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 415 records · Page 23Linked to original sources
PubMed1993

Vesicular fast axonal transport rates in young and old rat axons.

An isolated sciatic nerve preparation was used to measure the transport rates of more than 18,000 vesicles in 72 axons from young (3-4 months of age) and old (24-26 months of age) rats from two strains (Harlan Sprague-Dawley and Fisher-344). Average anterograde and retrograde vesicle transport rates were significantly slower in the older animals. The amount of slowing of anterograde vesicles was twice as great as the slowing of retrograde vesicles. Age-related slowing of vesicle transport was inversely proportional to vesicle speed, with the result that transport of the slowest and largest vesicles may essentially be blocked in older axons. One possible explanation for these data is that long-lived axonal cytoskeletal proteins are subject to age-related changes that impede vesicle transport.

Aging↗
PubMed1996

A newly-synthesized GPI-anchored protein, TAG-1/axonin-1, is inserted into axonal membranes along the entire length of the axon and not exclusively at the growth cone.

Evidence exists that some newly-synthesized membrane components are inserted into the membrane of the growing axon at the growth cone. We now examine the site of insertion of a glycosylphosphatidylinositol-anchored protein, TAG-1/axonin-1. The protein was cleaved from the plasma membrane by phosphatidylinositol-specific phospholipase C. Newly-synthesized TAG-1/axonin-1 was subsequently detected along the entire length of the axonal membrane, with no evidence for preferential insertion at the distal end. These results raise the possibility that different subsets of proteins are inserted at different locations in axonal membranes.

Animals↗
PubMed1986

Nerve repair and axonal transport. Distribution of axonally transported proteins during maturation period in regenerating rabbit hypoglossal nerve.

The distribution of fast migrating [3H]leucine-labelled proteins was studied in transected and repaired rabbit hypoglossal nerves. The nerves were repaired 90 days earlier with mesothelial chamber or epineurial suture technique. Fast migrating radiolabelled proteins were transported into the distal nerve segment and neurophysiological recordings from the tongue as well as the presence of myelinated axons in the distal nerve segment verified successful regeneration. The total amount of radioactivity was increased in repaired nerves as compared to contralateral nerves. In both groups there was a significant accumulation of radiolabelled proteins at the site of lesion. Nerves repaired with mesothelial chambers showed significantly more radioactivity in the distal nerve segment as compared to sutured nerves. The present study indicates long-standing effects on axonal transport system after both types of nerve repair. It is our opinion that axonal transport studies are a valuable complement when evaluating experimental nerve repair.

Animals↗
PubMed1984

A silver and gold technique for axons and axon-bundles in formalin-fixed central and peripheral nervous tissue.

We have modified the reduced silver procedure of Liesegang and added a gold treatment. The technique has been successfully and routinely used to impregnate both peripheral and central nervous tissues of mice of different ages, and central nervous tissue of man. It was applied on conventionally (formalin) fixed and cryostat-cut material. In the periphery, nerves, individual axons, and sensory and motor endings stained a dark purple. In the brain, both bundles of axons and individual fine axonal branches were stained. When counterstained by a Nissl method, an excellent overall image of CNS structure is obtained.

Age Factors↗
PubMed1994

Inflammation after axonal injury has conflicting consequences for recovery of function: rescue of spared axons is impaired but regeneration is supported.

Neural injury leads to tissue damage beyond that caused by the initial lesion, mainly as a result of a chain of autodestructive events triggered by the trauma. These events apparently include the activation of immune-derived cells and their products, as treatment with anti-inflammatory agents, such as corticosteroids, limits the damage and thus improves recovery. On the other hand, immune-derived substances, such as cytokines, are thought to play an important role in post-traumatic axonal regeneration. Thus, the need to reduce inflammation to limit the spread of damage appears to be in conflict with the need to permit inflammation to promote regeneration. Comprehension and resolution of this apparent conflict may lead to the development of treatment protocols aimed at rescuing axons spared by the initial injury, without hampering the potential regeneration of directly and indirectly injured axons. In this study, carried out on rats with crushed optic nerves, daily intraperitoneal injections of dexamethasone commencing prior to the injury significantly attenuated the injury-induced decrease in electrophysiological activity and reduced the area of tissue damage. On the other hand, dexamethasone treatment reduced the permissiveness of the injured nerves to neural adhesion and regrowth in vitro. This latter phenomenon was also observed in injured peripheral nerves. Results are discussed with respect to the possible establishment of an appropriate protocol for corticosteroid treatment of nerve injuries aimed at promoting neuronal rescue without compromising neuronal regeneration.

