Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Axonal Transport”

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 649 records · Page 36Linked to original sources
PubMed1996

Axonal transport of nitric oxide synthase in autonomic nerves.

By using mechanical nerve ligation or nerve pinch technique, we provide evidence that nitric oxide synthase (NOS) is transported in the preganglionic sympathetic axons, while postganglionic axons lack NOS transport. This finding corroborates the preganglionic sympathetic terminal as the site of NO synthesis, which is known to affect ganglionic transmission. Both vasoactive intestinal polypeptide (VIP) and substance P (SP) containing neurons of the nodose ganglion transport NOS in their axons. These results therefore suggest that NOergic innervation of autonomically innervated tissues is of parasympathetic and/or sensory, rather than sympathetic, origin.

Animals↗
PubMed1990

Impairment of retrograde axonal transport in wobbler mouse motor neuron disease.

The earliest horseradish peroxidase (HRP) neuronal labeling (the fastest retrograde transport) was determined by histochemical techniques at various intervals after intramuscular HRP injection in wobbler mice and normal littermates. In the clinically impaired forelimb system, the retrograde transport rate was 150-170 mm/day in wobbler mice and 170-230 mm/day in controls. However, there was no statistical difference between the two groups. The neuronal HRP accumulation at the early intervals was significantly less in wobbler mice than controls, suggesting that the amount of HRP transport was diminished in each axon. For the clinically intact hindlimb nerves, the rate was normal in wobbler mice, but the amount of neuronal HRP was significantly increased. Retrograde axonal transport appeared to be affected in a differential fashion, depending on the extent of disease.

Animals↗
PubMed1982

Protein synthesis and fast axonal transport in regenerating goldfish retinal ganglion cells.

To characterize the fast component of axonal transport in regenerating goldfish optic axons, the incorporation of L-2,3-[3H]proline into newly-synthesized proteins in the cell bodies of the retinal ganglion cells and the amount of transported labeled protein were determined at 2-36 days after cutting the optic tract. Both the incorporation and the amount of transported protein had doubled by 10 days after the lesion and continued to increase to about 5 times normal at 15 days, a time when a large proportion of the regenerating axon population had reached the optic tectum. Near-normal levels were recovered by 36 days. In contralateral control neurons, the incorporation of L-2,3-[3H]proline was unchanged from normal throughout, whereas the amount of labeled transported protein entering control axons was decreased by 55% at 2 and 10 days after the testing lesion, returning to normal by 15 days. An increase in fast transport velocity was seen in the regenerating axons beginning at 10 days after the lesion. However, a similar velocity increase was also seen in the contralateral control axons and in undamaged axons following removal of the cerebral hemispheres. Therefore, the velocity increase was not a specific consequence of axotomy.

Amino Acids↗
PubMed1982

[Alterations in axonal transport. Role in peripheral neuropathies (author's transl)].

In peripheral nerves, the use of radioisotopes or enzyme markers makes it possible to study the traffic of molecules and cell organelles, which flow along the axons in both directions. Such axonal transports ensure the renewal of most macromolecular components in the axons and hence contribute to maintain healthy peripheral nerve fibers. A lasting alteration of the mechanisms, which sustain transport or distribution of axonal constituents, could therefore initiate or reinforce pathological processes responsible for various human axonopathies. Investigation of axonal transport in genetic or toxic neuropathies in animals drows attention to the key-role played by neuronal dynamics in pathogenesis of nerve lesions.

Animals↗
PubMed1987

Reduced anterograde and retrograde accumulation of axonally transported phosphofructokinase in streptozotocin-diabetic rats: effects of insulin and the aldose reductase inhibitor 'Statil'.

This study examined anterograde and retrograde accumulation of axonally transported 6-phosphofructokinase activity, proximal and distal to sciatic nerve constrictions, in rats with streptozotocin-induced diabetes of 4 weeks' duration. There were deficits in accumulation on both sides of the constriction in untreated diabetic rats (proximal accumulation 66% of controls, p less than 0.05; distal accumulation 32% of controls, p less than 0.01). There was also a reduction in the phosphofructokinase activity per unit length unconstricted sciatic nerve in the untreated diabetic rats (87% of controls, p less than 0.05). Treatment of an age-matched group of diabetic rats with twice-daily insulin prevented all the above changes. There were significant increases, over untreated diabetic rats, in phosphofructokinase activity accumulated at constrictions (p less than 0.01 for both proximal and distal) and in unconstricted nerve (p less than 0.05). Indeed the activities measured in insulin-treated diabetic rats were virtually identical to those of controls. Treatment of a third group of diabetic rats with the aldose reductase inhibitor 'Statil' prevented or attenuated accumulations of polyol pathway metabolites and prevented depletion of myo-inositol in the sciatic nerve. In spite of these indications of effective aldose reductase inhibition, the drug was without effect on the deficits in accumulation of activity at ligatures or unconstricted nerve levels of phosphofructokinase activity. We conclude that short-term experimental diabetes in rats induced defects in both anterograde and retrograde axonal transport of 6-phosphofructokinase activity. These defects were prevented by intensive insulin treatment but were resistant to an effective aldose reductase inhibitor, indicating a lack of involvement of polyol pathway flux in their pathogenesis.

