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PubMed1996

Individual axon morphology and thalamocortical topography in developing rat somatosensory cortex.

The morphology of individual thalamocortical axons in developing rat primary somatosensory cortex was studied using lipophilic tracers. Anterograde labeling with lipophilic dyes demonstrated a topographical organization of thalamocortical projections exiting the thalamus as early as embryonic day (E) 16; retrograde labeling studies demonstrated topography of these projections as they reached the cortex as early as E18. At E17, axons course tangentially within the intermediate zone and turn or branch near the deepest layer of cortex (layer VIb), suggesting the presence of guidance cues in this region. Axons appear to grow and branch progressively within layers VIb and VIa during the following days; axons in the intermediate zone may give rise to radially directed branches. Individual axons appear to grow steadily and progressively into the cortex, with the leading front of axons at the transition zone between the cortical plate (CP) and the differentiating cortical layers. At birth (P0), thalamocortical axons extend radially through layers VIa and V and emit branches within these layers; some axons reach the CP. By P1, layer IV has begun to differentiate and axons begin to form a few simple branches in the vicinity of the layer IV cells. Over the ensuing week, axons generate more branches within layer IV, but the tangential extent of individual axon arbors does not exceed the width of a barrel. By P7, individual axons overlap within barrel clusters, and individual axons span the width of a cluster. These observations indicate that thalamic afferents develop by progressive growth of arbors that remain spatially restricted, rather than by overbranching and retracting arbors.

Aging↗
PubMed1999

Errors in lamina growth of primary olfactory axons in the rat and mouse olfactory bulb.

In the adult olfactory nerve pathway of rodents, each primary olfactory axon forms a terminal arbor in a single glomerulus in the olfactory bulb. During development, axons are believed to project directly to and terminate precisely within a glomerulus without any exuberant growth or mistargeting. To gain insight into mechanisms underlying this process, the trajectories of primary olfactory axons during glomerular formation were studied in the neonatal period. Histochemical staining of mouse olfactory bulb sections with the lectin Dolichos biflorus-agglutinin revealed that many olfactory axons overshoot the glomerular layer and course into the deeper laminae of the bulb in the early postnatal period. Single primary olfactory axons were anterogradely labelled either with the lipophilic carbocyanine dye, 1,1'-dioctodecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI), or with horse-radish peroxidase (HRP) by localized microinjections into the nerve fiber layer of the rat olfactory bulb. Five distinct trajectories of primary olfactory axons were observed in DiI-labelled preparations at postnatal day 1.5 (P1.5). Axons either coursed directly to and terminated specifically within a glomerulus, branched before terminating in a glomerulus, bypassed glomeruli and entered the underlying external plexiform layer, passed through the glomerular layer with side branches into glomeruli, or branched into more than one glomerulus. HRP-labelled axon arbors from eight postnatal ages were reconstructed by camera lucida and were used to determine arbor length, arbor area, and arbor branch number. Whereas primary olfactory axons display errors in laminar targeting in the mammalian olfactory bulb, axon arbors typically achieve their adult morphology without exuberant growth. Many olfactory axons appear not to recognize appropriate cues to terminate within the glomerular layer during the early postnatal period. However, primary olfactory axons exhibit precise targeting in the glomerular layer after P5.5, indicating temporal differences in either the presence of guidance cues or the ability of axons to respond to these cues.

Aging↗
PubMed1996

Addition of tetrodotoxin alters the morphology of thalamocortical axons in organotypic cocultures.

