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PubMed1986

Effects of retrograde axonal transport of Ricinus communis agglutinin I on neuroma formation.

The lectin Ricinus communis agglutinin I (RCAI) was topically applied to transected mouse sciatic nerve or to neuromas formed 2 months after a nerve transection. Fluorochrome-labelled ricin was transferred to the corresponding dorsal root ganglia where it accumulated selectively in the nerve cells, apparently as a consequence of retrograde axonal transport. The ricin caused an almost total loss of the dorsal root ganglionic neurons and, consequently, could prevent formation of neuromas or eliminate an already existing neuroma. The hybrid toxin wheat germ agglutinin (WGA)-ricin-A chain caused no apparent increased sensitivity for neuronal destruction. The drugs doxorubicin and ethidium bromide, similarly applied, labelled satellite and other cells in addition to neurons in the ganglia, and caused only a moderate neuronal loss. The presented method to eliminate neuromas by selectively destroying sensory neurons may provide a means to study pain mechanisms in neuromas.

Animals↗
PubMed2002

Axonally transported peripheral signals regulate alpha-internexin expression in regenerating motoneurons.

The class IV neuronal intermediate filament (IF) family proteins includes the neurofilament (NF) triplet proteins NF-L, NF-M, and NF-H and also the more recently characterized alpha-internexin-NF66. It is well established that NF-L, -M, and -H protein and mRNA are downregulated after peripheral nerve injury. We examined alpha-internexin protein expression after three facial nerve lesion paradigms: crush, transection, and resection. Alpha-internexin immunoreactivity was absent in the perikarya of uninjured facial motoneurons but increased dramatically in all three injury paradigms, with maximum immunoreactivity observed at 7 d after injury. Twenty-eight days after nerve crush or transection, there was a dramatic decrease in the number of alpha-internexin-positive cells. In contrast, alpha-internexin remained elevated 28 d after nerve resection, an injury that hinders regeneration and target reinnervation. In situ hybridization studies showed an increase in alpha-internexin mRNA expression in the facial nucleus at 7 and 14 d after injury. Retrograde transport of fluorogold from the whisker pads to the facial nucleus was seen only in motoneurons that lacked alpha-internexin immunoreactivity, supporting the idea that target reinnervation and inhibitory signals from the periphery regulate the expression of alpha-internexin. Blockage of axonal transport through local colchicine application induced strong immunoreactivity in motoneurons. Alpha-internexin expression was also examined after central axotomy of rubrospinal neurons, which constitutively show alpha-internexin immunoreactivity. After rubrospinal tractotomy, alpha-internexin immunoreactivity transiently increased by 7 d after injury but returned to control levels by 14 d. We conclude that alpha-internexin upregulation in injured motoneurons suggests a role for this IF protein in neuronal regeneration.

Animals↗
PubMed2004

cAMP, tubulin, axonal transport, and regeneration.

Mounting a regenerative response after injury is a multistep process for PNS neurons. The reason for failure of mammalian CNS neurons to regenerate successfully may involve more than one of those steps. Han et al. [Exp. Neurol. 189 (2004) 293] and others show that increasing cAMP levels in neuronal cell bodies elicits a partial regenerative response, altering expression of tubulin isotypes but not expression of other growth-associated genes or rate of axonal transport. This approach allows identification of specific steps in the regenerative response and the roles played by these steps.

Animals↗
PubMed1990

Accumulation of mercury in brainstem nuclei of mice after retrograde axonal transport.

Adult mice were injected intramuscularly in the region of the vibrissae muscles on the left side of the nose with a small volume of mercuric chloride dissolved in distilled water. The animals were killed after 1-6 weeks and fixed by whole-body perfusion. Frozen sections were taken from different levels of the brain stem and from the kidney. The sections were subjected to silver acetate autometallography for visualization of mercury. Mercury was found to accumulate in neurones of the facial nerve nuclei, of the motor trigeminal nuclei and of the trigeminal mesencephalic nuclei of the brain stem, after retrograde axonal transport. Mercury was also demonstrated in proximal tubular cells of the kidney. The mechanism for uptake of mercury at the neuromuscular junctions, and the fate of mercury within neurones are analysed. The possible significance of retrograde metal transport for the development of motor neurone disease is discussed.

