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PubMed1990

Acrylamide impairs fast and slow axonal transport in rat optic system.

Effects of single and repeated doses of acrylamide on fast and slow axonal transport of radio labeled proteins following the injection of L-[4,5-3H] leucine have been studied in the optic system of male Sprague-Dawley rats. A single dose of acrylamide (100 mg/kg) had no effect, but higher concentrations (200-300 mg/kg) altered the distribution of fast axonally transported materials in optic nerves and optic tracts. Repeated doses of acrylamide (30 mg/kg/day, 5 days per week for 4 weeks) produced degeneration of tibial nerves but spared optic nerves and optic tracts. Fast axonal transport rate in optic axons was reduced by 50% (reduced to 4 mm/h from 8 mm/h) in acrylamide treated animals. Acrylamide also slowed the velocity of slow axonal transport of labeled proteins in optic axons to 1.0 mm per day from 1.3 mm per day. Since acrylamide impaired the rate of both fast and slow axonal transport in the absence of overt morphological damage, it can be concluded that deficit in axonal transport is an important factor in the pathogenesis of axonal degeneration in acrylamide neuropathy.

Acrylamide↗

PubMed1985

Membrane ultrastructure of developing axons in glial cell deficient rat spinal cord.

In order to investigate axolemmal development in a glial cell deficient environment, normal and irradiated dorsal funiculus in rat lumbosacral spinal cord was examined by freeze-fracture electron microscopy. At 3 days of age, normal fibres are all unmyelinated and of small (less than 0.5 micron) diameter. The unmyelinated axons have a moderate density (approximately 850 microns-2) of intramembranous particles (IMPs) on P-fracture faces and a low IMP density (approximately 300 microns-2) on E-faces. IMPs are homogeneously distributed along both fracture faces. By 19 days of age, the normal dorsal funiculus is well populated with myelinated axons and glial cells, as well as a sizable population of unmyelinated fibres. Nearly all of the myelinated fibres have a large (greater than 1.0 micron) diameter; whereas, most unmyelinated axons are of small (less than 0.5 micron) calibre. The axolemma of unmyelinated axons is relatively undifferentiated, with an asymmetrical distribution of IMPs (P-face: approximately 1100 microns-2; E-face: approximately 450 microns-2). Myelinated fibres show nodal and paranodal regions with P-face and E-face ultrastructure similar to previous descriptions. Internodal axolemma appears relatively homogeneous, with P-faces being highly particulate (approximately 2100 microns-2) and a low IMP density (approximately 200 microns-2) on E-faces. Following irradiation of the lumbosacral spinal cord at 3 days of age, there is a severe reduction in the number of glial cells and myelinated fibres in this region when the tissue is examined at 19 days of age. Despite the deficiency of glial cells in this tissue, axonal and axolemmal development continue. Numerous large (greater than 1.0 micron) diameter axons are present in this irradiated tissue. Large diameter axons show a high (approximately 2000 microns-2) density of IMPs on P-faces; E-face IMP density remains at approximately 440 micron-2. Small calibre axons also have an asymmetrical distribution of particles (P-face: approximately 1100 microns-2; E-face: 280 microns-2). The axolemmal E-faces of some glial cell deprived fibres exhibit regions with greater than normal (approximately 750 microns-2) density of IMPs. These results demonstrate that some aspects of axonal and axolemmal development continue in a glial cell deficient environment, and it is suggested that axolemmal ultrastructure is, at least in part, independent of glial cell association.

Aging↗

PubMed1993

Close apposition among neighbouring axonal endings in a neuroma.

Axons in intact peripheral nerve trunks constitute independent afferent and efferent communication channels. However, when nerves are severed, several different forms of axon-axon cross-excitation develop in association with the injury site. In this study we have examined experimental sciatic nerve-end neuromas in rats with special interest in the compartmentalization of individual axons, and the barriers that separate close neighbours. At postinjury times at which functional coupling is known to occur, neuromas were found to contain many examples of axons in which adjacent membrane faces come into close contact without an intervening Schwann cell process. These occur in bundles containing from two to as many as 30 individual nerve fibres wrapped in a common Schwann cell sheath. The surface area of close apposition between axon pairs ranges up to several tens of micron2. Closely apposed axon profiles may be outgrowing branches of a single parent axon, but anterograde tracer data indicate that many belong to independent neurons. Closely apposed axons are separated from one another, and from associated Schwann cell processes, by a cleft about 130 A wide. No synapses, gap junctions or tight junctions were observed. Extracellular tracer studies using La3+ and Ruthenium Red indicated that the cleft system is patent, permitting the free diffusion of small molecules between the space adjacent to the axolemma and the bulk extracellular compartment. Together, these data provide a structural basis for interfibre interactions based on local electrical current flow (ephaptic crosstalk), as well as coupling mediated by K+ ions and neurotransmitter molecules.