Living organotypic cocultures of rat thalamic and cortical explants were used to examine the effects of blocking action potential activity on the morphological development of axons in the mammalian neocortex. Studies in vivo have suggested that blocking sodium channel-dependent activity influences the growth characteristics of thalamocortical axons during development. We have extended these observations by using an in vitro system that affords more direct observational analysis of the early events of axonal growth in an accessible cellular environment DiI-labeled thalamocortical axons grow exuberantly into the target cortex and establish axonal connections that reflect the events of early thalamocortical afferent development. Within these cocultures, the morphological features of DiI-labeled axons can be readily distinguished. Tracings of thalamocortical axons were quantitated with respect to number, length, and termination pattern of axonal branches, as well as number of varicosities. Addition of the voltage-dependent sodium channel blocker, tetrodotoxin, to cocultures did not change the general pattern of thalamocortical axonal ingrowth or the average length of collateral branches of these axons. However, in the presence of tetrodotoxin, axons were more highly branched, with an increased number of varicosities as compared to untreated cocultures. This pattern of axonal growth and branching may reflect the activity-dependent fine-tuning and trimming of collaterals that occur as thalamic afferents begin to refine their cortical territory. Our observations in thalamocortical cocultures are consistent with the view that neuronal activity modulates the pattern of axonal growth and development.

Animals↗
PubMed1981

The effect of buffer molarity on axonal exposure and axoaxonal apposition in the rat molar pulp.

Axons in the rat molar pulp have been examined morphometrically to determine axonal size and the degree of axonal exposure and axoaxonal apposition in tissue fixed by perfusion using 2% glutaraldehyde in cacodylate buffers ranging in molarity form 0.025 M to 0.4 M. Between 31.2% and 45.0% of the axons were incompletely ensheathed. This proportion of axons exposed was linearly related to the buffer molarity (P less than 0.05) and was approximately double that found in more central axons. Between 32.3% and 45.0% of the axons were in contact with other axons. This proportion was not linearly related to buffer molarity but was least ten times higher than that observed in more centrally positioned nerve fibers in the inferior alveolar nerves. Increasing buffer molarity reduced the size of the axons, a relationship not found in the more central axons. It is suggested that axonal exposure and axoaxonal apposition are constant, significant features of pulpal nerve fibers that may be related to the onset and spread of nociceptive activity. The permeability properties of pulpal axons may differ from those of more centrally placed axons.

Animals↗
PubMed2006

Development of layer-specific axonal arborizations in mouse primary somatosensory cortex.

In the developing neocortex, pyramidal neurons use molecular cues to form axonal arbors selectively in the correct layers. Despite the utility of mice for molecular and genetic studies, little work has been done on the development of layer-specific axonal arborizations of pyramidal neurons in mice. We intracellularly labeled and reconstructed the axons of layer 2/3 and layer 5 pyramidal neurons in slices of primary somatosensory cortex from C57Bl6 mice on postnatal days 7-21. For all neurons studied, the development of the axonal arborizations in mice follows a pattern similar to that seen in other species; laminar specificity of the earliest axonal branches is similar to that of mature animals. At P7, pyramidal neurons are very simple, having only a main descending axon and few primary branches. Between P7 and P10, there is a large increase in the total number of axonal branches, and axons continue to increase in complexity and total length from P10 to P21. Unlike observations in ferrets, cats, and monkeys, two types of layer 2/3 pyramidal neurons are present in both mature and developing mice; cells in superficial layer 2/3 lack axonal arbors in layer 4, and cells close to the layer 4 border have substantial axonal arbors within layer 4. We also describe axonal and dendritic arborization patterns of three pyramidal cell types in layer 5. The axons of tall-tufted layer 5 pyramidal neurons arborize almost exclusively within deep layers while tall-simple, and short layer 5 pyramidal neurons also project axons to superficial layers.

Animals↗
PubMed1982

Innervation of avian latissimus dorsi muscles and axonal outgrowth pattern in the posterior latissimus dorsi motor nerve during embryonic development.

