Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Axons”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources
PubMed1999

Rapid induction of functional and morphological continuity between severed ends of mammalian or earthworm myelinated axons.

The inability to rapidly restore the loss of function that results from severance (cutting or crushing) of PNS and CNS axons is a severe clinical problem. As a novel strategy to help alleviate this problem, we have developed in vitro procedures using Ca2+-free solutions of polyethylene glycol (PEG solutions), which within minutes induce functional and morphological continuity (PEG-induced fusion) between the cut or crushed ends of myelinated sciatic or spinal axons in rats. Using a PEG-based hydrogel that binds to connective tissue to provide mechanical strength at the lesion site and is nontoxic to nerve tissues in earthworms and mammals, we have also developed in vivo procedures that permanently maintain earthworm myelinated medial giant axons whose functional and morphological integrity has been restored by PEG-induced fusion after axonal severance. In all these in vitro or in vivo procedures, the success of PEG-induced fusion of sciatic or spinal axons and myelinated medial giant axons is measured by the restored conduction of action potentials through the lesion site, the presence of intact axonal profiles in electron micrographs taken at the lesion site, and/or the intra-axonal diffusion of fluorescent dyes across the lesion site. These and other data suggest that the application of polymeric fusiogens (such as our PEG solutions), possibly combined with a tissue adherent (such as our PEG hydrogels), could lead to in vivo treatments that rapidly and permanently repair cut or crushed axons in the PNS and CNS of adult mammals, including humans.

Animals↗
PubMed1999

Prior collateral sprouting enhances elongation rate of sensory axons regenerating through acellular distal segment of a crushed peripheral nerve.

Regenerating axons in crushed peripheral nerves grow through their distal nerve segments even in the absence of Schwann cell support, but their elongation rate is reduced by 30%. We examined whether prior exposure of sensory neurons to trophic factors achieved either by collateral sprouting or regeneration after conditioning lesion could enhance subsequent regeneration of their axons after crush, and compensate for loss of cell support. Collateral sprouting of the peroneal cutaneous sensory axons in the rat was evoked by transection of adjacent peripheral nerves in the hind leg. The segment of the peroneal nerve distal to the crush was made acellular by repeated freezing. Sensory axon elongation rate during regeneration was measured by the nerve pinch test. Prior axonal sprouting for two weeks increased the elongation rate of sensory axons through the acellular distal nerve segment back to normal value observed in control crushed nerves. The number of axons in the acellular distal segment at a fixed distance from the crush site was about 50% greater in sprouting than in control non-sprouting nerves. However, prior sprouting caused no further increase of axon elongation rate in control crushed nerves. Prior collateral sprouting, therefore, could in some respect compensate for loss of cell support in the distal nerve segment after crush lesion. This suggests that loss of cell-produced trophic factors is probably responsible for slower elongation rate through the acellular distal nerve segment. Surprisingly, prior conditioning lesion caused no enhancement of elongation rate of the sensory axons regenerating in the absence of cell support.

Animals↗
PubMed1999

Wnt factors in axonal remodelling and synaptogenesis.

Wiring' of the central nervous system is accomplished by the precise and co-ordinated behaviour of neuronal cells. Proper navigation of axons and formation of synaptic contacts with the correct targets are essential. Although several signalling molecules that control axon guidance, target selection and formation of synapses have been identified, little is known about how these proteins lead to changes in the axonal cytoskeleton. Wnt signalling factors have been shown to induce axonal remodelling in developing neurons. As several components of the Wnt signalling pathway are known, studies on Wnt factors could elucidate the mechanisms by which extracellular molecules regulate the neuronal cytoskeleton. Wnt-7a induces axonal spreading and subsequent increases in synaptic protein levels in mouse cerebellar neurons. These findings suggest a role for Wnt-7a in axon guidance and synapse formation in the developing cerebellum. Based on analyses of the axonal cytoskeleton, a model is proposed in which Wnt-7a induces axonal remodelling by inhibiting glycogen synthase kinase-3 beta (GSK-3 beta), a serine/threonine kinase. Inhibition of GSK-3 beta leads to a decrease in a phosphorylated form of microtubule-associated protein-1B (MAP-1B), a protein involved in microtubule assembly, and a concomitant decrease in the level of stable microtubules. This chapter discusses the novel role of Wnt factors in regulating the axonal cytoskeleton during neuronal development.

Animals↗
PubMed1999

High tolerance and delayed elastic response of cultured axons to dynamic stretch injury.

