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PubMed1998

The spatial relationships among cutaneous, muscle sensory and motoneuron axons during development of the chick hindlimb.

Previous studies have suggested that interactions with other axons are important in sensory axon pathfinding in the developing chick hindlimb. Yet the nature of these interactions remains unknown, in part because information about the spatial relationships among the different kinds of axons is lacking. To obtain this information, we combined retrograde axonal tracing with an immunofluorescent labelling approach that distinguishes between sensory and motoneuron axons. This allowed us to follow the trajectories of sensory axons having a known destination, while also identifying their neighbors. We found that as sensory and motoneuron axons meet in the spinal nerves and travel into the limb, sensory axons remain bundled together. The large bundles that are present proximally gradually split into smaller bundles as the axons course distally in the spinal nerves; more distally, some bundles join to again form large bundles. Younger, later-growing sensory axons appear to grow primarily along bundles of older sensory axons that grew out earlier. Starting from very proximal levels, axons projecting along an individual cutaneous nerve are found together in bundles that are situated in characteristic regions of each spinal nerve. Some of these bundles are initially interspersed with bundles of axons projecting along other nerves, thereby indicating that the initial position of a cutaneous axon in the spinal nerves does not strictly determine its subsequent trajectory. As they travel distally, bundles of axons projecting along one cutaneous nerve gradually join one another, becoming increasingly separated from axons having different destinations. In contrast, muscle sensory axons are situated adjacent to motoneuron axons innervating the same muscle for much of their course. This suggests that muscle sensory axons may be guided to the appropriate muscles by fasciculating along motoneuron axons. Taken together, the results show that sensory axons projecting along different nerves are different from one another and respond to cues in their environment to navigate through the spinal nerves and plexus. Thus, sensory neurons must be intrinsically specified with respect to their peripheral targets. Sensory axons appear to respond differentially to the axons they encounter, segregating from axons that project along different nerves and often growing with axons destined for the same nerve, suggesting that fasciculation may aid pathfinding.

Animals↗
PubMed2005

Mild axonal stretch injury in vitro induces a progressive series of neurofilament alterations ultimately leading to delayed axotomy.

We report a new model of transient axonal stretch injury involving pressurized fluid deflection of bundles of axons, resulting in a transient 1-6% increase in original axon length to investigate the slow progression of axonal alterations that are characteristic of diffuse axonal injury (DAI). We found no discernable difference in axon bundle morphology or cytoskeletal neurofilament protein arrangement between unstretched and stretched axonal bundles at 24 h post-injury. However, by 48 h post-injury, there was a stereotypical response of stretched axons involving characteristic neurofilament alterations that bear similarities to in vivo neuronal responses associated with DAI that have been reported previously. For instance, neurofilament protein immunoreactivity (SMI-312) was increased in axons contained within 51% of all injured axon bundles at 48 h compared to surrounding unstretched axon bundles, suggestive of neurofilament compaction. Furthermore, axonal bundle derangement occurred in 25% of injured axon bundles, with individual fibres segregating from each other and becoming undulating and wavy. By 72 h post-stretch, 70% of injured axon bundles underwent secondary axotomy, becoming completely severed at the site of initial stretch injury. While these results suggest a temporal series of stereotypical responses of axons to injury, we were able to distinguish very clear differences between mildly (100-103% increase in original axonal length) injured and strongly injured (106%+) axons. For instance, mildly injured axons developed increased neurofilament immunoreactivtity (SMI-312) within 48 h, and the marked development of ring-like neurofilament immunoreactive structures within axonal bundles, which were rarely axotomized. Conversely, at more severe strain levels increased neurofilament immunoreactivity was less apparent, while axons often became distorted and disorganised within axonal bundles and eventually became completely disconnected. Almost no ring-like neurofilament structures were observed in these severely injured axonal bundles. This suggests that axons do not respond in a stereotypical manner to a transient stretch insult, and indeed that variable degrees of stretch injury activate different responses within axons, with dramatically different outcomes. Hence, it is possible that the cytoskeletal characteristics that we have used in this study may be useful parameters for discriminating between mildly and severely injured axons following TBI.