Animals↗

PubMed1990

Axonal abnormalities in cerebellar Purkinje cells of the 'hyperspiny Purkinje cell' mutant mouse.

The hyperspiny Purkinje cell (hpc) is a murine, autosomal recessive mutation affecting cerebellar Purkinje cells. Axonal abnormalities in these neurons have been revealed by selective silver impregnation, specific immunohistochemical staining and electron microscopy. The main pathological feature consists of a massive axonal degeneration in the terminal domains of the Purkinje cell projection. This process starts approximately ten days postnatally, simultaneously with the onset of cerebellar symptoms, and evolves very rapidly. By 21 days, the vast majority of the terminal arbors have degenerated, resulting in an almost complete disruption of the corticonuclear projection. Axonal degeneration, although proceeding in a dying-back fashion, only provokes retrograde death in a small percentage of Purkinje cells (less than 15%). Purkinje cells exhibit other signs of axonal damage and axonal reaction: (a) Almost all of them bear gigantic varicosities (spheroids or torpedoes) along their transit through the granular layer. (b) In a small percentage of cases, a dendritic segment is inserted between the axon hillock and the initial segment (meganeurite). These ectopic dendrites receive a normal contingent of synaptic inputs, and are transient structures observed in four- to six-week-old mice. (c) The infra- and supraganglionic plexuses, formed by recurrent collaterals of Purkinje cell axons, have increased density and terminal domains. (d) In mice aged over 50 days, many Purkinje cells have developed 'arciform' axons, which is evidence of a compensatory reaction. The definite axonal pathology of hpc Purkinje cells confers to this mutation its own specificity, which differs from all other known mutations primarily affecting this neuronal population. Therefore, the hpc mutation offers a valuable tool to analyse some of the genetic factors involved in the differentiation and maintenance of cerebellar Purkinje cells.

Animals↗

PubMed1991

Two types of sympathetic axon innervating the juxtaglomerular arterioles of the rabbit and rat kidney differ structurally from those supplying other arteries.

Ultrastructural analyses of serial thin sections have revealed two structurally different types of sympathetic axon innervating the afferent and efferent juxtaglomerular arterioles and the intralobular arteries in the outer cortex of the rabbit kidney. Both types of axon have also been found in association with an afferent arteriole in rat kidney. One axon type consists of relatively large diameter unmyelinated axons bearing varicosities in the form of slight expansions. The varicosities have a distinct structural zonation: synaptic vesicles occupy the expansion which faces the smooth muscle cells, whereas the rest of the axon is filled with numerous microtubules. The other axon type has varicosities containing vesicles and mitochondria but few microtubules. The varicosities are generally small and the intervaricosities very thin. The relationship of both axon types with support cells and/or basal lamina is sometimes poorly defined. Both axon types are catecholaminergic as their vesicles take up 6-hydroxydopamine and both types form junctions with arteriolar smooth muscle cells. As well as differing from each other, both types of intrarenal axon differ in several respects from those which innervate other arterial vessels.

Animals↗

PubMed1980

Organization of identified axons innervating the dorsal longitudinal flight muscle of Drosophila melanogaster.

Axons innervating the dorsal longitudinal flight muscle of Drosophila were investigated with physiological, light microscopic and electron microscopic techniques. Five motor axons innervate the six muscle fibres which compose a dorsal longitudinal flight muscle. All five axons, designated 1-5, are identified physiologically and morphologically. Axons 1-4 separately innervate muscle fibres 1-4, while axon 5 innervates both muscle fibres 5 and 6, making five motor units. The branching pattern of the nerve and the organization of these axons within the nerve is very consistent from fly to fly, making identification of every axon possible in both the nerve trunk and finer branches. Morphologically, axons 1-2 and 3-4 make particular pairs with long shared pathways. Furthermore, the axons are unusually closely associated with each other within the nerve.