Although axonal injury is a common feature of brain trauma, little is known of the immediate morphological responses of individual axons to mechanical injury. Here, we developed an in vitro model system that selectively stretches axons bridging two populations of human neurons derived from the cell line N-Tera2. We found that these axons demonstrated a remarkably high tolerance to dynamic stretch injury, with no primary axotomy at strains <65%. In addition, the axolemma remained impermeable to small molecules after injury unless axotomy had occurred. We also found that injured axons exhibited the behavior of "delayed elasticity" after injury, going from a straight orientation before injury to developing an undulating course as an immediate response to injury, yet gradually recovering their original orientation. Surprisingly, some portions of the axons were found to be up to 60% longer immediately after injury. Subsequent to returning to their original length, injured axons developed swellings of appearance remarkably similar to that found in brain-injured humans. These findings may offer insight into mechanical-loading conditions leading to traumatic axonal injury and into potential mechanisms of axon reassembly after brain trauma.

Axons↗
PubMed1999

Local presentation of substrate molecules directs axon specification by cultured hippocampal neurons.

Axon specification is a crucial, early step in neuronal development, but little is known about how this event is controlled in vivo. To test the hypothesis that local presentation of growth-promoting molecules can direct axon specification, we cultured hippocampal neurons on substrates patterned with stripes of poly-L-lysine and either laminin (LN) or the neuron-glia cell adhesion molecule (NgCAM). Although undifferentiated neurites contacted both substrates equally, axons formed preferentially on LN or NgCAM. Time-lapse studies revealed that changes in the growth pattern of a cell indicative of axon specification began almost immediately after the growth cone of one of the neurites of the cell contacted LN or NgCAM. When cells were plated on alternating stripes of LN and NgCAM, cells with their somata on LN usually formed axons on NgCAM, whereas those with somata on NgCAM preferentially formed axons on LN. This suggests that the change from one axon-promoting substrate to another also provides a signal sufficient to specify the axon. These results demonstrate that contact with preferred substrate molecules can govern which neurite becomes the axon and thus direct the development of neuronal polarity.

Animals↗
PubMed2000

The development of abnormal axon trajectories after rotation of one eye in Xenopus.

The targeting of isthmotectal axons in the Xenopus binocular pathway is guided by both activity-dependent cues and activity-independent cues. Abnormal visual activity induced by unilateral eye rotation overrides activity-independent cues and causes isthmotectal axons to arborize at new locations during a critical period of development that ends approximately 3 months postmetamorphosis (PM). Horseradish peroxidase staining of isthmotectal axons reveals that they normally run rostrocaudally in the tectum; in contrast, those axons in animals with early eye rotation have circuitous trajectories. In this paper, by studying the trajectories and branching patterns of isthmotectal axons at different times after eye rotation, we aimed to investigate when and how activity cues determine the projection pattern of isthmotectal axons. As suggested by electrophysiological recording, isthmotectal axons initially grow normally and make arbors according to activity-independent cues despite the presence of abnormal visual input. Our findings demonstrate that the development of abnormal trajectories starts by 2 weeks PM in response to eye rotation and is a protracted process. It begins in the tectal regions in which the initial connections of isthmotectal axons are first formed according to activity-independent cues. At transitional stages (5 and 10 weeks), axons with arbors at two different locations are observed, with locations corresponding to the old and new termination sites, respectively. Later, at 10 weeks of age, the fainter horseradish peroxidase staining in arbors at old termination sites suggests that the older arbors are undergoing withdrawal.

Animals↗
PubMed2000

Comparison of neurotrophin and repellent sensitivities of early embryonic geniculate and trigeminal axons.