Animals↗
PubMed1992

Axon collaterals of mossy fibers from the pontine nucleus in the cerebellar dentate nucleus.

1. Single axons of pontine nucleus neurons (PN axons) receiving cerebral input were stained intra-axonally with horseradish peroxidase (HRP) in the cerebellum of cats. The axonal trajectory of single PN axons was reconstructed from serial sections of the cerebellum and the brain stem. 2. Axons were penetrated in the white matter near the dentate nucleus, and, after electrophysiological identification, PN axons were injected iontophoretically with HRP. The identification criteria for the PN axons were 1) their direct responses to stimulation of the contralateral pontine nucleus (PN), 2) their synaptic activation from the contralateral cerebral cortex, and 3) the decrease in threshold for evoking direct spikes in stimulation of the PN by conditioning stimuli applied in the cerebral cortex. 3. Two hundred thirty-three axons were electrophysiologically identified as PN axons receiving the input from the cerebral cortex. Ninety-six of them were stained successfully with HRP, and reconstructions were made from 40 well-stained PN axons. All of them gave rise to mossy fibers and terminated in the granular layer of the cerebellar cortex as typical mossy fiber rosettes. Out of these, 22 gave axon collaterals to the dentate nucleus. Virtually all of the axon branches observed in the dentate nucleus were axon collaterals of mossy fibers from the PN to the cerebellar cortex. In 7 of these 22 PN axons, cell bodies were retrogradely labeled with HRP, and all of them were found in the contralateral PN. 4. The stained-stem axons arising from the PN ran medially in the pons, crossed the midline, and then ascended dorsocaudally in the branchium pontis. After passing in the white matter anterior to or lateral to the dentate nucleus, they entered into the cerebellar cortex. On their way, one to three axon collaterals were given off from parent axons to the dentate nucleus. The diameter of these collaterals was very thin (mean, 0.6 microns), compared with the large diameter of the parent axons (mean, 2.1 microns). 5. Some axon collaterals were very simple and had only one terminal branch with or without short branchlets, whereas others were more complex, and single axon collaterals ramified before forming a terminal arborization. Axon collaterals of single PN axons mainly spread mediolaterally or dorsoventrally in the frontal plane but had a very narrow rostrocaudal extension. 6. Terminal branches usually bore swellings en passant along their length and one terminal swelling at their end. The number of swellings per axon collateral ranged 23-180 (116 +/- 52, mean +/- SD).(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1989

Comparison of the branching patterns of lateral and medial vestibulospinal tract axons in the cervical spinal cord.

The morphology of single physiologically-identified lateral and medial vestibulospinal tract (LVST and MVST) axons was analysed, using intracellular staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of axonal trajectories in the cat. Axons were penetrated in the cervical cord at C1-C8 with a microelectrode filled with 7% HRP. These axons were identified as vestibulospinal axons by their monosynaptic responses to stimulation of the vestibular nerve and further classified as either LVST or MVST axons by their responses to stimulation of the LVST and MVST. The stained axons could be traced over distances of 3-16 mm rostrocaudally. Within these lengths, both LVST and MVST axons were found to have multiple axon collaterals at different segments in the cervical cord. Up to seven collaterals were given off from the stems of MVST axons and LVST axons. The LVST axons included both neurones terminating at the cervical cord and those projecting further caudally to the thoracic or lumbar cord. Each collateral of these LVST axons, after entering into the gray matter, ramified successively in a delta-like fashion and terminated mainly in lamina VIII and in the medial part of lamina VII. Many boutons of both terminal and en passant types seemed to make contact with the cell bodies and proximal dendrites of neurones in the ventromedial nucleus (VM). Each collateral had a narrow rostrocaudal extension (0.2-1.6 mm, average 0.8 mm) in the gray matter in contrast to a much wider intercollateral interval (average 1.5 mm), so that there were gaps free from terminal boutons between adjacent collateral arborizations. The morphology of axon collaterals of MVST axons was very similar to that of LVST axons. The rostrocaudal extent of single axon collaterals was very restricted (0.3-2.1 mm) in contrast to the wide spread in a mediolateral or a dorsoventral direction. MVST axons had intensive projections to the upper cervical cord with multiple axon collaterals. One to seven collaterals of single MVST axons were found at C1-C3. Terminals of MVST axons were distributed in laminae VII, VIII and IX, including the VM, the nucleus spinalis n. accessorii (SA), and the commissural nucleus. Many terminals seemed to make contact with retrogradely-labelled motoneurones of neck muscles. Both axosomatic and axodendritic contacts were observed on motoneurones in various sizes. Some collaterals gave rise to terminal arborizations in both the VM and the SA. These results suggest that single LVST and MVST axons may control excitability of multiple dorsal axial muscles concurrently with their multiple axon collaterals at multisegmental levels.

