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PubMed1986

Intraocular colchicine inhibits competition between resident and foreign optic axons for functional connections in the doubly innervated goldfish optic tectum.

After unilateral optic tectum ablation in the goldfish, regenerating optic axons grow into the optic layers of the remaining ipsilateral tectal lobe and regain visual function. The terminal arbors of the foreign fibers are initially diffusely distributed among the resident optic axons, but within two months the axon terminals from each retina are seen to segregate into irregular ocular dominance patches. Visual recovery is delayed until after segregation. This suggests that the foreign fibers compete with the residents for tectal targets and that the segregation of axon terminations is an anatomical characteristic of the process. Here we investigate whether inhibiting axonal transport in the resident fibers inhibits competition with foreign fibers. The eye contralateral to the intact tectal lobe received a single injection of 0.1 microgram colchicine, which does not block vision with the intact eye. We measured visual function using a classical conditioning technique. Segregation of axon terminations was examined shortly following visual recovery by autoradiography. The no-drug control fish showed reappearance of vision with the experimental eye at 9 weeks postoperatively and ocular dominance patches were well developed. Colchicine administered to the intact eye (resident fibers) several weeks postsurgery decreased the time to reappearance of vision with the experimental eye by several weeks. Autoradiography revealed some signs of axonal segregation but the labeled foreign axons were mainly continuously distributed. Administration of colchicine at the time of tectum ablation, or of lumicolchicine at two weeks postoperatively produced normal visual recovery times. Fast axonal transport of 3H-labeled protein was inhibited by 1.0 and 0.5 microgram but not by 0.1 microgram of colchicine or by 1.0 microgram of lumicolchicine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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↗
PubMed1986

Current-distance relations of axons mediating circling elicited by midbrain stimulation.

Stimulation of mediocaudal midbrain in rats produces ipsiversive circling due to the stimulation of longitudinal axons. The refractory periods of these axons were measured by delivering trains of conditioning and testing pulses via a single electrode at various conditioning-testing (C-T) intervals. As C-T interval increased from 0.3 to 2.0 ms, the frequency required to produce a constant amount of circling halved. The current-distance relations of these axons were measured by placing two electrodes lateral to one another, and delivering conditioning pulses via one electrode and testing pulses via the second electrode. The required frequency decreased less at C-T intervals in the refractory period range using two electrodes rather than using a single electrode. This partial refractoriness suggests that only part of the axons were stimulated by both electrodes. The refractoriness increased as current increased or as interelectrode distance decreased. The overlap in the fields of stimulation at each current was calculated from the refractoriness observed in single and double electrode experiments. The results suggest that the axons mediating circling have a wide range of thresholds rather than a single threshold. The current required to activate an axon is roughly equal to K X r2, were K is a constant and r is the radial distance from electrode to axon. K must range from 400 to at least 3000 microA/mm2, to account for the circling data. For axons mediating medial forebrain bundle self-stimulation3, K must range from 1000 to at least 6400 microA/mm2. Estimation of the K distribution allows calculation of the effects of electrode size, placement and current on the recruitment of axons with different thresholds.

Animals↗
PubMed1987

Two immunohistochemically identified populations of calcitonin gene-related peptide (CGRP)-immunoreactive axons in human skin.

Double labelling immunofluorescence has shown two populations of unmyelinated sensory axons in human skin that contain immunoreactivity (IR) to calcitonin gene-related peptide (CGRP). One population also contains IR to substance P (SP), whilst the other also contains IR to somatostatin (SOM). Axons containing both CGRP-IR and SOM-IR comprised more than 75% of CGRP-IR axons associated with the epidermis; the rest of the CGRP-IR axons contained SP-IR. No axons contained both SP-IR and SOM-IR. Some dermal blood vessels were surrounded by axons containing both CGRP-IR and SP-IR, but most CGRP-IR perivascular axons contained SOM-IR without SP-IR. Sweat glands were well supplied with sensory axons containing CGRP-IR and weak SOM-IR but not SP-IR. Therefore, CGRP is a histochemical marker for a larger number of unmyelinated cutaneous afferents in human skin than is SP. CGRP itself may have a role in the mediation of responses to stimulation of at least two populations of sensory axons.

Axons↗
PubMed1988

Organelle dynamics in lobster axons: anterograde and retrograde particulate organelles.