Geniculate (gustatory) and trigeminal (somatosensory) afferents take different routes to the tongue during rat embryonic development. To learn more about the mechanisms controlling neurite outgrowth and axon guidance, we are studying the roles of diffusible factors. We previously profiled the in vitro sensitivity of trigeminal axons to neurotrophins and target-derived diffusible factors and now report on these properties for geniculate axons. GDNF, BDNF, and NT-4, but not NT-3 or NGF, stimulate geniculate axon outgrowth during the ages investigated, embryonic days 12-14. Sensitivity to effective neurotrophins is developmentally regulated and different from that of the trigeminal ganglion. In vitro coculture studies revealed that geniculate axons were repelled by branchial arch explants that were previously shown to be repellent to trigeminal axons (Rochlin and Farbman [1998] J Neurosci 18:6840-6852). In addition, some branchial arch explants and untransfected COS7 cells repelled geniculate but not trigeminal axons. Sema3A, a ligand for neuropilin-1, is effective in repelling geniculate and trigeminal axons, and antineuropilin-1, but not antineuropilin-2, completely blocks the repulsion by arch explants that repel axon outgrowth from both ganglia. Sema3A mRNA is concentrated in branchial arch epithelium at the appropriate time to mediate the repulsion. In Sema3A knockout mice, geniculate and trigeminal afferents explore medial regions of the immature tongue and surrounding territories not explored in heterozygotes, supporting our previous hypothesis that Sema3A-based repulsion mediates the early restriction of sensory afferents away from midline structures.

Animals↗
PubMed2000

Importance of timing of olfactory receptor-axon outgrowth for glomerulus development in Manduca sexta.

In the moth Manduca sexta, development of glomeruli in the antennal (olfactory) lobes (ALs) follows a precise timetable and involves interactions of olfactory receptor cell (ORC) axons with AL glial cells and neurons. To study the importance of timing for these intercellular interactions, we experimentally desynchronized the development of the ALs and the ORCs by altering the temperature of the developing antenna and brain for defined periods of time during development. Selective cooling of the antenna relative to the body resulted in a delay of ORC-axon outgrowth, and slightly warming the antenna while cooling the body caused precocious ingrowth of axons into the AL. Whereas cooling of the antenna for 24 hours caused only a delay in the formation of glomeruli, cooling for 48 hours led to significant disruption of glomerular development. Glial cells did not form normal glomerular borders, and glomeruli were shaped abnormally. Axons of pheromone-specific ORCs projected to their correct target, but terminal branches within the macroglomerular complex (MGC) were not clearly segregated. The results suggest that proper formation of glial glomerular borders requires interaction of ORC axons and glial cells within a sensitive period, whereas targeting of ORC axons appears to be effective over extended periods in development. Precocious ingrowth of ORC axons after warming the antenna and cooling the body for 48 hours resulted in enlarged protoglomeruli. Glial borders formed normally, but a subpopulation of MGC-specific ORC axons grew past the MGC. The decreased accuracy of targeting in these cases suggests that targeting mechanisms are not fully developed before the time when ORC axons normally would enter the brain.

Age Factors↗
PubMed2001

Cortical axon guidance by the glial wedge during the development of the corpus callosum.

Growing axons are often guided to their final destination by intermediate targets. In the developing spinal cord and optic nerve, specialized cells at the embryonic midline act as intermediate targets for guiding commissural axons. Here we investigate whether similar intermediate targets may play a role in guiding cortical axons in the developing brain. During the development of the corpus callosum, cortical axons from one cerebral hemisphere cross the midline to reach their targets in the opposite cortical hemisphere. We have identified two early differentiating populations of midline glial cells that may act as intermediate guideposts for callosal axons. The first differentiates directly below the corpus callosum forming a wedge shaped structure (the glial wedge) and the second differentiates directly above the corpus callosum within the indusium griseum. Axons of the corpus callosum avoid both of these populations in vivo. This finding is recapitulated in vitro in three-dimensional collagen gels. In addition, experimental manipulations in organotypic slices show that callosal axons require the presence and correct orientation of these populations to turn toward the midline. We have also identified one possible candidate for this activity because both glial populations express the chemorepellent molecule slit-2, and cortical axons express the slit-2 receptors robo-1 and robo-2. Furthermore, slit-2 repels-suppresses cortical axon growth in three-dimensional collagen gel cocultures.

Animals↗
PubMed2001

Fibroblast growth factor-2 promotes axon branching of cortical neurons by influencing morphology and behavior of the primary growth cone.