Animals↗

PubMed1981

A method to separate spatially the temporal sequence of axon-Schwann cell interaction during nerve regeneration.

This paper describes a surgical method of manipulating feline peripheral nerve regeneration to separate spatially the temporal sequence of events of axon-Schwann cell interaction during nerve fibre formation. The method allows regenerating axons from the peroneal nerve to reinnervate the distal stump of a axon- and myelin-free, Schwann cell-enriched, chronically denervated tibial nerve distal stump. Three zones can be morphologically delineated in the tibial nerve stump after three weeks of reinnervation: (1) a proximal myelinated zone, (2) a more distal, non-myelinated, axon-Schwann cell contact zone, and (3) a distal axon-free Schwann cell non-contact zone. The distal limit of the second zone can be determined accurately by the front of an axonally transported label. The large volume of available tissue makes this method suitable for interdisciplinary studies to elucidate the control of axon elongation, axon growth, and axon-Schwann cell inter-relationships.

Animals↗

PubMed1988

Regional heterogeneity in the distal motor axon: three zones with distinctive intrinsic components.

In this study we examined the distribution of cytoskeletal and other intrinsic axonal elements in motor nerve terminals in vivo. Components of axons were visualized with immunocytochemical staining of frozen longitudinal sections of muscle. Using these methods we compared the distribution of neurofilaments, tubulin, MAP2, actin and synaptic elements in distal regions of axons at and near neuromuscular junctions in rat muscles. Our results show that three discrete regions can be defined based on the anatomy and intrinsic components of distal axons. The preterminal axon, extending from its exit from the intramuscular nerve toward the neuromuscular junction, has a cytoskeletal composition similar to the more proximal axon with abundant staining of neurofilaments, tubulin, MAP2 and actin. The terminal arborization, a branched region of the axon extending through the endplate region, contains neurofilaments but little tubulin, actin, MAP2 or synaptic elements. Finally, the synaptic zone, demonstrated with antibodies to the synaptic vesicle protein synaptophysin, contains few cytoskeletal elements. We conclude that there is considerable regional heterogeneity in the composition of distal motor axons. The distribution of neurofilaments, other cytoskeletal elements and synaptic vesicle proteins varies among different discrete zones of terminal motor axons.

Animals↗

PubMed1996

Localization of synapsin I in normal fibers and regenerating axonal sprouts of the rat sciatic nerve.

The localization of synapsin I, a synaptic vesicle-associated protein, was investigated immunocyto-chemically in normal nerve fibers and regenerating axonal sprouts following crush-injuries to the rat sciatic nerve. In normal myelinated axons, weak synapsin I immunoreactivity was found in the axoplasmic/smooth endoplasmic domains, but not in the cytoskeletal domains comprising neurofilaments and microtubules. In non-myelinated axons without dense cytoskeletal structures, moderate immunoreactivity was distributed diffusely throughout the axoplasm. In the crush-injured nerves, intense synapsin I immunoreactivity was demonstrated by light microscopy in early regenerating sprouts emerging from nodes of Ranvier. These nodal sprouts subsequently elongated as regenerating axons through the space between the basal lamina and the myelin sheath (or Schwann cell plasma membrane). Intense synapsin I immunoreactivity was also found in the growth cones of such long regenerating axons. Electron microscopy revealed that synapsin I immunoreactivity was associated mainly with vesicular organelles in the nodal sprouts and growth cones of regenerating axons. Long regenerating axons exhibited no synapsin I immunoreactivity in the shaft, which contained an abundance of neurofilaments. However, vesicle accumulations remaining in the periphery of the shaft still exhibited intense synapsin I immunoreactivity. Thus, it can be concluded that synapsin I is localized at especially high density in the domains comprising vesicular organelles, which are characteristic of early nodal sprouts, as well as in growth cones of regenerating axons. These findings, together with the proposed functions of synapsin I investigated in other studies, suggest that synapsin I may play important roles in vesicular dynamics including the translocation of vesicles to the plasma membrane in sprouts and growth cones of regenerating axons.

Animals↗

PubMed1986

Progressive axonopathy: an inherited neuropathy of boxer dogs. 3. The peripheral axon lesion with special reference to the nerve roots.

