental question in central nervous system development is the timing of synaptogenesis in relation to invasion of targets by afferent axons. A related question is how growth cones transform into synaptic terminals. These two aspects of axon maturation were examined in developing mouse cerebellum, by labeling single axons with horseradish peroxidase, to study their form and cytology, and by immunocytochemical staining of a synaptic vesicle antigen, synapsin I, a phosphoprotein found on synaptic vesicles in all mature CNS synapses. From embryonic day 16 to postnatal day 3, horseradish peroxidase-labeled afferent axons extend well into the cerebellum and have simple forms. At embryonic day 16, axon growing tips are synapsin I-negative. Synapsin I is first expressed at embryonic day 17, and by embryonic day 18, fibers are stained throughout the cerebellum. Synapsin I expression coincides with a general increase in synaptic specializations, although growing tips continue to have the cytology of growth cones. During the period that axons have primitive shapes, synapsin I is distributed throughout the terminal arbor, corresponding to the presence of small vesicles along neurite lengths, even at non-synaptic sites. After postnatal day 3, when synaptic terminals develop into stereotypic shapes and engage in characteristic synaptic relations, synapsin I is restricted to boutons. Thus, the synapse-specific protein synapsin I is expressed in fetal mouse brain, long before nerve endings have the structure and connections of adult brain. In cerebellar axons, the expression of this protein follows axon arrival, coincides with the appearance of elementary synapses, and accompanies the transformation of growing tips into stereotypic synaptic boutons. The time course of expression of synapsin I, a phosphoprotein that may be involved in synaptic efficacy, suggests that transmitter release may influence early axon-target cell interactions.

Animals↗

PubMed2005

Cell death and axon regeneration of Purkinje cells after axotomy: challenges of classical hypotheses of axon regeneration.

Although adult mammalian neurons are able to regenerate their axons in the peripheral nervous system under certain conditions, they are not able to do it in the central nervous system. The environment surrounding the severed axons appears to be a key factor for axon regeneration. Many studies aiming to enhance axon regeneration in the CNS of adult mammals have successfully manipulated this environment by adding growth permissive molecules and/or neutralizing growth inhibitory molecules. In both cases, the number of axons able to regenerate was low and the different neuronal populations were not equal in their regenerative response, suggesting that manipulation of the environment is not always sufficient. This is particularly well illustrated in the cerebellar system, in which axotomized inferior olivary neurons regenerate when confronted with a permissive environment, whereas mature Purkinje cells do not. The intrinsic ability of a neuron to regenerate its axon is generally correlated with the intensity of its reaction to axotomy (expression of molecules, probability to die). Furthermore, molecules such as GAP-43 (growth-associated molecule) and c-Jun are involved in both axon regeneration and cell death suggesting that these two processes are linked. Surprisingly, Purkinje cells lose their capacity to regenerate their axon (even in the absence of myelin) during development before losing their capacity to react to an axotomy by cell death. These results emphasize the different reactions to axotomy between neuron types and underline that in Purkinje cells, the two cell decisions (axon regeneration and cell death) are differently regulated and therefore not part of the same signaling pathway.

Animals↗

PubMed2005

A little nip and tuck: axon refinement during development and axonal injury.

While building the nervous system, regions of some developing axons are eliminated; this can also happen as a result of axonal injury. During development, many axon branches that are formed in excess of an organism's needs are fated for removal in a process called axon pruning. By contrast, when axons are injured the axon segment distal to the injury site is compartmentalized and eliminated. In both cases, the end result is similar -- a region of an axon is selected for removal. Recent evidence suggests that there are some similarities in the cellular and molecular mechanisms that regulate axon elimination in development and during axonal injury.

Animals↗

PubMed2005

Myelin-associated glycoprotein and complementary axonal ligands, gangliosides, mediate axon stability in the CNS and PNS: neuropathology and behavioral deficits in single- and double-null mice.