Interstitial branching is an important mechanism for target innervation in the developing CNS. A previous study of cortical neurons in vitro showed that the terminal growth cone pauses and enlarges in regions from which interstitial axon branches later develop (Szebenyi et al., 1998). In the present study, we investigated how target-derived signals affect the morphology and behaviors of growth cones leading to development of axon branches. We used bath and local application of a target-derived growth factor, FGF-2, on embryonic pyramidal neurons from the sensorimotor cortex and used time-lapse digital imaging to monitor effects of FGF-2 on axon branching. Observations of developing neurons over periods of several days showed that bath-applied FGF-2 significantly increased growth cone size and slowed growth cone advance, leading to a threefold increase in axon branching. FGF-2 also had acute effects on growth cone morphology, promoting rapid growth of filopodia within minutes. Application of FGF-2-coated beads promoted local axon branching in close proximity to the beads. Branching was more likely to occur when the FGF-2 bead was on or near the growth cone, suggesting that distal regions of the axon are more responsive to FGF-2 than other regions of the axon shaft. Together, these results show that interstitial axon branches can be induced locally through the action of a target-derived growth factor that preferentially exerts effects on the growth cone. We suggest that, in target regions, growth factors such as FGF-2 and other branching factors may induce formation of collateral axon branches by enhancing the pausing and enlargement of primary growth cones that determine future branch points.

Animals↗
PubMedDate not supplied

The giant axonal neuropathy--clinical and hisotological aspects, differential diagnosis and a new case.

The giant axonal neuropathy (GAN) is morphologically characterized by axonal swellings and accumulations of neurofilaments in giant axons and other cell types. Curly hair is not a constant finding. The clinical course is progressive and mostly starts in early childhood. We report the case of a boy aged 6 years at the time of sural nerve and muscle biopsy. Suralis nerve showed a reduced numerical density of myelinated fibres with a consecutive endoneural fibrosis. Morphometric investigation revealed a pronounced reduction of fibres measuring 8-12 microm in diameter. Giant axons were seen in relatively low number and were not very large with a maximum diameter of 18 microm. They had a relatively thin myelin sheet proved also by the high G ratio in the histogram. Many onion bulb formations of Schwann cells were present. There are only few reports of giant axons with such low maximum diameter in cases with GAN, the lowest maximum diameters being reported in case reports on Japanese children. Up to now, this is the first report of a non-Japanese patient with a low maximum diameter of giant axons of less than 20 microm in peripheral nerve biopsy. Ultrastructurally, typical accumulations of neurofilaments and osmiophilic aggregates were found in giant axons. Other diagnoses with occurrence of giant axons could be excluded in view of the absence of specific findings. Sporadic or familial cases with giant axons are discussed. Sceletal muscle biopsy (M. quadriceps femoris) showed neurogenic affection with presence of small angulated atrophic muscle fibres.

Axons↗
PubMed2002

Metalloproteases and guidance of retinal axons in the developing visual system.

Axonal growth cones read cues in their environment that guide them to their target. Metalloproteases have been implicated in vitro in modulating the interaction of these cues with receptors in the growth cone. To determine whether metalloprotease function is important in the guidance of vertebrate axons in vivo, we applied hydroxamate-based metalloprotease inhibitors to Xenopus retinal ganglion cell (RGC) axons as they extended through the optic tract. In the presence of two different inhibitors, 0.5-20 microm N-[(2R)-2(hydroxamideocarbonylmethyl)-4-methylpantanoyl]-l-tryptophan methylamide and batimastat, RGC axons made similar dose-dependent guidance errors. Most axons failed to make the expected caudal turn in the diencephalon and continued straight, growing aberrantly toward and across the dorsal midline. As a result, few RGC axons innervated their midbrain target, the optic tectum. Similarly, if the inhibitors were applied after the axons made the turn, many failed to grow into the optic tectum and instead turned to grow along its anterior border. Interestingly, in many instances pathfinding defects were observed in the absence of problems with axon extension, although outgrowth was impaired at the higher doses of the inhibitors. These data provide compelling in vivo evidence that metalloproteases are important for both axon guidance and extension in the developing visual system.

Animals↗
PubMedDate not supplied

[Axonal degeneration in the pathogenesis of multiple sclerosis].

Axonal degeneration plays an important role in the cumulation of disability in patients with multiple sclerosis (MS). Pathological studies have demonstrated axonal damage, particularly in area of acute inflammation and demyelination, and in chronic lesions. The mechanism of axonal loss is uncertain, but may involve axonal degeneration which is secondary to demyelination. Mediators of inflammation, including cytokines and proteolytic enzymes may be responsible for axonal damage, as may be nitric oxide. Moreover, axonal destruction might be due to immune cells attack directed to axonal components. The method to evaluate the intensity of cerebral and spinal cord atrophy, both reflecting axonal damage, is still searched. It is thought that therapy affecting the axonal destruction would possibly reduce progression of disability in MS patients.

Axons↗
PubMed1992

Somatic gene transfer of nerve growth factor promotes the survival of axotomized septal neurons and the regeneration of their axons in adult rats.

