Trans-glial channels in ventral nerve roots of crayfish.

The sheath around the roots of the sixth abdominal ganglion in the ventral nerve cord of the crayfish consists of concentric layers of thin glial processes alternating with wide clefts containing filamentous connective tissue. Regions of each glial lamella are perforated by single, short, tubular channels: the trans-glial channels. In thin plastic sections examined in the electron microscope, the channels appear as slits that are 240 A wide and 450-550 A long which traverse glial lamellae less than 1,500 A thick. Branched tubular channels cross glial sheets that are thicker than 1,500 A. The thickest glial wrap is adaxonal; it closely encapsulates individual axons and its cell membrane is separated from the axolemma by a collagen-free space of only 150 A. The adaxonal glial cytoplasm contains unique, three-dimensional networks of interconnected tubules. Separate tubular lattices occur along these thicker processes. In replicas of freeze-fractured sheaths, the outer half of the plasma membrane belonging to the thin glial sheets exhibits many volcano-like protrusions which represent cross fractures through the necks of trans-glial channels. Corresponding depressions on the inner half of these membranes are sites where the plasma membrane invaginates to form the channels. Although some channels are randomly dispersed, others are lineraly positioned in restricted areas across successive glial layers. The number of channels is far more readily appreciated in replicas than in thin sections. The average frequency of channels is 16 per mu2 (range 8 to 33) in normal roots and does not differ significantly from the average of 13 per mu2 in proximal stumps of roots fixed three to four weeks after the roots were cut. The channels are not precisely aligned from one glial layer to the next but do appear to coincide approximately with the adaxonal tubular lattice. The combination of trans-glial channels and adaxonal tubular lattices may provide a complex conduit that could facilitate a rapid, passive flow of electrolytes and nutrients across the nerve sheath to the axonal surface. Horseradish peroxidase solutions bathing the ventral roots enter the trans-glial channels, extracellular clefts and finally the tubular lattices. This distribution supports the proposed role of the channels in a rapid extracellular passage of solutes. The channel profiles have a range of forms consistent with the supposition that they are not static but continually reforming. There are indications that, proximal to the cut, the areas of glial plasma membrane with channel profiles contain more junctional complexes between regenerating cells than between glial cells of normal sheaths. The channel profiles and aggregates of particles belonging to junctions are closely associated when they occupy the same region of the membrane.     

Distribution of ultrastructural tracers in crustacean axons

Ruthenium red and horseradish peroxidase were used to compare the uptake of exogenous molecules into crayfish motor axons and their sheaths in severed and intact peripheral nerves. Both tracers penetrated the axonal sheath and were subsequently seen lining small vesicles and tubules in the axoplasm. Tracer appeared to enter the axon via pinocytotic vesicles. There were no perceptible quantitative or qualitative differences in ruthenium red uptake between intact and severed axons. However, counts of tracer-filled vesicles in axons exposed to peroxidase showed that at least three times as much tracer penetrated the severed as opposed to the intact axons.     

Changes in ultrastructure and voltage-dependent currents at the glia limitans of the frog optic nerve following retinal ablation

The surface of the frog optic nerve consists of astrocytic processes separated by narrow extracellular clefts underlying a pial sheath of loose connective tissue. Macroscopic voltage dependent currents can be recorded from this surface using the loose patch-clamp technique. In this study the changes in ultrastructure and voltage dependent Na currents have been studied for up to 1 year following removal of the retina. During the first 1–4 weeks, many of the myelinated and unmyelinated axons of the retinal ganglion cells degenerate, and the debris is phagocytosed by macrophages and glial cells. However, some morphologically intact axons remain even 12 weeks after surgery. Finally, after 16 weeks all the axons have disappeared, leaving a nerve consisting only of glial cells, some of which contain phagosomes. At 40–52 weeks after enucleation, the nerve persists, at 20–40% of the normal diameter, consisting mostly of normal looking astrocytes. The amplitude of the voltage dependent Na currents recorded from nerves during the first 1–4 weeks after enucleation, with the pial sheath intact, decreases by about 50%. After 8 weeks, the Na current recorded from the surface is about 30% of control. At 16–52 weeks after removal of the retina, when there are no intact axons, the Na current is reduced by 90%. If, however, the pial sheath is stripped away, the Na currents recorded from the glial surface are 40–50% of control during this same 16- to 52-week period, suggesting that in the all-glia nerve, the currents are shunted by the relatively thicker pial sheath. In contrast to their normal TTX sensitivity, the voltage dependent Na currents recorded from these all glial nerves are insensitive to TTX (5 μM) but disappear when the external Na is replaced by TMA. The results suggest that in situ glial voltage dependent membrane properties depend on interactions between the glial cells and the neighboring axons. © 1993 Wiley-Liss, Inc.     