Adrenal Cortex Hormones↗
PubMed1980

Glio-axonic junctional like complexes at the Mauthner cell's axon cap of teleosts: a possible morphological basis for field effect inhibitions.

Differentiated contacts were identified by electron microscopy between glia and axons as they enter the axon cap which surrounds the initial segment of the teleost's Mauthner cell. At these regions, the cleft of adjacent membranes is 20-25 nm wide and contains clods of electron-dense material with a pseudo-periodicity of 10-30 nm. These junctions, referred to as 'septate-like junctions', presumably contribute to the compartmentalization of the axon cap and, therefore, to its elevated resistivity which underlies the generation of field effect inhibitions.

Animals↗
PubMed1983

Axonal trajectories of masticatory motoneurons: a genu formation of axons of jaw-opening motoneurons in the cat.

Axonal courses of jaw-opening motoneurons were examined in the cat by applying horseradish peroxidase to the central cut end of the nerve branch which supplies the mylohyoid and/or the anterior digastric muscle. The axons of mylohyoid and anterior digastric motoneurons, which are located in the ventromedial division of the trigeminal motor nucleus, initially swing dorsally before running ventrolaterally to leave the pons; axons proceeding in the more rostral levels make turns in the more dorsomedial tegmental regions, and those running in the most rostral levels form a small genu in the region near the midline under the floor of the fourth ventricle.

Animals↗
PubMed2000

Excitability changes of dorsal root axons following nerve injury: implications for injury-induced changes in axonal Na(+) channels.

Electrophysiological recordings were obtained from rat dorsal roots in a sucrose gap chamber to study changes in Na(+) currents following nerve injury. Application of 4-aminopyridine unmasks a prominent and well-characterized depolarization (delayed depolarization) following the action potential. In our previous studies, this potential, which is only present in cutaneous afferent axons, has been shown to correlate with activation of a slow Na(+) current. The delayed depolarization in the dorsal root was reduced 1 week after sciatic nerve ligation, suggesting a reduction in the kinetically slow Na(+) currents on dorsal root axons [control: 44. 2+/-7.3% (n=5); injury: 7.3+/-4.7% (n=5), P<0.001]. The refractory period of the action potential was reduced following nerve injury, in agreement with biophysical studies indicating faster "repriming" of fast Na(+) currents on cutaneous afferent cell bodies. Dorsal root ligation near the spinal cord also results in a reduction in the delayed depolarization. These results indicate that changes in Na(+) channel organization occur on dorsal root axons following either central or peripheral target disconnection, suggesting trophic support can be derived from either the CNS or the PNS.

Action Potentials↗
PubMed2001

Axon-glia interactions and the domain organization of myelinated axons requires neurexin IV/Caspr/Paranodin.

Myelinated fibers are organized into distinct domains that are necessary for saltatory conduction. These domains include the nodes of Ranvier and the flanking paranodal regions where glial cells closely appose and form specialized septate-like junctions with axons. These junctions contain a Drosophila Neurexin IV-related protein, Caspr/Paranodin (NCP1). Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis. In the absence of NCP1, normal paranodal junctions fail to form, and the organization of the paranodal loops is disrupted. Contactin is undetectable in the paranodes, and K(+) channels are displaced from the juxtaparanodal into the paranodal domains. Loss of NCP1 also results in a severe decrease in peripheral nerve conduction velocity. These results show a critical role for NCP1 in the delineation of specific axonal domains and the axon-glia interactions required for normal saltatory conduction.

Aging↗
PubMed2002

Neuropilin-2 mediates axonal fasciculation, zonal segregation, but not axonal convergence, of primary accessory olfactory neurons.