Intracerebral grafts consisting of primary fibroblasts genetically engineered to express NGF were used to assess the regenerative capacity of cholinergic neurons of the adult rat septum. Our data reveal that NGF-producing grafts sustain a significantly higher proportion of NGF receptor-immunoreactive septal neurons following axotomy (approximately 65-75%) than do grafts of noninfected fibroblasts. In addition, NGF promotes the regeneration of septal axons. Following the ablation of cholinergic septal projections to the hippocampus, NGF-producing grafts placed within the lesion cavity contain large numbers of AChE-positive axons; control grafts, on the other hand, lack such cholinergic axons. Ultrastructural examination reveals that unmyelinated axons within NGF-producing grafts use many different substrates for growth, including astrocytes and components of the extracellular matrix. Grafts of control fibroblasts possess the same cellular and matrix substrates but contain only a small population of axons, probably of peripheral origin. AChE-positive axons growing through NGF-producing grafts provide a new topographically organized input to the deafferented hippocampal dentate gyrus. Furthermore, regenerating septal axons terminate predominantly on the dendritic processes of granular neurons. The dentate gyrus ipsilateral to grafts of noninfected fibroblasts, on the other hand, remains devoid of AChE-positive fibers. From these results, we conclude that the availability of NGF is a necessary requirement to sustain axotomized cholinergic septal neurons and to promote axon regeneration and cholinergic reinnervation of dentate granular neurons by these lesioned neurons. The presence of many permissive substrates (e.g., astrocytes, basal lamina, and collagen) alone, however, is not sufficient to induce axon regrowth from adult septal neurons.

Acetylcholinesterase↗
PubMed2005

Apparent diffusion coefficients in spinal cord transplants and surrounding white matter correlate with degree of axonal dieback after injury in rats.

BACKGROUND AND PURPOSE: Abnormal apparent diffusion coefficient (ADC) values in injured spinal cord white matter and fibroblast transplants have been shown to correspond with qualitative histologic findings of axonal loss or regeneration. We proposed that ADC values would correlate with quantitative axonal tracing in the transected rubrospinal tract (RST). METHODS: Eleven rats received right-sided lateral funiculus lesions at C3-4 (disrupting the RST) and transplantation of fibroblasts that were unmodified or modified to secrete brain-derived neurotrophic factor (BDNF). Behavioral tests measured hindlimb function at 1, 2, 4, 6, 8, 10, and 12 weeks after injury. At 12 weeks after injury, the antegrade axon tracer biotinylated dextran amine was stereotactically injected into the red nucleus to label the injured RST axons. Animals were sacrificed 2 weeks later. Diffusion-weighted MR imaging of the excised, fixed spinal cord specimens was then performed at 9.4 T. RESULTS: In white matter surrounding transplants, ADC values transverse to axons were elevated and ADC values longitudinal to axons were decreased. These ADC values were more abnormal closer to the transplant, and this correlated with decreases in numbers of labeled RST axons. ADC values in BDNF-expressing fibroblast transplants were significantly lower than those in unmodified fibroblast transplants, and these lower values correlated with decreased axonal dieback. Behaviorally, all animals showed partial recovery, but animals with BDNF-expressing fibroblast transplants had slightly improved hindlimb function compared to those with unmodified fibroblast transplants. CONCLUSION: ADC values may be able to evaluate graft function after spinal cord injury by demonstrating the degree of axonal dieback and preservation.

Animals↗
PubMed2005

Ultrastructural characteristics of axons in traumatic neuromas of the human lingual nerve.