Progressive axonopathy is an autosomal recessive inherited neuropathy of Boxer dogs with lesions in the CNS and PNS. This paper describes the axonal changes in the lumbar and cervical nerve roots and tibial nerve. By 2 months of age the proximal paranodal areas of many larger diameter fibres show small axonal swellings, sometimes with attenuation or loss of the associated myelin sheath. Axoplasmic changes within swollen and non-swollen fibres include disorganization of the peripheral neurofilaments and small accumulations of vesicles and vesiculo-tubular profiles, particularly in the sub-axolemmal area. Occasional fibres, more often in the cervical roots, are massively distended with disorganized neurofilaments. The frequency of the membranous accumulations decreases with progression of the disease. Many axons show a markedly irregular or corrugated outline and are surrounded by an attenuated sheath. The peripheral axonal cytoskeleton is disorganized and misaligned, whereas the central structures maintain a more normal arrangement. Regenerating axonal clusters are common in the cervical ventral roots but occur infrequently in the lumbar roots. Similar axonal changes occur in the peripheral nerves but at a much lower frequency. Any membranous accumulations or cytoskeletal disorganization are more probable in the proximal tibial nerves, while the frequency of axonal degeneration and regeneration increases distally. The morphological appearances indicate gross disturbances in axon-sheath cell relationships and suggest that abnormalities in the transport of various axoplasmic organelles may be involved in the pathogenesis of the axonal lesion.

Animals↗

PubMed2002

Increased expression of the putative axon growth-repulsive extracellular matrix molecule, keratan sulphate proteoglycan, following traumatic injury of the adult rat spinal cord.

Keratan sulphate proteoglycan (KSPG) is a developmentally regulated barrier molecule, directing axonal growth during central nervous system (CNS) formation. The possible re-expression and functional significance of KSPG in preventing axon regeneration following spinal cord injury (SCI) is poorly understood. In the present investigation, the spatio-temporal expression of KSPG was studied following experimental SCI. There was no indication of sparing of axons at the lesion epicentre following severe compression injury. By 7 days post operation (p.o.) a diffuse increase of KSPG immunoreactivity (KSPG-IR) was observed in the parenchyma surrounding the lesion. This was followed by a delayed (21-28 days p.o.) and largely heterogeneous increase of KSPG-IR in the lesion epicentre, which revealed both cellular and extracellular matrix-like distribution patterns. Although no re-growth of anterogradely labelled corticospinal axons was observed, many 200-kDa neurofilament (NF)-positive axons could be detected growing into the connective tissue scar. This phase of spontaneous axonal re-growth was closely associated with a framework of glial cells (including Schwann cells from damaged local spinal nerve roots) that had migrated into the lesion site. The spontaneous nerve fibre re-growth could be detected in both KSPG-rich and KSPG-poor territories. The present data suggest that the lesion-induced up-regulation of KSPG-IR may have contributed to the lack of corticospinal axon re-growth. However, the lack of any direct spatio-temporal correlation between the distribution of raised KSPG-IR and spontaneous NF-positive axonal regeneration suggests that at least some populations of axons can resist the putative inhibitory effects of this extracellular matrix molecule.

Animals↗

PubMed2006

The fate of axons subjected to traumatic ultrastructural (neurofilament) compaction: an electron-microscopic study.

By means of a new head-injury apparatus, a 0.75-mm-deep depression was produced momentarily at a predetermined site of the rat calvaria. This immediately evoked ultrastructural (neurofilament) compaction in many myelinated axon segments in layers IV and V of the neocortex under the impact site. The affected axon segments run quasi-parallel to the brain surface in a diffuse distribution among normal axons. Other kinds of damage to the brain tissue were insignificant; the conditions were therefore favorable for investigation of the fate of the compacted axons. Quantitative analysis of the findings on groups of ten rats that were sacrificed either immediately after the head injury or following a 1 day or a 1 week survival period showed that around 50% of the compacted axons recovered in 1 day, and a further less than 10% did so in 1 week. Electron microscopy revealed that the non-recovering compacted axons underwent a sequence of degenerative morphological changes including homogenization, fragmentation and resorption of the fragments. However, the myelin sheaths around these degenerating axons remained apparently unchanged even in the long-surviving rats, and hardly any phagocytotic cells were encountered. On the other hand, many such myelin sheaths contained axolemma-bound, normal-looking axoplasm besides the above morphological signs of axon-degeneration. It is concluded that the non-recovering compacted axons undergo an uncommon (non-Wallerian) kind of degeneration, which is mostly reversible.