Particulate organelles in isolated axons from the walking legs of the lobster were detected with differential interference contrast optics and video microscopic techniques. The motion of the organelles was studied in normal axons, in axons whose surface membrane was rendered permeable with saponin, and in axoplasm extruded from the axons. In normal axons at 20-22 degrees C, organelles moved more rapidly in the anterograde direction than in the retrograde direction (respective mean velocities 1.73 micron/s and 0.63 micron/s). The instantaneous velocities of both sets of organelles were variable: those of the anterograde organelles varied less than those of retrograde organelles. The variation in instantaneous velocity was patterned; all organelles studied had velocities that fluctuated slowly with a major frequency at about 0.1 Hz. Some organelles oscillated about a fixed position at a similar major frequency. In axons with a permeabilized surface membrane there was no organelle motion unless adenosine 5'-triphosphate (ATP) was present in the bathing medium. Organelle motion reactivated with ATP was patterned in a way similar to that in normal intact axons. In extruded axoplasm in the presence of ATP, organelles moved along transport filaments that were assumed to be microtubules. Movement of organelles from one transport filament to another was not accompanied by changes in motion that could explain the normal fluctuation in velocity. The evidence indicates that the variable, or oscillatory, character of organelle motion in lobster axons is caused by an active component of the mechanisms of axonal transport.

Animals↗
PubMed1991

Light and electron microscopic analyses of intraspinal axon collaterals of sympathetic preganglionic neurons.

Experiments were performed in pigeons (Columba livia). Sympathetic preganglionic neurons (SPNs) in the first thoracic spinal cord segment (T1) were identified electrophysiologically using antidromic activation and collision techniques and then intracellularly labeled with horseradish peroxidase (HRP). In 6 of 10 HRP-labeled SPNs, the site of axon origin and intraspinal axonal trajectory could be specified. In 2 of the 6 HRP-labeled axons, the peripherally projecting process branched intraspinally. The presence or absence of SPN intraspinal axonal collateralization did not correlate with parent perikaryal subnuclear location or dendritic alignment. None of the collaterals were recurrent onto the SPN of origin. Light microscopically, the collateral branches appeared to end with punctate, bulbous swellings. The spinal regions of the terminal end swellings for the two axons did not overlap one another. In one instance the entire terminal field was confined within the principal preganglionic cell column (column of Terni). The other axon had collateral branches which terminated in the lateral white matter and in a ventrolateral region of lamina VII. A serial section, electron microscopic reconstructive analysis of the entire intraspinal collateral terminal field within the column of Terni revealed that: (a) the primary collateral process was unmyelinated and arose at a node of Ranvier; (b) after issuance of the collateral branch, the myelinated parent axon continued to increase its myelin wrapping throughout the spinal gray; (c) the bulbous swellings observed light microscopically corresponded to axon terminal boutons and regions of synaptic contact; (d) the axon collateral terminals were exclusively presynaptic to small caliber dendrites and formed only asymmetric specializations; and (e) the collateral terminals contained numerous mitochondria, and densely packed, electron-lucent, spherical vesicles.

Animals↗
PubMed1983

The polarity of axon growth in the wings of Drosophila melanogaster.

We have analyzed the growth of axons in the wings of the mutants Hairy wing and hairy of Drosophila melanogaster. These mutants produce many supernumerary bristle organs and sensilla campaniformia, whose axons grow between the two wing epithelia and can be visualized in both pupal and adult stages. The sensory axons of wild-type animals follow two paths in the wing, within longitudinal veins L1 and L3, and always grow with a distal to proximal polarity. In the mutants, all axons following these two paths likewise grow with correct polarity. Axons elsewhere in the wing, however, are found to grow in many different directions, including from proximal to distal and hence directly away from the central nervous system. A variety of patterns of axon growth and fasciculation are seen in different individuals. Only if the supernumerary axons encounter the two normal paths do they reliably grow toward the base of the wing. We conclude that these two paths provide polarity information for axon growth, information which is either not used or not available elsewhere in the wing in spite of the obvious morphological polarization of every epithelial cell. The time course of neural differentiation suggests that the normal sensory cells of mutant wings, which grow axons relatively early, may be the source of polarity information for the later-differentiating supernumerary cells.