Animals↗
PubMed1992

Morphology of single medial vestibulospinal tract axons in the upper cervical spinal cord of the cat.

The morphology of single medial vestibulospinal tract (MVST) axons was investigated by iontophoretic injection of horseradish peroxidase into single axons at the upper cervical cord in pentobarbital-anesthetized cats. MVST axons were identified by their monosynaptic responses to stimulation of the vestibular nerve and their direct responses to stimulation of the medial longitudinal fusciculus (MLF). Reconstructions of the axonal trajectory were made from 22 uncrossed and 19 crossed MVST axons at C1-C4. MVST axons ran in the ventral funiculus and gave rise to multiple axon collaterals to the upper cervical gray matter at different segments. These axons could be traced over the distance of 2.5-15.3 mm. Within these lengths, up to 9 axon collaterals were identified per axon (mean +/- s.d., 3.3 +/- 2.0, n = 41). Axon collaterals ramified in the gray matter several times and spread in a delta-like manner in both the transverse and horizontal planes. There were usually gaps free from terminal arborizations between adjacent axon collaterals, since the rostrocaudal extension of individual axon collaterals (mean = 820 microns) was very much limited in contrast to wide intercollateral intervals (mean = 1,510 microns). Axon terminals were distributed mainly in laminae IX, VIII, and VII, and sometimes in laminae VI-IV. Most abundant terminals were observed in lamina IX, including the ventromedial (VM), the spinal accessory (SA) nuclei and the nucleus dorsomedial to the VM nucleus (DM nucleus). A majority of individual axon collaterals provided some terminal branches to at least one of the above three motor nuclei. Axon collaterals projecting to laminae VIII-VI without terminals in the motor nuclei were rarely observed. Individual MVST axons had a preferential terminal distribution in each motor nucleus, but all three motor nuclei were covered by axon terminals of an ensemble of all MVST axons, indicating that all neck muscles innervated by these three motor nuclei are influenced by vestibular inputs through MVST axons. Most collaterals from a single axon produced circumscribed terminal arborizations in one or two common areas in the transverse plane (mainly in lamina IX) that were in line with one another in the longitudinal axis of the cord. This longitudinal arrangement of discontinuous terminal arborizations in lamina IX from a single axon may correspond to a continuous sagittal column of motoneurons for a particular muscle.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Changes in axonal physiology and morphology after chronic compressive injury of the rat thoracic spinal cord.