Aldehyde Reductase↗
PubMed1982

Ganglioside-induced acceleration of axonal transport following nerve crush injury in the rat.

The role of gangliosides in the re-establishment of neuronal continuity was examined in rats whose peroneal nerve had been crushed by a standardized procedure. Neuronal continuity was determined by the ability of the nerve to transport horseradish peroxidase retrogradely back to the spinal cord. The number of retrogradely labeled neurons provided an index of the degree of axonal transport that was re-established. Comparison of ganglioside-treated animals with saline-treated controls showed that ganglioside treatment advanced the re-establishment of retrograde axonal transport by 3 days.

Animals↗
PubMed1982

Microtubules and the capacity of the system for rapid axonal transport.

Current information favors the view that microtubules are required for rapid axonal transport of proteins and organelles but are normally present in surplus. Different types of axons tolerate losses of between 35 and 65% of their microtubules during exposure to low temperatures or antimitotic drugs before transport is impaired. Greater losses of microtubules are associated with progressive and marked failure of transport. The normal surplus of microtubules may explain why adrenergic axons of rabbit peroneal nerve have spare transport capacity, which enables them to transport between two and three time as much material as they do ordinarily. Spare capacity for transport is diminished or absent when nerves are incubated at temperatures that lead to a partial loss of microtubules. These observations are considered in the light of the hypothesis that the local density of microtubules determines the maximal local concentration of material that can be carried by rapid transport along vertebrate axons.

Adrenergic Fibers↗
PubMed1983

Characterization of axonally transported glycoproteins in regenerating garfish olfactory nerve.

This study examined changes in composition and concanavalin A (Con A) binding of axonally transported glycoproteins and their pronase-generated glycopeptides in regenerating garfish olfactory nerve. A previous study had demonstrated a regeneration-related increase in the proportion of [3H]glucosamine label in lower-molecular-weight Con A-binding glycopeptides derived from transported glycoproteins. Further analysis of carbohydrate composition shows that these molecules resemble mannose-rich oligosaccharides in composition and are increased in absolute amount in regenerating nerve. Subcellular analysis shows that the Con A-binding glycopeptides are enriched in membrane subfractions, particularly in a high-density fraction that morphologically resembles isolated cell surface coat. Regeneration-related changes in intact axonally transported glycoproteins were also detected. Sodium dodecyl sulfate gel electrophoresis of transport-labeled glycoproteins disclosed growth-correlated increases in radioactivity associated with 180-200K, 105-115K, and 80-90K components, while a 150-160K molecular weight class of glycoproteins was diminished in relative labeling. Intact glycoproteins displaying an affinity for Con A were also augmented in regenerating nerve, the increases occurring primarily in molecules in the 50-140K range.

Animals↗
PubMed1982

Synthesis, and central and peripheral axonal transport of substance P in a dorsal root ganglion-nerve preparation in vitro.

A preparation of the rat L5 dorsal root ganglion with 6 mm lengths of dorsal root and peripheral branch attached was incubated in vitro over a 9 h period. The substance P-like immunoreactivity (SPLI) of the preparation increased linearly with time and SPLI was transported down both branches. The turnover-time of ganglion SPLI was 3.6 h. Four times as much SPLI accumulated in the peripheral branch as in the dorsal root. When axonal transport was inhibited by demecolcine, SPLI was formed at the same rate but accumulated in the ganglion. Anisomycin inhibited SPLI synthesis after a delay of 2 h. It was apparent that the SPLI of the preparation was contained in two pools, only one of which underwent rapid axonal transport. The mobile pool of axonal SPLI comprised 30% of the total and moved with a velocity of 4.9 mm . h-1.

Animals↗
PubMed1992

Changes of fast axonal transport by taxol injected subepineurally into the rat sciatic nerve.

In contrast to the complete and long-lasting inhibition of tubulin transport, taxol has no effect on fast axonal transport examined immediately after its sub-epineural application to rat sciatic nerve. However, a significant accumulation of rapidly migrating radioactivity appears at the site proximal to the injection when examined a few weeks after treatment, probably due to mechanical obstruction caused by abnormal aggregation of a huge number of intra-axonal microtubules. It also decreases slightly in amount within a few weeks post-treatment, which may be due to reduction of the number of axons caused by degeneration.