Animals↗
PubMed1984

Axon growth in embryonic chick and quail retinal whole mounts in vitro.

Whole retinae of 4- to 10-day-old chick and quail embryos were spread on membrane filters and kept in culture for up to 4 days. Axon growth during culture was demonstrated by silver staining, anterograde labeling of fibers with RITC, time-lapse recording, and SEM. Fiber growth was observed in specimens from chick embryos up to 7 days old, with a growth maximum at E6 and from quail embryos up to E6 with the maximum at E5. Newly growing axons followed the optic fiber pattern already existing and, like axons in vivo, grew predominantly toward the optic fissure. Directional and orientational adaptation of newly growing axons to the preexisting fibers increased with the donor age. Retinae from donors up to E5 in chick and up to E4 in quail showed a high proportion of axons which crossed the optic fissure during the culture period and invaded the opposite retinal fiber layer. These fibers showed a correct radial orientation while growing in the opposite direction to normal. Likewise, in cultures from these young donors some fibers grew out initially in the diametrically opposite direction to normal toward the tissue periphery. Since all of the wrongly directed axons grew at the same rate as normal and adapted correctly to the already formed axon pattern, this suggests independent signals for the direction and orientation of growing fibers. Treatment of mounted retinae with collagenase or trypsin removed the vitreal retinal surface, leaving the existing axon pattern intact. Subsequently, new axons grew profusely in culture, but lost both their orientational and directional characteristics.

Animals↗
PubMed1989

The growth of axons in three-dimensional astrocyte cultures.

The environment of the adult central nervous system (CNS) does not support axon regeneration. We have been unable to replicate this behaviour using monolayer cultures of glia, so we have developed a technique for three dimensional culture of glial cells. We have examined the growth of axons from embryonic and postnatal retina and dorsal root ganglia (DRG's) through purified three-dimensional astrocyte cultures. Neither postnatal DRG's nor adult retina were able to grow axons through astrocytes from cultures 3 weeks or more old, although some DRG axons grew in astrocyte cultures which were 10 days or less old. However axons from embryonic DRG's and retina grew axons profusely into even elderly astrocyte cultures. All the tissues grew axons into three-dimensional Schwann cell cultures. The behaviour of axons in three-dimensional glial cultures therefore reproduces the behaviour of axons in vivo.

Age Factors↗
PubMed1987

Growth of retinal ganglion cell axons following optic nerve crush in adult hamsters.

Regrowth of retinal ganglion cell axons was examined 2 to 60 days after intraorbital optic nerve crush lesions in adult hamsters. Anterograde axonal transport of intraocularly injected wheat germ agglutinin-horseradish peroxidase conjugate was used to label the axons after specific postinjury time periods. Labeled axons were present in the region of the optic nerve lying between the eye and the crush site at all times, but their numbers appeared to decrease with increasing survival time. Labeled axons were first detected in the segment of optic nerve lying distal to the crush site 1 week after injury and had extended as far as 2.3 mm beyond the crush site by 60 days postinjury, growing at a rate similar to that at which the collateral branches of developing ganglion cell axons extend into their targets. Although most axons failed to regrow after these lesions, the slow reextention exhibited by members of a small population of axons indicates that the degenerating adult mammalian optic nerve provides an adequate environment for a particular mode of regrowth by injured axons of the central nervous system.

Animals↗
PubMed1991

The role of Schwann cells in the regeneration of peripheral nerve axons through muscle basal lamina grafts.

Evacuated muscle is a possible substitute for nerve autografts in the repair of damaged peripheral nerves. Previous experiments have shown that killed or evacuated muscle grafts are as effective as nerve autografts for bridging gaps of up to 4 cm between proximal and distal nerve stumps. Evacuated muscle grafts are made of extracellular matrix components, which are good substrates for axon growth in vitro. However, experiments in vivo have generally demonstrated that live Schwann cells are essential for successful axon regeneration. In the present experiments we have used immunohistochemical techniques with anti-S100 and anti-neurofilament antibodies to visualize axon growth and Schwann cell migration into muscle grafts over the first 10 days following grafting. We only saw axons growing into grafts accompanied by Schwann cells, and most though not all Schwann cells were associated with axons. Schwann cell migration from the proximal stump in association with axons was much faster and more extensive than from the distal stump. We examined muscle grafts over the first 20 days after grafting by electron microscopy. Regenerating axons were always associated with Schwann cells, which were mostly in the basal lamina-lined tubes left by the evacuated myofibrils. A comparison between evacuated muscle grafts and grafts in which the muscle had been killed but not evacuated revealed that 7 days after grafting there were more than twice as many regenerated axons in and distal to the evacuated grafts, but that by 20 days the numbers of axons were similar in the two groups.