The mechanisms that underlie axonal pathfinding of vomeronasal neurons from the vomeronasal organ (VNO) in the periphery to select glomeruli in the accessory olfactory bulb (AOB) are not well understood. Neuropilin-2, a receptor for secreted semaphorins, is expressed in V1R- and V3R-expressing, but not V2R-expressing, postnatal vomeronasal neurons. Analysis of the vomeronasal nerve in neuropilin-2 (npn-2) mutant mice reveals pathfinding defects at multiple choice points. Vomeronasal sensory axons are severely defasciculated and a subset innervates the main olfactory bulb (MOB). While most axons of V1R-expressing neurons reach the AOB and converge into distinct glomeruli in stereotypic locations, they are no longer restricted to their normal anterior AOB target zone. Thus, Npn-2 and candidate pheromone receptors play distinct and complementary roles in promoting the wiring and patterning of sensory neurons in the accessory olfactory system.

Animals↗
PubMed2000

Slit proteins: key regulators of axon guidance, axonal branching, and cell migration.

In the past year, Slit proteins have been identified as important regulators of axon guidance and cell migration in Drosophila and vertebrates. Remarkably, they were simultaneously identified as negative regulators, repelling various axonal and cell migrations in both invertebrates and vertebrates, and as positive regulators, stimulating branching and extension of at least one class of axons in vertebrates.

Animals↗
PubMed1996

The selectivity of motor axons during regeneration with sensory axons.

This study investigated the influence of selective sensory regeneration on less selective motor regeneration in a rat femoral nerve model. The proximal stump of the motor branch to the quadriceps muscle was sutured to the distal stumps of one motor and one sensory branch. Regenerated sensory axons were degenerated secondarily, and motor regeneration was later evaluated. The distal sensory stump attracted both regenerating sensory and motor axons. Misdirected motor axons in the distal branches were not pruned over time. The authors hypothesized that motor regeneration may be been influenced by selective sensory regeneration or non-selective neurotropic attraction.

Animals↗
PubMed1997

Nitric oxide donors reversibly block axonal conduction: demyelinated axons are especially susceptible.

Diseases such as multiple sclerosis and Guillain-Barré syndrome are characterized not only by widespread loss of myelin from nerve fibres, but also by widespread inflammation in the central and peripheral nervous systems, respectively. While the demyelination alone is sufficient to block conduction and thereby cause symptoms, there is increasing evidence that the inflammation may also contribute significantly to the conduction block, although the mechanisms are not understood. Nitric oxide is an important inflammatory mediator which is elevated within the central nervous system in multiple sclerosis and which can be experimentally applied to tissues using nitric oxide donors. We report that such compounds cause reversible conduction block in both normal and demyelinated axons of the central and peripheral nervous systems. Notably, conduction in demyelinated and early remyelinated axons is particularly sensitive to block by nitric oxide, so that at lower concentrations, including those expected at sites of inflammation, demyelinated axons are selectively affected. We therefore propose that inflammation may directly cause symptoms via nitric oxide release, and that the inhibition of such release may open a new therapeutic avenue for demyelinating disease.

Animals↗
PubMed1993

Axonal neurofilamentous accumulations: a comparison between human and canine giant axonal neuropathy and 2,5-HD neuropathy.

The neuropathy produced by the hexacarbon 2,5-hexanedione (2,5-HD) resembles human and canine inherited giant axonal neuropathy (GAN) in the presence of giant axonal swellings that contain accumulations of neurofilaments. The accumulations are both paranodal and internodal in GAN and 2,5-HD induced neuropathy. Detailed morphometry on the neurofilaments reveals that the changes in human and canine GAN are closely similar and differ from those of 2,5-HD neuropathy, suggesting that the mechanisms underlying the formation of the axonal neurofilamentous accumulations differ between the two conditions. In both human and canine GAN, the neurofilaments are more closely spaced and are of greater diameter than in 2,5-HD neuropathy. The changes in the NF in GAN may be the consequence of flattening of the side-arms of the neurofilaments against the axis of the filaments.