The distribution of the innervation to the anterior latissimus dorsi (ALD) and posterior latissimus dorsi (PLD) muscles of the chicken are described on the day of hatching and 6 weeks later using electron microscopy. In the ALD muscle, there are 5,000 muscle fibres and 374,000 endplates supplied by about 169 skeletomotor axons; in the PLD muscle, there are 12,000 focally innervated muscle fibers supplied by about 20 skeletomotor axons. On the cell surface of the muscle fibers the mean total subsynaptic area contacted by each motor axon is comparable in the ALD and PLD muscles. The growth pattern of the axons in the PLD motor nerve was described from the ninth day in ovo up to 6 weeks after hatching. The axons arrive in the PLD muscle in two successive waves: first, the large somatic axons which are already present before the ninth day in ovo and second, the small autonomic axons which continue to accumulate until hatching. The total number of somatic axons decreases from the ninth day until the hatching day when it reaches its definitive value. This decrease takes place during a period when the numbers of myofibers and of endplates dramatically increase, and it coincides with the axonal segregation by the Schwann cells. The myelination of the axons starts on the 15th day in ovo and is essentially complete upon hatching. Despite the decreasing number of somatic axons in the PLD nerve, the decrease in number of nerve endings per PLD endplate and the increasing number of PLD endplates per PLD muscle, it was found that between the 16th day in ovo and 6 weeks after hatching the mean number of axonal branches per PLD motor axon does not decrease.

Aging↗
PubMed1984

The morphology of optic tract axons arborizing in the superior colliculus of the hamster.

Single axons innervating the superficial layers of the hamster's superior colliculus (SC) were visualized using an HRP-filling technique. Five types of axons were distinguished. Experiments involving the removal of retinal and/or cortical input showed that three of these axon types originated in the contralateral retina with the fourth type most likely originating in the visual cortex. The origin of the fifth type, a widely branched varicose axon, is apparently subcortical. The two major types of presumed retinotectal axons (types U and L1) project to the stratum griseum superficiale (SGS) in a bilaminar pattern. Type U axons take relatively direct paths from the layer of optic fibers to form dense terminal arbors in the upper half of the SGS. Terminal fields for type U fibers showed fairly consistent dimensions. Their rostrocaudal extent ranged from 90 micron to 190 micron, averaging about 120 micron. Type L1 axons were thicker than type U axons and terminated in deeper regions of the SGS and in the stratum opticum (SO). Single axons of this type often gave rise to multiple branches which took separate, circuitous paths to a common terminal field. Terminal fields for type L1 axons varied more in extent than did type U fields, but 58% of them had fields 90-150 micron in extent. Each of the axon types found can be related to previous studies of populations of tectal afferents. The two major types of retinofugal axons fit a scheme of parallel ascending pathways. The findings also have interesting implications for the study of axonal development.

Animals↗
PubMed1986

Postnatal loss of axons in normal rat sciatic nerve.

Myelinated and unmyelinated axons were counted in sciatic nerves of newborn, 5-day-old, 14-day-old, and adult rats. Myelinated axons increase from essentially none at birth to approximately 8,000 in adulthood, but total axon numbers decrease steadily from 33,954 at birth to 22,872 in adulthood. Thus there is a significant postnatal loss of axons from rat sciatic nerve. This loss is, in our opinion, not associated with the death of the cells that give rise to these axons. This is thus an example of a regressive event that probably is of importance in normal neural development, namely the postnatal elimination of axons unaccompanied by death of the neurons that give rise to axons. These findings presumably imply a considerable amount of proximal peripheral axon branching, and the postnatal elimination of axons in the sciatic nerve presumably results from a reduction of this branching. Thus postnatal elimination of processes on, for example, somatic muscle cells may be at least partially the result of long axon elimination rather than local withdrawal of presynaptic processes, as is usually thought to be the case. In addition, an increased number of axons resulting from early postnatal manipulations may indicate cessation of axon loss rather than formation of new axons.

Age Factors↗
PubMed1986

Simple and complex retinal ganglion cell axonal rearrangements at the optic chiasm.

The rearrangements that retinal ganglion cell (RGC) axons undergo near the optic chiasm were determined by ablating either the nasal, temporal, dorsal, ventral, or peripheral retina. The axons of the remaining intact RGCs were then labelled with cobaltous lysine. RGC axons change their relationship with respect to the axes of the brain and with respect to one another. Toward the caudal end of the optic chiasm, the optic tract begins to rotate axially such that its rostral edge ultimately becomes located medially. Thereby, the column of ventronasal RGC axons shifts from a rostral to a medical position. In addition, columns of axons from other retinal sectors move with respect to one another. Ventrotemporal RGC axons, located initially at the caudal edge of the tract, move toward and come to be positioned laterally to, the column of ventronasal RGC axons. The column of dorsonasal RGC axons moves from the rostral to the lateral side of the column of dorsotemporal RGC axons. Concurrently, the axons within each column reorganize internally. Each chronological lamina of axons within a column twists such that the nasal and temporal axons within each column invert their positions with respect to the edges of the column. All of these reorganizations take place between the caudal end of the optic chiasm and the division of the main optic tract into the optic brachia. Furthermore, the rearrangements that occur do not involve any alterations in the positions of central and peripheral RGC axons with respect to the surface of the diencephalon. The results are discussed with respect to mechanisms that might influence the organization of the visual pathways.