Animals↗
PubMed1981

An increase in smooth endoplasmic reticulum and a decrease in Golgi apparatus occur with ionic conditions that block initiation of fast axonal transport.

The ultrastructure of bullfrog spinal ganglia was analyzed after incubation in media containing concentrations of calcium and cobalt known to inhibit export of proteins from the soma to the axon. Although most somal organelles were morphologically unchanged by the various incubation media, striking changes were seen in the smooth endoplasmic reticulum (SER) and the Golgi apparatus (GA). In order of effect, calcium-free medium (CFM), normal medium supplemented with cobalt (NM--Co), and CFM supplemented with cobalt (CFM--Co) produced increasing amounts of SER coupled with decreasing densities of GA stacks. In the extreme case, CFM--Co incubation resulted in a nearly 10-fold increase in SER volume as well as in a virtually complete depletion of GA stacks. Axons originating within the ganglion were also examined and showed little change after the various incubations. The rank order of the altered incubation media in producing morphological changes was the same as the relative effectiveness of the media in depressing the fast axonal transport of [3H]protein within the dorsal root ganglion neurons. The morphological and biochemical results are discussed with respect to establishing the localization of the calcium-dependent step(s) that has been proposed to occur in the neuronal soma during the initiation of axonal transport.

Animals↗
PubMed1980

Facilitated ultracytochemical demonstration of retrograde axonal transport of horseradish peroxidase in peripheral nerve.

p-Phenylenediamine/pyrocatechol mixture (PPD-PC) was evaluated as a reagent for the ultracytochemical demonstration of retrograde axonal transport of horseradish peroxidase (HRP). HRP crystals were applied to the proximal stumps of the severed infraorbital nerves in rats. After 48 h the rats were sacrificed by perfusion, and the trigeminal ganglia ipsilateral to the severed nerves were processed for HRP cytochemistry and then prepared for electron microscopy. PPD-PC was rapidly oxidized in HRP-labeled neurons to form a dark brown-black osmiophilic reaction product which was more readily visible than the DAB product in the sections. This facilitated selection by light microscopy of areas in the epoxy wafers for ultrathin sectioning. In thin sections viewed under the electron microscope, the osmicated electron opaque PPD-PC reaction product was present in membrane-bound structures including smooth endoplasmic reticulum and granules of various sizes. The PPD-PC reaction product formed after 10-min incubation appeared to be more electron opaque than the DAB reaction product formed after 20 min. PPD-PC was found to be much less readily oxidized than DAB by endogenous hemoproteins. This methodology facilitated the ultracytochemical localization of HRP in neurons following retrograde axonal transport.

3,3'-Diaminobenzidine↗
PubMed1995

Differential role of the low affinity neurotrophin receptor (p75) in retrograde axonal transport of the neurotrophins.

The receptor mechanisms mediating the retrograde axonal transport of the neurotrophins have been investigated in adult rats. We show that transport of the TrkB ligands NT-4 and BDNF to peripheral neurons is dependent on the low affinity neurotrophin receptor (LNR). Pharmacological manipulation of LNR in vivo using either an anti-LNR antibody or a soluble recombinant LNR extracellular domain completely blocked retrograde transport of NT-4 and BDNF to sensory neurons, while having minimal effects on the transport of NGF in either sensory or sympathetic neurons. Furthermore, in mice with a null mutation of LNR, the transport of NT-4 and BDNF, but not NGF, was dramatically reduced. These observations demonstrate a selective role for LNR in retrograde transport of the various neurotrophins from distinct target regions in vivo.

Animals↗
PubMed1987

Orthograde and retrograde axonal transport of dopamine-beta-hydroxylase in ileal mesenteric nerves of rats with chronic streptozotocin diabetes.

Rats with chronic streptozotocin-induced diabetes develop a neuropathy involving the ileal mesenteric nerves. Distal portions of these postganglionic sympathetic axons develop markedly dilated, dopamine-beta-hydroxylase (DBH)-containing dystrophic swellings. These findings led us to develop a quantitative method to examine orthograde and retrograde axonal transport of DBH in ileal mesenteric nerves. Surprisingly, no significant alteration in orthograde or retrograde axonal transport of DBH was identified.

Animals↗
PubMed1992

The neurotrophins BDNF, NT-3, and NGF display distinct patterns of retrograde axonal transport in peripheral and central neurons.