Animals↗

PubMed1998

Focal accumulation of intra-axonal mitochondria in demyelination of the cat optic nerve.

Mitochondrial accumulation has been reported at sites of degenerating nerve fibres. The reason for focal accumulation of mitochondria within axons has not previously been investigated. The aim of this study was to quantitate changes in mitochondrial concentration within demyelinated axons and determine if these changes were due to obstruction of the free passage of organelles within the fibre. The average number of mitochondria per unit area of axon within axons of normal cat optic nerve and optic nerve in which demyelination had been induced with anti-galactocerebroside (GC) was determined using transmission electron microscopy. Increased numbers of mitochondria were demonstrated at the site of demyelination, peaking at approximately two and a half times the value for normal non-lesioned nerves at 6-7 days after anti-GC administration [0.66+/-0.06 (SD) mitochondria per microm2 of axon compared to 0.28+/-0.04 in controls; P < 0.05]. The mitochondrial concentration gradually decreased over the next 20 days towards normal values. The concentration of mitochondria within non-myelinated axons of cat retina (0.55+/-0.18) was also determined and shown to be comparable to the values for the demyelinated optic axons (0.66+/-0.06). It is proposed that the accumulation of mitochondria within demyelinated axons reflects the adaptive process of the axon during the early restoration of impulse conduction rather than the obstruction of the free passage of organelles within the fibre.

Animals↗

PubMed2004

Quantitative analysis of granule cell axons and climbing fiber afferents in the turtle cerebellar cortex.

The turtle cerebellar cortex is a single flat sheet of gray matter that greatly facilitates quantitative analysis of biotylinated dextran amine labeled granule cell and olivocerebellar axons and Nissl-stained granule and Purkinje neurons. On average, ascending granule cell axons are relatively thicker than their parallel fiber branches (mean +/- SD: 0.84 +/- 0.17 vs 0.64 +/- 0.12 microm, respectively). Numerous en passant swellings, the site of presynaptic contact, were present on both ascending and parallel fiber granule cell axons. The swellings on ascending axons (1.82 +/- 0.34 microm, n = 52) were slightly larger than on parallel fibers (1.43 +/- 0.24 microm, n = 430). In addition, per unit length (100 microm) there were more swellings on ascending axons (11.2 +/- 4.2) than on parallel fibers (9.7 +/- 4.2). Each parallel fiber branch from an ascending axon is approximately 1.5 mm long. Olivocerebellar climbing fiber axons followed the highly tortuous dendrites of Purkinje cells in the inner most 15-20% of the molecular layer. Climbing fibers displayed relatively fewer en passant swellings. The spatial perimeter of climbing fiber arbors (area) increased 72% from anteriorly (1797 microm2) to posteriorly (3090 microm2) and 104% from medially (1690 microm2) to laterally (3450 microm2). Differences in the size and spacing of en passant swellings on granule cell axons suggest that ascending axons may have a functionally more significant impact on the excitability of a limited number of radially overlying Purkinje cells than the single contacts by parallel fiber with multiple orthogonally aligned Purkinje cell dendrites. The spatially restricted distribution of climbing fibers to the inner most molecular layer, the paucity of en passant swellings, and different terminal arbor areas are enigmatic. Nevertheless, these finding provide important anatomical information for future optical imaging and electrophysiological experiments.

Afferent Pathways↗

PubMed2003

Stimulus-dependent translocation of egg-laying hormone encoding mRNA into the axonal compartment of the neuroendocrine caudodorsal cells.

To get insight into the stimulus-dependent translocation of mRNA encoding neuropeptides to the axonal compartment of neurons, we investigated this process in the egg-laying hormone producing caudodorsal cells of the mollusk Lymnaea stagnalis. The axonal compartment including the nerve terminals of these neurons harbors high amounts of mRNA encoding the egg-laying hormone precursor. We determined how a sensory stimulus, that results in egg-laying, affected the amount of egg-laying hormone encoding transcripts in the axon endings. Four hours after stimulation high amounts of transcripts were detected in the axonal compartment and maximum values were reached after 8 h. Transcript levels in the somata were affected in a similar fashion, although the increase was not as pronounced as in the axons. Next, we investigated the ultrastructural localization of egg-laying hormone encoding transcripts in axons and axon terminals by means of electron microscopic in situ hybridization and showed that transcripts were localized in the axoplasm. By means of conventional electron microscopy we showed that axon terminals of egg-laying hormone producing neurons contained large amounts of polyribosomes. Together, these data support the notion that egg-laying hormone encoding transcripts are translated in the axonal compartment.