Administration, Oral↗
PubMed1990

Effect of gamma-butyrolactone on the retrograde axonal transport of neurotensin in dopaminergic neurones.

gamma-Butyrolactone is a drug known to inhibit the flow of electrical impulses in dopaminergic neurones and to prevent dopamine release in the striatum. In this study, we investigated the effects of this compound on the retrograde transport of neurotensin in the nigrostriatal dopaminergic pathway. The amount of radioactivity measured in the substantia nigra after injection of iodinated neurotensin into the striatum and the time course of its accumulation were not found to be modified in gamma-butyrolactone-treated rats. We therefore conclude that the retrograde axonal transport of neurotensin in the nigrostriatal pathway is not affected by reduced dopaminergic firing or by inhibition of the striatal release of dopamine.

4-Butyrolactone↗
PubMed1994

The relationship of efferent projections from the area postrema to vagal motor and brain stem catecholamine-containing cell groups: an axonal transport and immunohistochemical study in the rat.

The area postrema has been implicated as a major station for the processing of visceral sensory information, involved primarily in eliciting rapid homeostatic responses to fluid and nutrient imbalances. Yet the precise relationship of efferent projections from the area postrema to medullary motor and relay nuclei involved in such functions remains unclear. In this study, axonal transport and immunohistochemical techniques were used to investigate the relationship of efferent projections from the area postrema to vagal motor neurons and medullary catecholamine-containing cell groups in the rat. The results may be summarized as follows: (1) The area postrema gives rise to dense inputs to the commissural and medial parts of the nucleus of the solitary tract. Many of these projections are intimately associated with catecholamine-containing neurons in the A2 and C2 cell groups, including a particularly prominent input to a caudally placed cluster of adrenergic neurons (the C2d cell group) in the dorsal aspect of the medial part of the nucleus of the solitary tract. (2) The area postrema provides a dense input to the external lateral part of the parabrachial nucleus. (3) The area postrema does not project significantly to vagal motor neurons in either the dorsal motor nucleus or the nucleus ambiguus, although the possibility for inputs to distal dendrites of dorsal vagal motor neurons cannot be excluded. (4) En route to the parabrachial nucleus, axons of area postrema neurons traverse the regions of the A1, C1 and A5 cell groups, although these fibers make few arborizations, suggesting little functional contact. Together, these results suggest that sensory information received by the area postrema is dispatched to a restricted set of neurons in the commissural, medial, and dorsal parts of the nucleus of the solitary tract, most probably including catecholamine-containing cells in the A2, C2, and C2d cell groups, and to the external lateral portion of the parabrachial nucleus. The targets of area postrema projections are, in turn, in a position to effect adaptive changes in the activities of hypothalamic neurosecretory neurons, vagal motor neurons, and limbic forebrain regions in response to perturbations in fluid and nutrient homeostasis.

Animals↗
PubMedDate not supplied

Reduced axonal transport of 10S acetylcholinesterase in dystrophic mice.

Extracts of extensor digitorum longus muscle, atria, brain, and sciatic nerve from phenotypically normal and dystrophic ReJ/129 mice were subjected to sucrose density gradient ultracentrifugation, and the amounts of acetylcholinesterase (AChE) activity associated with each major enzyme form were determined. Normal muscle showed approximately equivalent amounts of the 4S, 10S, and 16S forms of AChE, while dystrophic muscle was relatively deficient in 10S AChE and relatively oversupplied with 4S AChE. This abnormality was not present in the other tissues examined. However, as measured by the 24-hour accumulation of enzyme activity proximal to a ligature on the sciatic nerve, the axonal transport of 10S AChE was only about one third as great in dystrophic as in normal nerve. This result is consistent with the view that the reduction in the amount of this enzyme form in dystrophic muscle could be related to disturbances in a transport-dependent trophic interaction between nerve and muscle.

Acetylcholinesterase↗
PubMed1983

Concentration dependence of rapid axonal transport: a study of the transport kinetics of [35S]methionine-labeled protein in postganglionic sympathetic fibers of the bullfrog.

The kinetics of transport of radiolabeled proteins in sympathetic axons of the bullfrog sciatic nerve were examined after injection of [35S]methionine into the S9 sympathetic ganglion. Under resting conditions at 20 degrees C, the fastest moving material was carried distally at 5.7 +/- 0.3 mm/hr. Various manipulations of temperature in the proximal part of the nerve were used to alter the amount of protein transported into the distal region, which was always kept at 20 degrees C. The velocity in this test region was found to increase to over 9 mm/hr when material that had accumulated at a cold block for 4 hr was released by rewarming. This acceleration was transient, and base line velocity was regained after 2 hr. In order to increase the local concentration of transported protein by a second method, the proximal part of several nerves was warmed to 28 degrees C. Maximal transport velocity in the 20 degrees C test region rose to 6.2 +/- 0.12 mm/hr. To decrease the local concentration of transported protein, the proximal part of other nerves was cooled to 15 degrees C. Maximal transport velocity in the 20 degrees C test region fell to 4.7 +/- 0.7 mm/hr. We conclude that there is a small but real tendency for the velocity of rapid axonal transport in this neural system to be positively related to the availability of material suitable for transport.