Animals↗
PubMed1995

The duration of sprouted cerebrovascular axons following intracranial infusion of nerve growth factor.

We reported previously that a 2-week infusion of the trophic protein nerve growth factor (NGF) into the lateral ventricle of the adult rat brain elicits a sprouting response by perivascular axons associated with the intradural segment of the internal carotid artery. In the present study, we used electron microscopy to determine whether the sprouted axons persist following cessation of NGF delivery and, if not, to determine the time course of their disappearance. Our results demonstrate that NGF-induced sprouted axons do not persist following cessation of NGF delivery. The total number of axons at 1 week following the end of the NGF infusion was elevated compared to control values, but significantly reduced compared with NGF cases sacrificed immediately following the infusion period. Three weeks following the end of the NGF infusion, the total number of axons was similar to controls although there were no signs of axonal degeneration. These results suggest that continued elevation of NGF levels is necessary to maintain the sprouted axons and that endogenous levels of NGF, or other factors produced by the vascular target tissue, are not sufficient to maintain the newly formed axons. The demonstration that mature perivascular axons proliferate and disappear as a function of exogenous NGF exposure supports the accumulating evidence for continued plasticity in the mature nervous system.

Animals↗
PubMed1983

Flat, whole-mount nerve preparations: a useful tool for studying the process of regenerating axon outgrowth.

A method, which is based on the use of flat, whole-mount nerve preparations, has been developed for studying the process of regenerating axon outgrowth, employing the rat sciatic nerve as a model. At various intervals after a nerve crush, animals are perfused with aldehyde fixatives, the nerve dissected out, and its epineurium removed. Next the nerve is flattened between two glass slides, removed and reacted (floating), then whole-mounted on a micro slide and cover-slipped. Regenerating axons have been labeled by means of the horseradish peroxidase tracing technique, a histochemical technique for acetylcholinesterase, or an indirect immunocytochemical technique utilizing antibodies against tubulin. With all these techniques, individual outgrowing axons and their bundles can be clearly visualized. Regenerating axons labeled by horseradish peroxidase are readily traced along their entire undulating courses from the distal margin of the crush zone to axonal tips, which mark the leading edge of several waves of outgrowing axons. It appears that such flat, whole-amount nerve preparations can be useful for obtaining: (1) accurate estimates of the rate of regenerating axon elongation, (2) values characterizing the duration of the initial delay of axonal outgrowth, and (3) information concerning the nature of axonal subpopulations that elongate at different rates.

Acetylcholinesterase↗
PubMed1988

Excessive numbers of axons after early enucleation and blockade of metamorphosis in the oculomotor nerve of Xenopus laevis.

The number of axons in the oculomotor (OM) nerve of Xenopus laevis tadpoles was counted in unoperated and in unilaterally enucleated animals, raised in 0.4 g/l thiourea (TU), a thyroid-blocking agent, which arrested their development at premetamorphosis. In unoperated animals the number of axons starts to decrease with metamorphosis. When raised in TU, the tadpoles do not metamorphose and show no axon loss; rather, there is a moderate increase in axon number (13%) after 6 months of thiourea-treatment. Thus metamorphosis is necessary for the initiation of axon loss. In unilaterally enucleated tadpoles, increased axon loss occurs at metamorphosis in the OM nerve of the operated side, but the contralateral OM nerve shows no loss at all. When these animals are treated with TU, there is, as compared with the effects of the TU-treatment in unoperated animals, an increase of 7% in the ipsilateral side and of 28% in the contralateral one. Thus thyroxine blockade prevents the effects of unilateral enucleation and induces an excessive number of axons during the period observed. We postulate that through blockade of metamorphosis, axon elimination is arrested, while their production continues, and that these effects are accentuated by manipulation of the axonal target.

Age Factors↗
PubMed1991

Long-term survival of anucleate axons and its implications for nerve regeneration.