Complementary interacting molecules on myelin and axons are required for long-term axon-myelin stability. Their disruption results in axon degeneration, contributing to the pathogenesis of demyelinating diseases. Myelin-associated glycoprotein (MAG), a minor constituent of central and peripheral nervous system myelin, is a member of the Siglec family of sialic acid-binding lectins and binds to gangliosides GD1a and GT1b, prominent molecules on the axon surface. Mice lacking the ganglioside biosynthetic gene Galgt1 fail to express complex gangliosides, including GD1a and GT1b. In the current studies, CNS and PNS histopathology and behavior of Mag-null, Galgt1-null, and double-null mice were compared on the same mouse strain background. When back-crossed to >99% C57BL/6 strain purity, Mag-null mice demonstrated marked CNS, as well as PNS, axon degeneration, in contrast to prior findings using mice of mixed strain background. On the same background, Mag- and Galgt1-null mice exhibited quantitatively and qualitatively similar CNS and PNS axon degeneration and nearly identical decreases in axon diameter and neurofilament spacing. Double-null mice had qualitatively similar changes. Consistent with these findings, Mag- and Galgt1-null mice had similar motor behavioral deficits, with double-null mice only modestly more impaired. Despite their motor deficits, Mag- and Galgt1-null mice demonstrated hyperactivity, with spontaneous locomotor activity significantly above that of wild type mice. These data demonstrate that MAG and complex gangliosides contribute to axon stability in both the CNS and PNS. Similar neuropathological and behavioral deficits in Galgt1-, Mag-, and double-null mice support the hypothesis that MAG binding to gangliosides contributes to long-term axon-myelin stability.

Animals↗

PubMed1995

Optic nerve axon count and axon diameter in patients with ocular hypertension and normal visual fields.

BACKGROUND: At postmortem examination, the authors obtained eight eyes of five individuals with elevated intraocular pressure and normal visual fields to study the axon count and mean axon diameter. METHODS: Automated image analysis was used to calculate the total axon count and mean axon diameter per nerve and per nerve segment for each eye. The authors applied the method of identification analysis to compare each study eye with a corresponding normal eye of patients of the same age. RESULTS: There was no statistically significant difference compared with control subjects for total axon count or segmental axon count for any of the eyes. Two eyes showed a statistically significant difference for mean axon diameter for the whole nerve but not for individual segments of the nerve. CONCLUSIONS: Some eyes subjected to varying duration and magnitude of intraocular pressure elevation with normal visual fields may maintain normal axon counts and mean axon diameters.

Aged↗

PubMed1992

Neurolin, a cell surface glycoprotein on growing retinal axons in the goldfish visual system, is reexpressed during retinal axonal regeneration.

The mAb E 21 recognizes a cell surface glycoprotein selectively associated with fish retinal ganglion cell axons that are in a state of growth. All retinal axons and ganglion cells in goldfish embryos stained for E 21. In adult fish, however, E 21 immunoreactivity exhibited a patterned distribution in ganglion cells in the marginal growth zone of the continuously enlarging fish retina and the new axons emerging from these cells in the retina, optic nerve, and optic tract. The E 21 antigen was absent from older axons, except the terminal arbor layer in the tectum, the Stratum fibrosum et griseum superficiale where it was uniformly distributed. Upon optic nerve transection, the previously unlabeled axons reacquired E 21 positivity as they regenerated throughout their path to the tectum. Several months after ONS, however, E 21 staining disappeared from the regenerated axons over most of their lengths but reappeared as in normal fish in the terminal arbor layer. The immunoaffinity-purified E 21 antigen, called Neurolin, has an apparent molecular mass of 86 kD and contains the HNK1/L2 carbohydrate moiety, like several members of the class of cell adhesion molecules of the Ig superfamily. The NH2-terminal amino acid sequence has homologies to the cell adhesion molecule DM-Grasp recently described in the chicken. Thus, retinal ganglion cell axons express Neurolin during their development and are able to reexpress this candidate cell adhesion molecule during axonal regeneration, suggesting that Neurolin is functionally important for fish retinal axon growth.

Activated-Leukocyte Cell Adhesion Molecule↗

PubMed1995

Axonal synthesis of phosphatidylcholine is required for normal axonal growth in rat sympathetic neurons.