Animals↗
PubMed1995

Failure of axon regeneration in postnatal rat entorhinohippocampal slice coculture is due to maturation of the axon, not that of the pathway or target.

Horizontal slices which included the entorhinal area in continuity with the hippocampus were taken from the ventral levels of the cerebral hemispheres of rat pups from two age groups, from the 6th to the 8th postnatal days ('young') and the 12th to the 15th days ('old'). The slices were divided into an entorhinal part and a hippocampal part (which consisted of the hippocampus proper, dentate gyrus and subiculum) by a knife cut passing through the deep white matter of the entorhinal area. The slices were recombined in their normal orientation by matching the cut edges in the following age combinations: young/young, old/old, young/old and old/young. After 14 days in culture, crystals of biocytin were placed on the superficial layers of the entorhinal area. In the young/young combination the same placement of biocytin simultaneously labelled projections passing in both directions across the interface, i.e. (i) orthograde transport of biocytin taken up by entorhinal projection neurons resulted in labelling of axons passing from the entorhinal area across the interface between the cocultures to reach the correct terminal zone in the outer molecular layer of the dentate gyrus, and (ii) retrograde transport of biocytin taken up by axons and their terminals in the entorhinal area labelled the slender subicular and adjacent hippocampal field CA1 pyramidal cells whose axons project to the entorhinal area. In the old/old cocultures there were no projections in either direction. In the mixed age combinations, young entorhinal cortical tissue projected correctly across the interface to old dentate gyrus, but old entorhinal tissue did not project to young dentate gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1980

Somatopetal transport of horseradish peroxidase following incorporation into axonal sprouts and axons in neuromas after nerve transection.

Horseradish peroxidase (HRP) applied to the proximal stump of the facial nerve of the mouse 5 h after section diffused into the endoneurium and was incorporated by endocytosis into axons densely packed with organelles. By 24 h to 16 days after the section, uptake of the tracer into profiles of outgrowing axonal sprouts rich in vesicles and vacuoles was registered. Subsequently HRP accumulated in corresponding perikarya. Tracer transport from neuromas was demonstrated 32 and 64 days after section. In this way influences from outgrowing nerve sprouts and axons in neuromas may reach nerve cell bodies.

Animals↗
PubMed1991

The axonal transport motor 'kinesin' is bound to anterogradely transported organelles: quantitative cytofluorimetric studies of fast axonal transport in the rat.

Monoclonal antibodies to the axonal transport ATPase kinesin were used in an immunofluorescent study on mammalian nerves. Following crushing of the sciatic nerve and the ventral roots of adult rats, immunoreactive material was found to accumulate rapidly, mainly proximal to a crush but also, to some degree, distal to a crush. The strongest immunofluorescence was observed after incubation with the H2 antibody against the heavy subunit of kinesin. Using the cytofluorimetric scanning (CFS) procedure, the accumulated amounts were quantified and it was found that the retrogradely accumulating kinesin-like immunoreactivity (IR) was about 4-12% of the anterogradely transported kinesin-IR. The results were compared to the vesicle marker p38 (synaptophysin), which was found to accumulate to a significant extent on both sides of the crush. Cytofluorimetric scanning measurements indicated that nearly 50% of the anterogradely accumulated p38-IR was recycling to the cell body. The results demonstrate that kinesin in the living axon is affiliated with anterogradely transported organelles. Retrogradely transported organelles appeared to carry very little kinesin-IR, suggesting that kinesin may be subject to turnover, distinct from that of p38, in the distal regions of the axon.

Adenosine Triphosphatases↗
PubMed2006

Getting axons onto the right path: the role of transcription factors in axon guidance.

The normal function of the nervous system requires that the constituent neurons are precisely 'wired together'. During embryogenesis, each neuron extends an axonal process, which can navigate a considerable distance to its target. Although a number of the receptors and guidance signals that direct axonal growth have been identified, less is known about the transcription factors that regulate the expression of these molecules within the neuron and its environment. This review examines recent studies in vertebrates and Drosophila that address the identity of the transcription factors that either control the repertoire of guidance receptors and signals that permits an axon to take a particular trajectory or act themselves as novel extracellular guidance factors.

Animals↗