Animals↗
PubMed1989

Axonal redirection at the dorsoventral intraretinal boundary.

Cobaltous-lysine applied to the goldfish optic nerve backfilled retinal ganglion cells and their axons. Confined to the ventronasal and ventrotemporal retina was a small population of retinal ganglion cells whose axons traveled dorsally and parallel to the retinal margin. On reaching the boundary between dorsal and ventral retina, the axons arched, joined radially oriented bundles of axons, and traveled toward the optic disk. Control studies showed that the axons came from retinal ganglion cells rather than from retinopetal cells. The somatic area of retinal ganglion cells (RGCs) with circumferential axons was 30-50 microns, and was similar to that of average ganglion cells. The axons of these cells coursed between the optic fiber and ganglion cell layers or between the ganglion cell and inner plexiform layers. Many somata were displaced slightly toward the inner plexiform layer, but were not really displaced ganglion cells. The aberrant axonal trajectory may be related to the slightly displaced location of the cell. However, ganglion cells that are displaced to the edge of the inner nuclear layer usually have radially coursing axons. We digitized the coordinates of the bending points and the dorsoventral retinal boundary. On average, the bending points occurred within 100 microns of the dorsoventral retinal border. These findings suggest that some molecular, rather than mechanical, factor at the dorsoventral retinal boundary alters the course of the circumferential axons. Furthermore, because there are cells with circumferential axons throughout the ventral retina, the data imply that at least ventral RGC axons avoid mingling with the axons from dorsal RGCs.

Animals↗
PubMed1990

Regeneration of adult dorsal root axons into transplants of fetal spinal cord and brain: a comparison of growth and synapse formation in appropriate and inappropriate targets.

Cut dorsal root axons regenerate into transplants of embryonic spinal cord and form synapses that resemble those found in the dorsal horn of normal spinal cord. One aim of the present study was to determine whether these axons also regenerate into and establish synapses within transplants of embryonic brain. A second aim was to compare the patterns of growth in embryonic brain and spinal cord transplants. Embryonic spinal cord or brain was transplanted into the lumbar enlargement of adult Sprague-Dawley rats, the L4 or L5 dorsal root was cut, and the cut root was juxtaposed to the transplant. The transplants included whole pieces or dissociated cell suspensions of embryonic day 14 (E14) spinal cord, or whole pieces of E14 neocortex, E18 occipital cortex, E15 cerebellum, or E18 hippocampus. One month later the regenerated dorsal root axons were labeled by immunocytochemical methods to demonstrate calcitonin gene-related peptide (CGRP). CGRP-immunoreactive axons regenerated into all the transplants examined and formed synapses in the neocortex and cerebellum transplants in which they were sought. Synapses were far rarer in neocortex and cerebellum than we had observed previously in transplanted spinal cord, and the patterns of growth differed in transplants of spinal cord and brain. In solid transplants of spinal cord, regenerated axons remained relatively close to the interface with the dorsal root, branched, and formed bundles. Areas of dense ingrowth were separated by regions with few labeled axons. In transplants of brain regions, the regenerated axons were few, unbranched, and appeared as individual fibers rather than in bundles, but they were distributed widely in neocortex transplants. The results of quantitative studies confirmed these observations. The area fraction occupied by regenerated axons in solid spinal cord transplants was significantly larger than in occipital cortex or cerebellum transplants. Distribution histograms of the area occupied in transplants demonstrated that regenerated axons were distributed sparsely but homogeneously in transplants of brain, whereas spinal cord transplants were heterogeneous for regenerated axons and contained areas in which growth was dense or sparse. In contrast, several measurements of axon distribution, including area, longest axis, and length of lateral extension, indicated that CGRP-labeled axons spread more widely in occipital cortex transplants than in solid transplants of spinal cord or cerebellum. The results indicate that embryonic CNS tissues that are not normal targets support or enhance the growth of severed dorsal roots and suggest that the conditions that constitute a permissive environment for regenerating axons are relatively nonspecific.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Immunolocalization studies of putative guidance molecules used by axons and growth cones of intersegemental interneurons in the chick embryo spinal cord.