The goal of this study was to assess the relative importance of the axonal synthesis of phosphatidylcholine for neurite growth using rat sympathetic neurons maintained in compartmented culture dishes. In a double-labeling experiment [14C]choline was added to compartments that contained only distal axons and [3H]choline was added to compartments that contained cell bodies and proximal axons. The specific radioactivity of labeled choline was equalized in all compartments. The results show that approximately 50% of phosphatidylcholine in distal axons is locally synthesized by axons. The requirement of axonal phosphatidylcholine synthesis for neurite growth was investigated. The neurons were supplied with medium lacking choline, an essential substrate for phosphatidylcholine synthesis. In the cells grown in choline-deficient medium for 5 d, the incorporation of [3H]palmitate into phosphatidylcholine was reduced by 54% compared to that in cells cultured in choline-containing medium. When phosphatidylcholine synthesis was reduced in this manner in distal axons alone, growth of distal neurites was inhibited by approximately 50%. In contrast, when phosphatidylcholine synthesis was inhibited only in the compartment containing cell bodies with proximal axons, growth of distal neurites continued normally. These experiments imply that the synthesis of phosphatidylcholine in cell bodies is neither necessary nor sufficient for growth of distal neurites. Rather, the local synthesis of phosphatidylcholine in distal axons is required for normal growth.

Animals↗

PubMed2002

Axonal injury in children after motor vehicle crashes: extent, distribution, and size of axonal swellings using beta-APP immunohistochemistry.

The brains of 32 children (3 months to 16 years) who died as a result of motor vehicle collisions were examined for axonal injury using beta-APP immunohistochemistry. The extent and distribution of axonal injury was assessed and quantified throughout the forebrain, brainstem and cerebellum. The mean diameter of immunoreactive axons in the corpus callosum was measured for this pediatric group and, for comparison, a small adult sample. beta-APP immunoreactivity was seen in 14 pediatric cases (survival 35 mins to 87 h), most frequently in the parasagittal white matter (12/14), the corpus callosum (11/14), the brainstem (10/14) and cerebellum (9/14). In 2 cases, axon swelling was visualized in the internal capsule after only 35-45-min survival, earlier than has previously been reported. No immunoreactivity was seen in the remaining 18 cases who died within 1 h. The extent and distribution of axonal injury throughout the brain showed a rapid early increase with increasing survival time and then a slower progression. The diameter of individual callosal axons increased with increasing survival times, rapidly over the first 24 h and then more slowly. There was no statistical difference (p < 0.05) for callosal axon diameters at different survival times between the children and the adults sampled here. The extent and distribution of axonal injury throughout the brain appears to be similar in children to that previously reported in adults. The spatial and temporal spread of axonal damage suggests there may be therapeutic potential for the process to be arrested or slowed in its early stages.

Accidents, Traffic↗

PubMed2003

Post-acute alterations in the axonal cytoskeleton after traumatic axonal injury.

All previous analyses of axonal responses to traumatic axonal injury (TAI) have described the ultrastructure of changes in the cytoskeleton and axolemma within 6 h of injury. In the present study we tested the hypothesis that there are, in addition, ultrastructural pathological changes up to 1 week after injury. TAI was induced in the adult guinea pig optic nerve of nine animals. Three animals were killed at either 4 h, 24 h, or 7 days (d) after injury. Quantitative analysis of the number or proportion of axons within 0.5-micro m-wide bins showed an increase in the number of axons with a diameter of less than 0.5 micro m at 4 h, 24 h, and 7 d, the presence of lucent axons at 24 h and 7 d and that the highest number of injured axons occurred about half way along the length of the nerve. A spectrum of pathological changes occurred in injured fibers-pathology of mitochondria; dissociation of myelin lamellae but little damage to the axon; loss of linear register of the axonal cytoskeleton; differential responses between microtubules (MT) and neurofilaments (NF) in different sizes of axon; two different sites of compaction of NF; loss of both NF (with an increase in their spacing) and MT (with a reduction in their spacing); replacement of the axoplasm by a flocculent precipitate; and an increased length of the nodal gap. These provide the first ultrastructural evidence for Wallerian degeneration of nerve fibers in an animal model of TAI.

Animals↗

PubMed2000

Topography and severity of axonal injury in human spinal cord trauma using amyloid precursor protein as a marker of axonal injury.