AIMS: To determine the ultrastructural characteristics of axons in traumatic neuromas of the human lingual nerve during the surgical removal of lower third molar teeth and to establish whether any characteristics were different between patients with dysesthesia and patients without dysesthesia. METHODS: Transmission electron microscopy was used to determine the ultrastructural morphological characteristics of human lingual nerve neuromas (n = 34) removed at the time of microsurgical nerve repair. From a sample population of myelinated and nonmyelinated fibers within the neuromas, fiber diameter, myelin thickness, g-ratio, and the number of mitochondria per axon were quantified. Comparisons were made with normal control lingual nerve specimens (n = 8) removed at the time of organ donor retrieval. RESULTS: Significant differences in ultrastructural morphology were found between the neuromas and control nerves. The neuromas contained a higher proportion of small (2- to 8-microm diameter) myelinated nerve fibers than controls, and the mean myelinated fiber diameter was significantly lower in neuromas than in controls. Mean myelin sheath thickness was significantly thinner in neuromas (0.6 +/- 0.1 microm) than in controls. However, the g-ratio, which is a measure of the myelination status of the nerve fibers in relation to their diameter, was found to be similar in each group, suggesting a normal process of myelination in the damaged axons. Nonmyelinated axon diameter was also significantly smaller in the neuromas than in the controls, and Schwann cells were found to sheathe more nonmyelinated axons in neuromas than in controls. The ratio of nonmyelinated to myelinated axons was significantly higher in neuromas than in controls. However, no significant differences were found between patients with dysesthesia and those without dysesthesia. CONCLUSION: Damage to the lingual nerve results in marked changes to axon diameter, myelin sheath thickness, and Schwann cell-axon relationships. These ultrastructural changes could contribute to the altered electrophysiological properties of axons trapped within neuromas. However, no significant differences in the ultrastructural characteristics studied were found between specimens from patients with or without symptoms of dysesthesia.

Adolescent↗
PubMed1991

Growth of regenerating goldfish axons is inhibited by rat oligodendrocytes and CNS myelin but not but not by goldfish optic nerve tract oligodendrocytelike cells and fish CNS myelin.

Encounters of regenerating goldfish retinal axons with oligodendrocytes and CNS myelin of mammals and fish were monitored in in vitro assays. Upon contact with highly branched rat oligodendrocytes, goldfish axons collapsed or grew around but never crossed these cells. However, in the presence of the antibody IN-1 against the oligodendrocyte-associated growth-inhibitory proteins, axons did grow over highly branched oligodencrocytes. In contrast to the mammalian oligodendrocytes, goldfish optic nerve/tract-derived oligodendrocytelike cells allowed the growth of axons across their surface and even along their processes. The fish growth cones avoided entering the region of rat CNS myelin applied to polylysine/laminin-coated coverslips or failed to elongate on this substrate. They were, however, able to pass over CNS myelin of fish. When exposed to rat CNS myelin as the sole substrate, axonal outgrowth from fish retinal explants was inhibited almost entirely. However, outgrowth on fish CNS myelin was substantial, but many more axons extended on fish or rat brain membranes that were depleted of myelin. Thus, goldfish retinal axons are sensitive to the axon-growth-inhibiting cell-surface molecules of mammalian oligodendrocytes as well as CNS myelin. Fish optic nerve oligodendrocytelike cells and fish CNS myelin lack these inhibitory properties and are growth permissive. These in vitro experiments suggest that the success of axonal regeneration in the fish optic nerve is causally related to the presence of growth-permissive properties and to the absence of growth inhibitors on fish optic nerve/tract oligodendrocytelike cells.

Animals↗
PubMed1986

Analysis of the carbohydrate composition of axonally transported glycoconjugates in sciatic nerve.

Glycosidase enzyme digestion in combination with postembedding lectin cytochemistry was used to study the carbohydrate composition of axonally transported glycoproteins. A cold block procedure for the interruption of axonal transport was employed to increase selectively the population of anterograde moving components on the proximal side of the transport block. Electron-microscopic observations revealed that a cold block applied to the sciatic nerve of an anesthetized rat produced an increase in axonal smooth membrane vesicles at a site directly proximal to the cold block. Postembedding lectin cytochemistry of the sciatic nerve demonstrated a substantial increase in concanavalin A (Con A), wheat germ agglutinin (WGA), and succinylated WGA binding sites in axons directly proximal to the cold block. Endoglycosidase H (endo H) digestion prior to lectin cytochemistry characterized a large population of the axonally transported Con A binding sites as polymannose and/or hybrid N-linked oligosaccharides (endo H-susceptible). A distinct population of neuraminidase-resistant WGA binding sites was also found in axons directly proximal to the transport block. The concomitant increase in smooth membrane vesicles and lectin binding sites in axons at the transport block supports the hypothesis that a system(s) of smooth membrane inside the axon is involved in the transport of glycoproteins from the cell soma to their cell surface destinations. Results of glycosidase digestions and lectin cytochemistry experiments suggest that many of the axonally transported glycoprotein carbohydrates are polymannose and/or hybrid N-linked oligosaccharides. This observation is especially interesting in relation to our previous reports, which indicated that most lectin binding sites on the neuronal cell surface are composed of complex oligosaccharides.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