Animals↗
PubMed1985

[Efferent connections of the caudate nucleus of the cat studied using retrograde axonal transport of horseradish peroxidase].

The origin of descending efferent pathways from the caudate nucleus was studied by retrograde axonal transport of horseradish peroxidase. Widespread topically organized projections were observed to the paleostriatum and the substantia nigra and less numerous to the thalamus. The main source of these projections were small and medium-size cells. A particular role of the subthalamic nucleus in the descending efferent system of the caudate nucleus is pointed out: this nucleus besides projections to the caudate nucleus itself possesses direct connections with principal output structures of the latter--the the paleostriatum and substantia nigra.

Animals↗
PubMed1977

The effect of the retrograde axonal transport of nerve growth factor on the morphology of adrenergic neurones.

An injection of nerve growth factor (NGF) into one eye of neonatal rats results in an increase in the tyrosine hydroxylase activity of the ipsilateral superior cervical ganglion. This effect was seen maximally after the intraocular injection of a depot preparation of NGF linked to cellulose. The sympathetic neurones that innervate the eye can be identified by autoradiography after the retrograde axonal transport of either NGF or tetanus toxin labelled with [125I]iodine. It was only those cells having their terminals in the vicinity of the depot preparation. This demonstrates that NGF transported from the periphery to the cell bodies is effectively retained within the transporting cell and is not released to act on extracellular receptors within the ganglion. It is suggested that this specificity of action for NGF reaching the ganglion in this fashion is important during normal development in determining the survival of adrenergic neurones.

Animals↗
PubMed1976

The effect of nicotine on intra-axonal transport in cholinergic motor neurons of the rat; influence of acutely administered, non-toxic doses.

The intra-axonal transport of acetylcholine (ACh) and ACh-metabolizing enzymes in rat sciatic nerves was studied following nicotine treatment. The nicotine was administered in a low dose (30 mug/kg) s.c. every second h for 18-22 h, to mimic the serum-concentrations of a cigarette smoker. Control rats received s.c. injections of the vehicle. The main effects were observed regarding the ACh-esterase (AChE) activity. In unoperated nerves the level was decreased by about 10%. In 12 h crushed nerves the accumulation of enzyme activity proximal to the crush was markedly reduced in the nicotine-treated group, indicating a reduction in amount of proximo-distally transported enzyme activity. The ACh-levels were unchanged except at 12 h postoperatively when a small increase proximal to the crush was observed. The choline-acetyl transferase (CAT) activity in unoperated nerves was similar in both groups of rats; the 7 h accumulation above the crush, however, was somewhat reduced after nicotine treatment. The possible causes of the observed nicotine induced changes are so far not known.

Acetylcholine↗
PubMed2000

Axonal transport of NADPH-diaphorase and [(3)H]nitro-L-arginine binding, but not [(3)H]cGMP binding, by the rat vagus nerve.

Previous studies have shown that the NO(ccirf)-cGMP pathway may be functionally relevant in the nodose ganglion and at afferent terminations of the vagus nerve. The technique of unilateral vagal ligations, using double ligatures, was combined with the techniques of NADPH-diaphorase histochemistry, as an index of nitric oxide synthase (NOS) activity, and autoradiography using the radioligands [(3)H]nitro-L-arginine and [(3)H]cGMP, to examine axonal transport of NOS and cGMP-dependent effectors by the rat vagus nerve. A population of perikarya in the nodose ganglia was NADPH-diaphorase positive, and binding of both [(3)H]nitro-L-arginine and [(3)H]cGMP was found on the nodose ganglia. Following vagal ligation, NADPH-diaphorase reactivity accumulated proximal to the proximal ligature and distal to the distal ligature. Vagus nerve transection beyond the distal ligature eliminated NADPH-diaphorase reactivity at the distal ligature. Similarly, [(3)H]nitro-L-arginine binding was found over the nodose ganglion; and after vagal ligation, an accumulation of [(3)H]nitro-L-arginine binding was seen adjacent to the proximal ligature, though little binding was found adjacent to the distal ligature. No accumulation of [3H]cGMP binding was found adjacent to either the proximal or the distal ligatures. These findings suggest that the rat vagus nerve bidirectionally transports NOS, the enzyme involved in biosynthesis of NO(ccirf) by nitroxidergic nerves. As anticipated, [(3)H]nitro-L-arginine, a competitive inhibitor of the amino acid precursor for NO(ccirf), binds only to a centrifugally transported moiety that we conjecture is NOS, while cGMP apparently is not subject to transport. These data further support the use of NO(&z.ccirf;) in transmission at vagal afferent terminals.