The pattern of retrograde axonal transport of the target-derived neurotrophic molecule, nerve growth factor (NGF), correlates with its trophic actions in adult neurons. We have determined that the NGF-related neurotrophins, brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), are also retrogradely transported by distinct populations of peripheral and central nervous system neurons in the adult. All three 125I-labeled neurotrophins are retrogradely transported to sites previously shown to contain neurotrophin-responsive neurons as assessed in vitro, such as dorsal root ganglion and basal forebrain neurons. The patterns of transport also indicate the existence of neuronal populations that selectively transport NT-3 and/or BDNF, but not NGF, such as spinal cord motor neurons, neurons in the entorhinal cortex, thalamus, and neurons within the hippocampus itself. Our observations suggest that neurotrophins are transported by overlapping as well as distinct populations of neurons when injected into a given target field. Retrograde transport may thus be predictive of neuronal types selectively responsive to either BDNF or NT-3 in the adult, as first demonstrated for NGF.

Animals↗
PubMed1984

A new methodological approach for studying axonal transport: cytofluorometric scanning of nerves.

A new technique for studying axonal transport has been developed. The technique, which is based on histofluorescence techniques, enables the measurement of several different accumulated substances and parameters within a single nerve in relation to a nerve crush or local cooling. Any substance that can be made to fluoresce can be measured. The tissue is treated according to the formaldehyde-induced fluorescence method of Hillarp and Falck for visualization of monoamines, or according to the indirect immunofluorescence method. For immunofluorescence the nerve is cryostat-sectioned and various sections can be incubated with primary antisera against different antigens. After incubation and mounting the sections are placed in a cytofluorimeter (Leitz MPV II). They are passed under a measuring slit at a steady speed by a motor driven cross-table. The fluorescence intensity passing through the measuring slit is continuously registered by a recording unit with an integrator. This recorder produces a graphical nerve accumulation profile, and the area under the profile, relating to the fluorescence, is expressed in arbitrary units. This article presents data on the accumulation of noradrenaline, dopamine beta-hydroxylase, and tyrosine hydroxylase in crush-operated rat sciatic nerve. The time-course accumulations for noradrenaline (visualized by the Falck and Hillarp method) and dopamine beta-hydroxylase (visualized by immunofluorescence) demonstrated a striking similarity, which is to be expected since the two substances are stored in the same organelle. Tyrosine hydroxylase (visualized by immunofluorescence) showed a slower accumulation with time, but faster than would be expected had the enzyme been 100% soluble. Colchicine but not lumi-colchicine blocked the transport of noradrenaline organelles. With the new scanning technique we have the potential to study accumulation profiles of several different substances within a single nerve. Morphometric data, morphological observations, and photograph documentation of the same nerve section are also available.

Animals↗
PubMed1981

'Acrylamide-induced' neuropathy and impairment of axonal transport of proteins. II. Abnormal accumulations of smooth endoplasmic reticulum as sites of focal retention of fast transported proteins. Electron microscope radioautographic study.

The distribution of fast axonally transported proteins was studied by electron microscope radioautography in ciliary ganglia of chickens treated or not treated with acrylamide. At 3 h after the intracerebral injection of [3H]lysine, the preganglionic axons of the untreated chickens displayed few silver grains, mainly associated with smooth endoplasmic reticulum (SER) profiles. In most axons of acrylamide-treated chickens, a similar pattern was observed, except in axons which exhibited focal and intense labeling underneath the axolemma: clusters of silver grains indeed overlayed peripheral accumulations of tubulovesicular profiles of SER, dense core vesicles and mitochondria. After impregnation with heavy metals, electron microscope observation of 1 micrometer thick sections showed a locally disorganized SER forming a complex network of tubules intermingled with vesicles and mitochondria. Such a local disorganization of the peripheral SER in the distal part of the axons, could be responsible for the focal stasis of fast transported proteins; it seems to be one of the earliest changes detectable in axons damaged by acrylamide treatment.

Acrylamides↗
PubMed1986

Alpha-tubulin is not detyrosylated during axonal transport.

We have examined the question of whether alpha-tubulin is detyrosylated during axonal transport in retinal ganglion cell axons and axons of spinal motor neurons. The degree of tyrosylation of alpha-tubulin was estimated from immunocytochemistry and immunoblotting with two anti-alpha-tubulin monoclonals, one of which (YL1/2) recognizes only the tyrosylated form of alpha-tubulin. In the case of retinal ganglion cells, the axons were depleted of tyrosylated alpha-tubulin both in the retina and proximal region of the optic nerve. Distal regions of the axons, in the optic tract, gave a pattern of staining consistent with a reduction in the total level of alpha-tubulin at the expense of detyrosylated alpha-tubulin. Axons within the L5 ventral root, the sciatic nerve and tibial nerve were consistently unstained by YL1/2 indicating that these axons were depleted in tyrosylated alpha-tubulin in all 3 segments. The results indicate that alpha-tubulin destined for axonal microtubules is detyrosylated close to or in cell bodies and not progressively during its transport. Therefore the segregation of detyrosylated alpha-tubulin to axonal microtubules may occur at their site of assembly.

Animals↗