Animals↗

PubMed2003

Axonal injury in multiple sclerosis.

The pivotal role of axons in the pathophysiology and pathogenesis of multiple sclerosis (MS) is increasingly becoming the focus of our attention. Axonal injury, considered at one time to be a late phenomenon, is now recognized as an early occurrence in the inflammatory lesions of MS. There is converging evidence from histopathologic, as well as magnetic resonance imaging and magnetic resonance spectroscopy studies, that axons play a crucial and dynamic role during the evolution of MS pathology and the development of clinical disability. It has been repeatedly demonstrated that neurologic functional impairment correlates best with axonal, rather than myelin, injury. The pathophysiology of axonal injury remains speculative. Although generally considered to be sequelae of demyelination, it is possible that axonal injury in MS is indeed a primary event. The discovery that axonal injury can be reversible has provided an impetus to institute early therapy. The finding that irreversible axonal transection occurs in early lesions has underscored now, more than ever before, the need to curtail inflammation and the need to institute early treatment with disease-modifying agents. The axon will undoubtedly remain the focus of our attention regarding research on MS now and in the future.

Axons↗

PubMed1979

Electron microscopic localization of substance P and enkephalin in axon terminals related to dendrites of catecholaminergic neurons.

Morphological and pharmacological data suggest that catecholaminergic neurons receive afferent axons positively labeled for the peptides, substance P and [Met5]-enkephalin. In the present study, electron microscopic immunocytochemistry was used to determine whether a positive reaction for these peptides could be localized to axon terminals forming synapses with catecholaminergic neurons in the locus coeruleus and A2 regions of rat brain. Adjacent sections through these areas were incubated with antiserum to either substance P, [Met5]-enkephalin, or tyrosine hydroxylase, a specific marker for catecholaminergic neurons. The sections were subsequently processes by the peroxidase-antiperoxidase immunocytochemical technique. In both the locus coeruleus and A2 region, tyrosine hydroxylase was localized primarily to perikarya and dendrites of intrinsic neurons; whereas substance P and enkephalin-like immunoreactivity was localized to axons and axon terminals. The axon terminals showing positive reactions for substance P and [Met5]-enkephalin were morphologically similar to each other and to one type of axon terminal which formed synapses with dendrites labeled for tyrosine hydroxylase. This type of axon terminal always formed asymmetric synaptic junctions and contained 3-4 large (75-100 nm) dense vesicles (LDVs) and many small (40-60 nm) clear vesicles (SCVs). The reaction product for substance P and [Met5]-enkephalin was distributed throughout the lumen of the LDVs and formed a rim of labeling around the outer boundaries of the SCVs. These findings demonstrate that substance P and [Met5]-enkephalin-positive reactions are selectively localized to subcellular organelles in axon terminals in the locus coeruleus and A2 region of rat brain. They further suggest that the labeled axon terminals form synapses with dendrites of the catecholaminergic neurons.

Animals↗

PubMed1982

The effect of ligation combined with section on anterograde axonal transport in rabbit hypoglossal nerve.

The axonal transport of radiolabeled slow phase proteins and fast phase glycoproteins was studied in rabbit hypoglossal nerve one week after axotomy. The nerves were ligated and cut to prevent axonal regeneration into the distal stump. In this situation of obstructed axonal outgrowth, the axonal transport of these components into the proximal part of the nerve was increased. This increase, however, was significantly less pronounced compared with the increase previously found after nerve crush, when the axons were free to regenerate. The results suggest that the axonal transport response concerning structural axonal proteins after nerve lesions depends on the type of trauma, and that the neuronal export of these components during regeneration is modified if axonal outgrowth is impaired. The results are discussed in the light of the present understanding of the role of axonal transport in nerve regeneration.

Afferent Pathways↗