Animals↗
PubMed1991

Two 68-kDa proteins in slow axonal transport belong to the 70-kDa heat shock protein family and the annexin family.

The major 68-kDa protein found selectively in the faster of the two subcomponents of slow axonal transport [group IV or slow component b (SCb)] in the rat sciatic nerve has been characterized. It was found to contain two distinct classes of proteins, S1 and S2, both of which have isoelectric points of 5.7, but differ in their solubility in the presence of calcium. The S1 protein, which contributes up to 70% of the 68-kDa component, was soluble in the presence or absence of calcium, whereas the S2 protein was bound to the cytoskeleton in a calcium-dependent manner. Further characterization of the two proteins by peptide mapping and immunological methods revealed that the S1 protein belonged to a family of proteins related to the 70-kDa heat shock protein, whereas the S2 protein was identical to 68-kDa calelectrin (annexin VI). Selective occurrence in SCb of these proteins with potential abilities to regulate protein-protein or protein-membrane interactions suggests that they may play important roles in the control of cytoskeletal organization in the axon, because SCb contains mainly cytoskeletal proteins in a more dynamic form compared with the slowest rate component, slow component a, which is enriched in the stably polymerized form of these proteins.

Animals↗
PubMed2006

Matrix-mediated gene transfer to brain cortex and dorsal root ganglion neurones by retrograde axonal transport after dorsal column lesion.

BACKGROUND: In previous studies, we showed that the immobilisation of DNAs encoding basic fibroblast growth factor, neurotrophin-3 and brain-derived neurotrophic factor in a gene-activated matrix (GAM) promotes sustained survival of axotomised retinal ganglion cells after optic nerve injury. Here, we evaluated if the immobilisation of DNAs in a GAM could be an effective approach to deliver genes to axotomised dorsal root ganglion (DRG) neurones after spinal cord injury and if the matrix component of the GAM would modulate the deposition of a dense scar at the injury site. METHODS: We evaluated the expression of the thymidine kinase (TK) reporter gene in brain cortex and DRG after a bilateral T8 dorsal column (DC) lesion using PCR, RT-PCR and in situ hybridisation analyses. Collagen-based GAMs were implanted at the lesion site and the cellular response to the GAM was assessed using cell-specific markers. RESULTS: At 1 week post-injury, PCR analyses confirmed that DNATK was retrogradely transported from the DC lesion where the GAM was implanted to the brain cortex and to caudal DRG neurones, and RT-PCR analyses showed expression of mRNATK. At 7 weeks post-injury, DNATK was still be detected in the GAM and DRG. In situ hybridisation localised DNATK and mRNATK within fibroblasts, glia, endothelial and inflammatory cells invading the GAM and in DRG neurones. Interestingly, the presence of a GAM also reduced secondary cavitation and scar deposition at the lesion site. CONCLUSIONS: These results establish that GAMs act as bridging scaffolds in DC lesions limiting cavitation and scarring and delivering genes both locally to injury-reactive cells and distally to the cerebral cortex and to DRG neuronal somata through retrograde axonal transport.

Animals↗
PubMed1984

Inferior olivary neurons: 3-acetylpyridine effects on glucose consumption, axonal transport, electrical activity and harmaline-induced tremor.

The effects of 3-acetylpyridine (3-AP) on the neurons in the inferior olive (IO) were studied by several methods to establish the time-order of events due to the neurotoxicity of 3-AP in the rat. It was found that IO metabolism, studied with [14C]2-deoxyglucose, began to decrease detectably 1 h after 3-AP and was totally suppressed at 3 h. Retrograde axonal transport of lectin horseradish peroxidase (HRP) from cerebellar cortex to the IO was also totally suppressed 3 h after 3-AP and in fact showed a time course similar to that for the suppression of metabolism. Harmaline produced tremor has been shown to induce rhythmic activity and increase glucose consumption in the IO. When injected in 3-AP treated animals, harmaline produced its usual effects at 2 h after the 3-AP but had no effects after 3 h. The present results indicate that the neurotoxic effects of 3-AP are not simply graded in time, but tend to have the greatest effects between the 2nd and 3rd hour following its administration.

Alkaloids↗