STUDY DESIGN: Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI. OBJECTIVES: To topographically map and semiquantitate axonal injury in spinal cord compression of sufficient severity to produce para- or quadriplegia. SUMMARY OF BACKGROUND DATA: Amyloid precursor protein is carried along the axon by fast axoplasmic transport and has been extensively used as a marker of traumatic axonal injury. METHODS: The study group comprised 18 cases of spinal cord compression (17 due to fracture dislocation of the vertebral column and 1 iatrogenic compression from Harrington rods) and two normal control. All the cords were examined according to a standard protocol, and at least 10 segmental levels were immunostained using a monoclonal antibody to amyloid precursor protein and immunopositive AI was semiquantitated using a grading system to provide the axonal injury severity score (AISS). The focal injury at the site of cord compression (haemorrhage, haemorrhagic necrosis, ischaemic necrosis) was also semiquantitated to provide the focal injury area score (FIAS). AI occurring around the site of focal compression (focal axonal injury severity score or FAISS) was distinguished from AI distant to the focal injury (nonfocal axonal injury severity score or NFAISS). RESULTS: All 18 cases showed widespread amyloid precursor protein immunoreactive axonal injury and the AISS ranged from 28 to 60%. In all cases, the FAISS was greater than the NFAISS and there was a statistically significant relationship between the AISS and the FIAS. CONCLUSION: Acute spinal cord compression of sufficient severity to produce permanent paralysis causes widespread axonal damage that is maximal at the site of compression but also present throughout the length of the cord in segments far distant from the site of the focal injury.

Adolescent↗

PubMed1993

Persistence of axonal transport in isolated axons of the mouse.

We have examined the hypothesis, for the case of mouse axons, that isolating an axon from its cell body will lead to a rapid failure of fast axonal transport as anterogradely moving organelles vacate the axon in a proximo-distal direction, and retrogradely moving organelles vacate it in the opposite direction. We used CD1 and BALB/c mice and the Wallerian degeneration-resistant mutant C57BL/Ola. Sciatic nerves were cut high in the thigh; at various times up to 8 days later nerves were removed from the animal and individual myelinated axons from the segment distal to the cut were examined by video light microscopy to detect rapid organelle transport. Bidirectional fast organelle transport did decrease in amount with time but not nearly as rapidly as predicted, and anterograde and retrograde organelle velocities remained normal through time. In the C57BL/Ola mouse some structurally preserved axons contained organelles that transported at normal velocities in the anterograde and retrograde directions for as long as 8 days after axotomy. To test one of the possible origins of transported organelles in long-surviving axons we examined organelle transport very close to narrow lesions in axons bathed in a medium compatible with intracellular function. No organelles crossed the lesion but bidirectional organelle transport took place proximal and distal to the lesion; the amounts were compatible with the interpretation that approximately 30% of organelles reversed transport direction on either side of the lesion. We propose that at least some of the organelles that undergo persistent transport in axons isolated from their cell bodies shuttle back and forth between the ends of the isolated segment.

Animals↗

PubMed1986

Multiple axon collaterals of single corticospinal axons in the cat spinal cord.

To investigate intraspinal branching patterns of single corticospinal neurons (CSNs), we recorded extracellular spike activities from cell bodies of 408 CSNs in the motor cortex in anesthetized cats and mapped the distribution of effective stimulating sites for antidromic activation of their terminal branches in the spinal gray matter. To search for all spinal axon branches belonging to single CSNs in the "forelimb area" of the motor cortex, we microstimulated the gray matter from the dorsal to the ventral border at 100-micron intervals at an intensity of 150-250 microA and systematically mapped effective stimulating penetrations at 1-mm intervals rostrocaudally from C3 to the most caudal level of their axons. From the depth-threshold curves, the comparison of the antidromic latencies of spikes evoked from the gray matter and the lateral funiculus, and the calculated conduction times of the collaterals, we could ascertain that axon collaterals were stimulated in the gray matter rather than stem axons in the corticospinal tract due to current spread. Virtually all CSNs examined in the forelimb area of the motor cortex had three to seven branches at widely separated segments of the cervical and the higher thoracic cord. In addition to terminating at the brachial segments, they had one to three collaterals to the upper cervical cord (C3-C4), where the propriospinal neurons projecting to forelimb motoneurons are located. About three quarters of these CSNs had two to four collaterals in C6-T1. This finding held true for both fast and slow CSNs. About one third of the CSNs in the forelimb area of the motor cortex projected to the thoracic cord below T3. These CSNs also sent axon collaterals to the cervical spinal cord. CSNs in the "hindlimb area" of the motor cortex had three to five axon branches in the lumbosacral cord. These branches were mainly observed at L4 and the lower lumbosacral cord. None of these CSNs had axon collaterals in the cervical cord. CSNs terminating at different segments of the cervical and the thoracic cord were distributed in a wide area of the motor cortex and were intermingled. To determine the detailed trajectory of single axon branches, microstimulation was made at a matrix of points of 100 or 200 micron at the maximum intensity of 30 microA, and their axonal trajectory was reconstructed on the basis of the location of low-threshold foci and the latency of antidromic spikes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