Severed distal segments of nerve axons (anucleate axons) have now been reported to survive for weeks to years in representative organisms from most phyla, including the vertebrates. Among invertebrates (especially crustaceans), such long-term survival might involve transfer of proteins from adjacent intact cells to anucleate axons. In lower vertebrates and mammals, long-term survival of anucleate axons is more likely attributed to a slow turnover of axonal proteins and/or a lack of phagocytosis by macrophages or other cell types. Invertebrate anucleate axons that exhibit long-term survival are often reactivated by neurites that have grown from proximal nucleate segments. In mammals, induction of long-term survival in anucleate axons might allow more time to use artificial mechanisms to repair nerve axons by fusing the two severed halves with polyethylene glycol, a technique recently developed to fuse severed halves of myelinated axons in earthworms.

Animals↗
PubMed1991

Distribution of axons showing calcitonin gene-related peptide- and/or substance P-like immunoreactivity in the sensory trigeminal nuclei of the cat.

Distribution of axons with calcitonin gene-related peptide (CGRP)-like and/or substance P (SP)-like immunoreactivity (LI) within the sensory trigeminal nuclei was examined in the cat before and after trigeminal rhizotomy. Axons with CGRP-LI or SP-LI were seen throughout the principal sensory trigeminal nucleus (Vp) and spinal trigeminal nuclei, including the medullary dorsal horn (MDH). They were densely distributed particularly in the dorsolateral part of the dorsal subnucleus of the Vp, ventromedial marginal zone of the ventral subnucleus of the Vp, dorsomedial and ventromedial parts of the oral spinal trigeminal nucleus, ventromedial and lateral marginal zones of the interpolar spinal trigeminal nucleus, and lamina I, outer part of lamina II and lamina V of the MDH. Most of the CGRP-LI axons exhibited SP-LI, while many SP-LI axons did not show CGRP-LI. After trigeminal rhizotomy, almost all CGRP-LI axons disappeared from the ipsilateral sensory trigeminal nuclei, while a considerable number of SP-LI axons remained intact throughout the nuclei; these SP-LI axons did not show CGRP-LI. The results indicate that CGRP-LI axons within the sensory trigeminal nuclei exhibit SP-LI and are of peripheral origin, and that SP-LI axons without CGRP-LI are of central origin.

Animals↗
PubMed1991

Myelin maintenance by Schwann cells in the absence of axons.

Formation and maintenance of myelin sheaths in the peripheral nervous system are regulated by unknown molecular interactions that are thought to depend upon physical contact between Schwann cells and axons. However, recent studies describing axons surrounded by two concentric myelin internodes in the superior cervical ganglion (SCG) of normal rodents have demonstrated that the outer myelin internodes are maintained without physical contact with the axon. To determine whether the centrally enclosed axon has a trophic effect in maintaining these remote outer internodes, we have produced axonal degeneration by surgical or chemical means. The results indicate that maintenance of myelin internodes totally displaced from axonal contact depends neither upon the presence of the axon nor on diffusible axonal factors. A further implication of these studies is that myelin breakdown during Wallerian degeneration is regulated by a positive signal which originates in degenerating nerves, rather than solely by loss of axonal trophic substances.

Animals↗
PubMed1991

Evidence for axonal loss in regions occupied by senile plaques in Alzheimer cortex.

The studies described have sought to determine what, if any, relationship exists between axons and the senile plaque, a hallmark histopathological feature of Alzheimer's disease. A double stain was performed on both early and late Alzheimer frontal cortex tissues in order to examine the interaction between axons stained with antibodies against the 200,000 mol. wt neurofilament subunit (NFP-200) of the axon cytoskeleton and Thioflavin-S, a fluorescent dye that stains plaques. Serial photomicrographs of plaques were taken and axon and plaque profiles were three-dimensionally reconstructed. Analysis of computer-processed images revealed that there were fewer axons within plaques than in regions lying one and two plaque distances away. When axons were observed passing through plaques, swelling and disruption of normal morphology was frequently present. Statistical analyses of axon counts within and around placques showed a gradient of axon density, with increased numbers occurring at progressive distances from the placque. Similar patterns were seen for early and late stages of the disease. The results of this study indicate that disruption of the axonal cytoskeleton may occur within the regions occupied by plaques.

Alzheimer Disease↗