The spinal cord is rarely transected after spinal cord injury. Dysfunction of surviving axons, which traverse the site of spinal cord injury, appears to contribute to post-traumatic neurological deficits, although the underlying mechanisms remain unclear. The subpial rim frequently contains thinly myelinated axons which appear to conduct signals abnormally, although it is uncertain whether this truly reflects maladaptive alterations in conduction properties of injured axons during the chronic phase of spinal cord injury or whether this is merely the result of the selective survival of a subpopulation of axons. In the present study, we examined the changes in axonal conduction properties after chronic clip compression injury of the rat thoracic spinal cord, using the sucrose gap technique and quantitatively examined changes in the morphological and ultrastructural features of injured axonal fibers in order to clarify these issues. Chronically injured dorsal columns had a markedly reduced compound action potential amplitude (8.3% of control) and exhibited significantly reduced excitability. Other dysfunctional conduction properties of injured axons included a slower population conduction velocity, a longer refractory period and a greater degree of high-frequency conduction block at 200 Hz. Light microscopic and ultrastructural analysis showed numerous axons with abnormally thin myelin sheaths as well as unmyelinated axons in the injured spinal cord. The ventral column showed a reduced median axonal diameter and the lateral and dorsal columns showed increased median diameters, with evidence of abnormally large swollen axons. Plots of axonal diameter versus myelination ratio showed that post-injury, dorsal column axons of all diameters had thinner myelin sheaths. Noninjured dorsal column axons had a median myelination ratio (1.56) which was within the optimal range (1.43-1.67) for axonal conduction, whereas injured dorsal column axons had a median myelination ratio (1.33) below the optimal value. These data suggest that maladaptive alterations occur postinjury to myelin sheath thickness which reduce the efficiency of axonal signal transmission.In conclusion, chronically injured dorsal column axons show physiological evidence of dysfunction and morphological changes in axonal diameter and reduced myelination ratio. These maladaptive alterations to injured axons, including decrease in myelin thickness and the appearance of axonal swellings, contribute to the decreased excitability of chronically injured axons. These results further clarify the mechanisms underlying neurological dysfunction after chronic neurotrauma and have significant implications regarding approaches to augment neural repair and regeneration.

Action Potentials↗
PubMed1994

Microtubule-associated protein 1b (MAP1b) is concentrated in the distal region of growing axons.

Microtubule-associated protein 1b (MAP1b) is expressed at especially high levels in neurons actively extending axons, and although it appears to be required for axon growth, the nature of its role is unknown. We reasoned that a detailed description of the localization of MAP1b in growing axons would help define how MAP1b participates in axon growth. Therefore, we have stained cultured sympathetic neurons with various antibodies against MAP1b, and then used digital image processing and analysis procedures to quantify MAP1b distribution, phosphorylation and association with microtubules (MTs) in actively elongating axons. MAP1b is present on MTs all along the axon. Quantitative analyses showed that MAP1b has a nonuniform distribution along growing axons. It is present at relatively low and constant levels along the axon shaft until approximately 130 microns from the axon tip, where the amount of MAP1b begins to increase sharply and reaches a peak close to the growth cone. The peak amount of MAP1b in the distal axon is an order of magnitude greater than the average amount in the axon shaft. The enrichment of MAP1b in the distal axon was observed for total MAP1b and assembled MAP1b, and was even more pronounced for phosphorylated MAP1b. This distribution pattern remains after correcting the relative amount of MAP1b along the axon for variations in axonal volume. Thus, the concentration of MAP1b in the distal axon exceeds by severalfold that in the rest of the axon. The amount of assembled MAP1b relative to the amount of MT polymer also varies along the axon, and is greatest distally near the growth cone. This pattern of MAP1b localization in axons focuses attention on the distal axon and growth cone as the principal sites of MAP1b function in axon growth. We discuss the possibility that MAP1b regulates MT dynamics in the distal axon so that it is properly coordinated with growth cone events involved in axon extension.

Antibodies, Monoclonal↗
PubMed1984

Axons of the dorsal division of the medial geniculate body of the cat: a study with the rapid Golgi method.