The earliest developing interneurons in the chick spinal cord can be divided into two groups: neurons in the ventral region whose axons pioneer the primitive longitudinal pathway (PL-cells) and neurons whose axons project circumferentially (C-cells) along the lateral marginal zone and join the ipsilateral or contralateral ventrolateral longitudinal pathways. To begin to examine the molecular cues for axonal pathway formation of these interneurons, we screened a variety of molecules from embryonic day (E) 2 to E6.5 [stage 14-30 of Hamburger and Hamilton (1951) J. Morphol. 88:49-92]. These include cell adhesion and related molecules (G4, F11, neurofascin, N-cadherin, TAG-1-like molecule), extracellular matrix (ECM) molecules (laminin, fibronectin, heparan sulfate proteoglycan, laminin-heparan sulfate proteoglycan complex, and collagen type IV), and receptors for ECM molecules (beta 1-class integrin). PL-cells first expressed neurofascin at stage 14+ before the onset of axonogenesis. When the PL-cells began to extend their axons at stage 15, they expressed G4 and avian TAG-1-like molecules, as well as neurofascin, on both cell bodies and longitudinal axons. In the following stages, PL-cells continued to strongly express neurofascin and G4 on their fasciculating axons, suggesting the involvement of these glycoproteins in growth and fasciculation. C-cells began to express G4 and TAG-1-like molecules on cell bodies and axons at stage 15-16 shortly after axonal growth. In the following stages, C-cells expressed several cell adhesion molecules differentially on their axonal segments. The proximal segment of C-axons in the circumferential pathway strongly expressed a TAG-1-like molecule, whereas the distal segment in the longitudinal pathway strongly expressed G4 and neurofascin. The commissural axonal segment in the floor plate expressed TAG-1-like molecule, neurofascin, N-cadherin, and beta 1-class integrin. The basement membrane around the spinal cord was enriched with ECM glycoproteins (laminin, fibronectin, heparan sulfate proteoglycan, and collagen type IV) during the stages examined (stage 15-27), and commissural C-cell axons became strongly integrin positive in the floor plate where they contacted the basement membrane. These data indicate that interneurons may use multiple molecules during axonal pathway formation, depending on cell type, pathway position, and developmental stage.

Animals↗
PubMed1991

Cytoskeletal components and calibers in developing fish Mauthner axon (Salmo gairdneri Rich.).

In developing axons of many vertebrates, microtubular density is inversely correlated with fiber caliber. It is suggested that microtubules are causally related to axonal caliber. For this reason, cytoskeletal analysis during development of the fish Mauthner axon, which displays a giant caliber, is of particular interest. The Mauthner axon originates from the Mauthner cell in the medulla and runs in the fasciculus longitudinalis medialis in the spinal cord. At embryonic, larval and postlarval stages in trout (Salmo gairdneri Rich.), the following parameters were measured on conventional electron micrographs of Mauthner axon cross sections; axonal caliber, number of microtubules per axons, and microtubular and neurofilament densities. Results at each stage point to an inverse correlation between axonal caliber (x) and microtubular density (y) expressed by the equation y = axb (R = 0.932). Furthermore, three periods of Mauthner axon development are identified on the basis of the cytoskeletal content: (1) embryonic; the Mauthner axon has small caliber with a high microtubule density, (2) elongation period (larval stages); the axon enlarges and a transient peak of microtubules, corresponding to the caliber increment, is observed, and (3) postlarval; the axon enlarges still further (greater than 500 microns 2) but has the lowest microtubular content. During this period neurofilaments are the main axonal component.