Oligodendrocytes repel axons and cause axonal growth cone collapse.

We have examined the interactions between axons regenerating from dorsal root ganglia (DRGs) derived from newborn rats and oligodendrocytes cultured by three different techniques. Cultures examined after 2 days have a profuse outgrowth of axons from the DRGs, forming a dense mat on the culture surface. However, the axons avoid growing on oligodendrocytes; axons are seen all around these cells, but do not grow over them. We have also performed time-lapse video studies of the interactions between axonal growth cones and oligodendrocytes. Axons grow normally until their growth cone comes into direct contact with an oligodendrocyte, following which the growth cone remains motile for 30-60 min, but without making any progress over the cell. The growth cone then suddenly collapses, and the axon retracts, leaving a thin strand in contact with the cell. After this a new growth cone is usually elaborated and the process repeated. Oligodendrocytes are therefore inhibitory to axonal growth, and this may partially explain the failure of axons to regenerate in the mammalian central nervous system.

Animals↗

PubMed1989

Axonal injury in the optic nerve: a model simulating diffuse axonal injury in the brain.

A new model of traumatic axonal injury has been developed by causing a single, rapid, controlled elongation (tensile strain) in the optic nerve of the albino guinea pig. Electron microscopy demonstrates axonal swelling, axolemmal blebs, and accumulation of organelles identical to those seen in human and experimental brain injury. Quantitative morphometric studies confirm that 17% of the optic nerve axons are injured without vascular disruption, and horseradish peroxidase (HRP) studies confirm alterations in rapid axoplasmic transport at the sites of injury. Since 95% to 98% of the optic nerve fibers are crossed, studies of the cell bodies and terminal fields of injured axons can be performed in this model. Glucose utilization was increased in the retina following injury, confirming electron microscopic changes of central chromatolysis in the ganglion cells and increased metabolic activity in reaction to axonal injury. Decreased activity at the superior colliculus was demonstrated by delayed HRP arrival after injury. The model is unique because it produces axonal damage that is morphologically identical to that seen in human brain injury and does so by delivering tissue strains of the same type and magnitude that cause axonal damage in the human. The model offers the possibility of improving the understanding of traumatic damage of central nervous system (CNS) axons because it creates reproducible axonal injury in a well-defined anatomical system that obviates many of the difficulties associated with studying the complex morphology of the brain.

Animals↗

PubMed1990

[Abnormalities of axonal transport as pathogenesis of axonal degeneration in peripheral neuropathy].

Axonal transport is a universal property of nerve cells. Role of axonal transport abnormalities in the pathogenesis of peripheral neuropathies was discussed. Applications of isotope-labeling technique to the study of axonal transport in experimental neuropathy have provided insights into the pathogenesis of axonal degeneration. As a model of dying-back neuropathy, axonal transport has been studied in sciatic motor neurons of rats with neuropathy induced by p-bromophenylacetylurea (BPAU) using this technique. The velocity of rapid anterograde transport was unaffected in this neuropathy and amount of retrograde axonal transport was reduced. The lag time between precursor injection and the onset of transport was shorter in BPAU-treated rats than controls. Whereas, in experimental ethylene oxide (EO) neuropathy rats, rapid transport velocity was markedly reduced in spite of very mild results of morphometric study. Those rapid axonal transport abnormalities may explain some aspects of the pathogenesis of peripheral neuropathies. In BPAU neuropathy model, disturbance of assembly of membrane-limited vesicles in Golgi processing may play a role in turnaround defect which causes dying-back neuropathy. EO neuropathy model suggests the possibility of oxygen utilization disturbance may causes energy dependent rapid transport velocity. Moreover, environments surrounding axon are also important for function of axonal transport. Present information leads to the conclusion that abnormalities in the supply and deposition of transported materials occur in early course of peripheral neuropathy and may contribute to development of the neuropathy.