The arrangement of eight groups of axons afferent to the nuclei of the dorsal division of the medial geniculate body is described in rapid Golgi impregnations from young cats. Three kinds of axons travel predominantly in the brachium of the inferior colliculus and enter the medial geniculate body ventromedially: group I, thin axons resembling ivy tendrils ending along dendrites; group II, thicker axons with a sinuous course and few branches; group IV, coarse thick axons with grumous collaterals and massive peridendritic terminals near principal cells and interneurons. Three kinds of axons enter from the parabrachial region and pass laterally: group III, very thin axons with many collaterals forming dense terminal nests; group V, runcinate axons with sparse, thin collaterals; group VI, either medium-sized (group VIa) or thin (group VIb) smooth axons, perhaps corticofugal, and ending near principal neuron dendrites; group VII, thick axons, entering from the auditory radiation, with large, grapelike terminal arbors; and group VIII, thin and forming peridendritic festoons on principal cells after entering from the brachium of the superior colliculus. There appears to be some, though not complete, segregation of axons in the dorsal division nuclei. Thus axons of groups I, III, IV, and VI are found in each nucleus, although group VI axons are conspicuous in the superficial dorsal nucleus, and group IV endings are much more elaborate in the dorsal and deep dorsal nuclei than in the superficial dorsal nucleus. Each axon type has a specific pattern of terminal branches, which contributes to the texture of the neuropil in each nucleus. Golgi type II axons accentuate these textural differences. Thus each nucleus has a specific pattern of neuropil by virtue of the relative proportions of the different groups of axons ending there and the density and architecture of the axonal plexus. For example, both the dorsal nucleus and the deep dorsal nucleus receive the same groups of afferent axons, but the axonal plexus is more diffusely and evenly distributed in the dorsal nucleus, whereas the neuropil of the deep dorsal nucleus is highlighted by aggregates of grumous endings, more irregularities in the distribution of the axonal plexus, and many more fibers of passage. The extrinsic axons in the dorsal division come from the inferior and superior colliculi, the lateral tegmental system of the midbrain, and the cerebral cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Axonal pathfinding during the regeneration of the goldfish optic pathway.

Retinal ganglion cells in fish and amphibians regenerate their axons after transection of the optic nerve. Fiber tracing studies during the third month of regeneration show that the axons have reestablished a basically normal fiber order in the two brachia of the optic tract; axons originating in the ventral hemiretina are concentrated in the dorsal brachium, axons from the dorsal hemiretina in the ventral brachium. Attardi and Sperry (Exp. Neurol. 7:46-64, 1963) first suggested that the reestablishment of the fiber order reflects path-finding by the regenerating axons. Recently, however, Becker and Cook (Development 101:323-337, 1987) have claimed that the fiber order observed at later stages of regeneration is due to secondary axonal rearrangements and that the initial brachial choice is random. In order to evaluate whether regenerating axons are capable of navigating in the optic tract and brachia and on the tectum, the present study examined the pathway choices and the morphology of regenerating axons en route to their tectal targets in goldfish. Subsets of axons were labeled at various time intervals (2 to 30 days) following an optic nerve crush, by intraretinal application of the lipophilic fluorescent tracer 1,1-dioctadecyl-3-3-3'-3'-tetramethylcarbocyanine (DiI). After a survival time of 18 to 72 hours (to allow for diffusion of DiI along the axons), the experimental animals were perfused with fixative and their right and left optic pathways (nerve, tract, and tectum) were dissected free and separated at the chiasm. Fluorescently labeled axons were traced in whole-mounted pathways. Pathway choices were examined at the brachial bifurcation where axons from ventral and dorsal hemiretinae normally segregate. DiI was found to label axons reliably up to their growth cones, even at the earliest stages of regrowth. The pathway choices of the axons were nonrandom. The majority of the ventral axons reached the appropriate, dorsal hemitectum through the appropriate dorsal brachium of the tract. Dorsal axons reached the ventral hemitectum mainly through the ventral brachium. This suggests the presence of specific guidance cues, accessible to the regenerating axons. Differences in the complexity of the growth cones of the regenerating axons (simple in the nerve and tectal fiber layer, complex in the tract and the synaptic layer of the tectum) provide further evidence for specific interactions between the regenerating axons and their substrates along the pathway. These results argue that regenerating retinal axons in fish are capable of axonal path-finding.

Animals↗