Animals↗
PubMed1992

Analysis of neuritic outgrowth from severed giant axons in Lumbricus terrestris.

This study analyzes the detailed morphometric pattern at various postoperative times of neuritic outgrowths from the proximal and distal stumps of two uniquely identifiable axons. Morphological patterns of neuritic outgrowths from stumps of severed axons were compared for medial and lateral giant axons in the central nervous system of the earthworm Lumbricus terrestris. Outgrowths from proximal and distal stumps were labeled by injection of fluorescent dye into axonal stumps and assessed according to morphometric parameters. Outgrowths from axonal stumps of severed giant axons were statistically indistinguishable for most morphometric measures of neuritic quantity, shape, direction, and location. There were two exceptions to this general rule: 1) proximal stumps of medial giant axons produced significantly more neurites than distal stumps of medial giant axons, and 2) proximal stumps of lateral giant axons produced significantly longer neurites than proximal stumps of medial giant axons. No measure of neuritic outgrowth showed a significant change from the second through seventh postoperative week, suggesting that most outgrowth occurred in the first two postoperative weeks and that neuritic morphology remained stable through the seventh postoperative week. Neurites grew across the lesion site in relatively straight trajectories parallel to the longitudinal axis of the ventral nerve cord and often grew alongside the appropriate axonal stump across the lesion site. The length of neurites growing in close apposition to appropriate axonal stumps or giant axons was much greater than expected, had outgrowth been randomly directed. These data provide a basis for future investigations of the mechanisms that regulate neuritic outgrowth.

Animals↗
PubMed1993

Development of the thalamic reticular and perireticular nuclei in rats and their relationship to the course of growing corticofugal and corticopetal axons.

This study examines the connections of the thalamic reticular and perireticular nuclei during development. In addition, because these nuclei lie directly in the path of corticofugal and corticopetal axons during development, we have examined the relationship of these growing axons to the reticular and perireticular cell groups. Neurones were labelled by applying DiI, wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP), or HRP to the dorsal thalamus and/or cerebral cortex of rats at different stages of development. The axons of neurons in the reticular nucleus reach the dorsal thalamus as early as embryonic day (E) 14. At this age, and during later prenatal development, a small DiI implant limited to the presumptive lateral geniculate nucleus labels reticulothalamic and thalamocortical axons which travel in a clearly defined bundle through the thalamus. During late gestation, thalamocortical (approximately E15) and corticothalamic (approximately E17) axons pass directly through the reticular nucleus toward their targets. It is not until birth that collaterals are seen extending into the nucleus from the parent axons. Neurones in the perireticular nucleus, in contrast to those in the reticular nucleus, are not labelled from the lateral geniculate nucleus until after birth. The perireticular nucleus is very large at a stage when the first thalamocortical axons leave and when the first corticothalamic axons approach the thalamus. These axons are seen to change course sharply in the region of the internal capsule, where there are many perireticular cells. Corticothalamic axons turn toward the reticular nucleus, and thalamocortical axons turn toward the cortical subplate. Corticospinal and corticobulbar axons, on the other hand, pass directly through the perireticular region toward their more caudal targets. After these axons have reached their targets, the perireticular nucleus reduces dramatically in size.

Afferent Pathways↗
PubMed1994

Morphology of retinal axons induced to arborize in a novel target, the medial geniculate nucleus. I. Comparison with arbors in normal targets.