Animals↗

PubMed1985

The neuronal endomembrane system. III. The origins of the axoplasmic reticulum and discrete axonal cisternae at the axon hillock.

The axoplasmic reticulum (AR) and the discrete element (e.g., vesicles, vesiculotubular bodies, multivesicular bodies, etc.) constitute the endomembrane system of the axon. It is reported here that the AR of bullfrog sciatic nerve readily fills with osmium deposits during osmium impregnation. In contrast, the discrete elements and mitochondria are highly resistant to impregnation. Hence this preparation is well suited to address the nature of possible interactions between AR and rough endoplasmic reticulum (RER) in the axon hillock. It is also ideal to study the origin of the axonal discrete elements within the cell body as well as their interaction with other somal endomembrane system components. Tissues used in the present study were spinal ganglia, sciatic nerve, and spinal roots from Rana catesbeiana. Thick sections (1 to 2 microm) of this material were studied by high voltage electron microscopy. In some cases, osmium impregnation was followed by en bloc staining with lead aspartate. This made visible membranous structures that had not filled with osmium deposits during impregnation. Serial 170-nm-thick sections of this latter material were prepared and serial stereo pair electron micrographs of axon hillocks were collected. These were used to reconstruct three-dimensionally the AR and to study its relationship with RER and with discrete elements. The impregnated AR within the axon hillock was found to terminate as many proximally pointing finger-like projections. A large portion of these projections were found to form connections with RER. Some, however, terminated as true blind endings. Single unimpregnated discrete cisternae were found throughout the cytoplasm of the cell body, axon hillock, and axon. Large clusters of unimpregnated vesicles were usually found in close association with the trans face of the Golgi apparatus. These results indirectly support the hypothesis that vectors of fast axonal transport, namely the discrete elements, form directly at the trans face of the Golgi apparatus. From here they move toward and subsequently down the axon without any membrane fission-fusion events with either RER or AR. AR, although it forms continuities with RER, retains a distinctly different chemical composition from RER as evidenced by its much higher affinity for osmium. Thus, it should be considered as an endomembrane component separate from, although intimately related to the RER.

Animals↗

PubMed1978

Quantitative studies on the maturation of central and peripheral parts of individual ventral motoneuron axons. I. Myelin sheath and axon calibre.

The entire lengths of central and peripheral myelin sheaths on the same ventral motoneuron axons of young rats were studied during the rapid early phase of myelination which occurs during the first 2 weeks after birth. Sheath thickness varied along central internodes at all ages, though this variation was less in the more mature sheaths. Usually there was a single level of maximum thickness, most often near the middle of the internode, but frequently close to one end. Some sheaths varied little in thickness along their lengths; a few were bimodal. The number of turns decreased on either side of the maximum as the sheath was traced towards the bounding nodes. Comparison of serially adjacent sheaths along the same axon showed no relationship between their mean thickness or patterns of longitudinal thickness variation. Patterns of thickness variation in peripheral sheaths were very similar to those found centrally. At a given age, however, peripheral sheaths were less variable along more than twice that of central internodes belonging to the same fibre. At first, the unrolled glial unit was oval in outline while the unrolled Schwann cell was trapezoidal. Subsequently, both eventually became trapezoidal. The calibre of central and peripheral stretches of the same ventral motoneuron axons were also compared with one another in young rats during the first 2 weeks after birth. At each age, the great majority of axons were thicker peripherally than centrally. The mean circumference of the peripheral segment exceeded that of the central by a factor which averaged 1.3 over the period studied. Circumference varied from one level to another along both central and perpheral stretches of the same axons. The degree of this variation differed considerably from one axon to another. In many central fibres, and in all peripheral stretches of fibres, calibre variation followed no particular pattern. However, the calibre of some central axon segments gradually increased as the fibre was traced distally towards the cord surface. A proportion of axons was dilated just deep to the cord surface. These dilatations were frequently myelinated. No association was found between patterns of longitudinal variation in axon calibre and in sheath thickness along the same fibre.

Aging↗