Ferret retinal axons can be induced to innervate the medial geniculate nucleus (MGN) by a combination of brain lesions early in development. Our previous work suggests that the retinal ganglion cells responsible for this plasticity are W cells. The present study continues this work with a morphological investigation of normal retinal ganglion-cell axons and retinal ganglion-cell axons induced to arborize in the MGN. Retinal axons were bulk filled with horseradish peroxidase placed in the optic tract, and individual axons were serially reconstructed from sagittal sections. The control population consisted of fine-caliber axons arborizing in the superior colliculus (SC) and in the ventral C laminae of the lateral geniculate nucleus (LGN) of normal ferrets. We also compared the axons in the MGN of lesioned ferrets to intracellularly filled X and Y axons from normal ferrets as reported by Roe et al. ([1989] J. Comp. Neurol. 288:208). We have found that the retino-MGN axons in the lesioned ferrets do not resemble X or Y axons in normal ferrets in axon diameter, arbor volume, bouton number, or bouton density. However, they do resemble the fine-caliber, presumed W axons arborizing in the C laminae of the LGN and in the SC of normal ferrets. Thus, this study, in combination with previous studies, suggests strongly that W retinal ganglion cells are responsible for the retinal input to the MGN in lesioned animals. In addition, we find that the retino-MGN axons are of two types, branched and unbranched, which may correspond to different subtypes of retinal W cells.

Animals↗
PubMed2006

Developmental regulation of sensory axon regeneration in the absence of growth cones.

The actin filament (F-actin) cytoskeleton is thought to be required for normal axon extension during embryonic development. Whether this is true of axon regeneration in the mature nervous system is not known, but a progressive simplification of growth cones during development has been described and where specifically investigated, mature spinal cord axons appear to regenerate without growth cones. We have studied the cytoskeletal mechanisms of axon regeneration in developmentally early and late chicken sensory neurons, at embryonic day (E) 7 and 14 respectively. Depletion of F-actin blocked the regeneration of E7 but not E14 sensory axons in vitro. The differential sensitivity of axon regeneration to the loss of F-actin and growth cones correlated with endogenous levels of F-actin and growth cone morphology. The growth cones of E7 axons contained more F-actin and were more elaborate than those of E14 axons. The ability of E14 axons to regenerate in the absence of F-actin and growth cones was dependent on microtubule tip polymerization. Importantly, while the regeneration of E7 axons was strictly dependent on F-actin, regeneration of E14 axons was more dependent on microtubule tip polymerization. Furthermore, E14 axons exhibited altered microtubule polymerization relative to E7, as determined by imaging of microtubule tip polymerization in living neurons. These data indicate that the mechanism of axon regeneration undergoes a developmental switch between E7 and E14 from strict dependence on F-actin to a greater dependence on microtubule polymerization. Collectively, these experiments indicate that microtubule polymerization may be a therapeutic target for promoting regeneration of mature neurons.

Actins↗
PubMed1995

Development of wing sensory axons in the central nervous system of Drosophila during metamorphosis.

The development of new, adult-specific axonal pathways in the central nervous system (CNS) of insects during metamorphosis is still largely uncharacterized. Here we used axonal labeling with DiI to describe the timing and pattern of growth of sensory axons originating in the wing of Drosophila as they establish their adult projection pattern in the CNS during pupal life. The wing of Drosophila carries a small number of readily identifiable sensory organs (sensilla) whose neurons are located in the periphery and whose axons travel along specific routes within the adult CNS. The neurons are born and undergo axonogenesis in a characteristic order. The order of axon arrival in the CNS appears to be the same as that of their development in the periphery. Within the CNS, the formation of four prominent axon bundles leading to distant termination sites is followed by the formation of a compact axon termination site near the point of wing nerve entry into the CNS. This sensillum-specific pattern persists into adulthood without discernible modification. We also find a small number of axons filled with DiI prior to the formation of the four permanent bundles. We have only been able to fill them for a few hours in early pupal life and therefore consider them to be transient. The bundles of wing sensory axons travel within tracts that contain other axons as well. Using immunocytochemistry, the tracts start to be histologically identifiable at around 12 h after pupariation (AP), and grow substantially as metamorphosis proceeds. Wing sensory neurons are found in the tracts by 18-20 h AP and the full adult pattern is established by 48 h AP. When sensory axons first enter the CNS, they fan out in the region where their appropriate tracts are located, but they do not wander extensively. They quickly form bundles that become increasingly compact over time. Calculations show that the rate of axon extension within the CNS varies from bundle to bundle and is equal to or greater than that of the same axons growing through wing tissue.

Animals↗