Regenerating crayfish motor axons assimilate glial cells and sprout in cultured explants

Phasic and tonic motor nerves originating from crayfish abdominal ganglia, in 2-3-day-old cultured explants, display at their transected distal ends growth zones from which axonal sprouts arise. The subcellular morphology of this regenerative response was examined with thin serial-section electron microscopy and reveals two major remodeling features. First, the external sprouts that exit the nerve are a very small part of a much more massive sprouting response by individual axons comprising several orders of internal sprouts confined to the nerve. Both internal and external sprouts have a simple construction: a cytoskeleton of microtubules and populations of mitochondria, clear synaptic vesicles, membranous sacs, and extrasynaptic active zone dense bars, features reminiscent of motor nerve terminals. Close intermingling of the sprouts of several axons give rise to a neuropil-like arbor within the nerve. Thus, extensive sprouting is an intrinsic response of crayfish motor axons to transection. Second, an equally dramatic remodeling feature is the appearance of nuclei, which resemble those of adjacent glial cells, within the motor axons. These nuclei often appear where the adjoining membranes of the axon and glial cell are disrupted and where free-standing lengths of the double membrane are present. These images signify a breakdown of the dividing membranes and assimilation of the glial cell by the axon, the nucleus being the most visible sign of such assimilation. Thus, crayfish motor axons respond to transection by assimilating glial cells that may provide regulatory and trophic support for the sprouting response.     

Protein metabolism in transected peripheral nerves of the crayfish.

The significance of the protein metabolism in crayfish peripheral nerve was studied in relation the ability of crayfish motor axons to survive for over 200 days following axotomy. In contrast to frog peripheral nerves, the crayfish nerves appear to more closely resemble ganglia in their profiles of synthesis expressed on sodium dodecyl sulfate (SDS) gels, and have higher incorporation rates of [3H]leucine into protein than ganglia. Since anisomycin inhibits over 95% of protein synthesis in crayfish peripheral nerve, it was concluded that this local protein synthesis was dependent upon a eukaryotic ribosomal mechanism. Radioautography of isolated nerves reveals newly synthesized proteins in glial sheaths, and also within the axoplasm of large motor fibers. Based upon the data available at present, a hypothesis that the glia surrounding the axons are responsible for the local protein synthesis, and that some of these newly synthesized proteins are transported into the axon, is presented. Transection of crayfish peripheral nerves proximal to the neuron cell bodies produced a more than two-fold increase in [3H]leucine incorporation, but no significant changes in labeling profiles of the proteins on SDS gels. The data suggest that while an active local protein synthesis may be necessary for the maintenance of several crayfish motor axons, it is not a sufficient condition.     

Biochemical studies of trophic dependences in crayfish giant axons.

Data from previous histological studies indicate that long-term survival of crayfish medial giant axons might be due in part to trophic support from cells of the surrounding glial sheath which often hypertrophy in response to transection of the medial giants. The biochemical studies reported herein show that segments from transected ventral nerve cords (VNC) always incorporate more [3H]leucine into protein than do corresponding segments from intact VNCs. Furthermore, the relative amount of [3H]leucine incorporation in severed segments seems to be influenced by distance and direction from the lesion site as well as time after lesioning. Similar spatiotemporal parameters were previously shown to be correlated with extent of glial hypertrophy around severed medial giant axons. Quantitative autoradiography of medial giant axons after incubation in [3H]leucine revealed that the grain density of label in glial sheaths surrounding severed medial giants was over two-fold greater than in sheaths around corresponding control axons. Moreover, the grain density in the axoplasm of severed medial giants was nearly four-fold greater than the grain density in the axoplasm of control axons. Data from experiments using short or long labeling intervals suggests that labeling in the medial giant axoplasm may be due more to transfer from glial sheath cells than from inherent axonal synthetic mechanisms. In light of this and other data, we concluded that long-term survival of severed medial giant axons is probably due to the direct transfer of trophic substances from cells of the glial sheath into the axon.     

A morphometric study of optic axons regenerated in a sciatic nerve graft of adult rats

PURPOSE: In the present study we have morphometrically examined a regeneration model in which axons normally residing in CNS have regrown and are interacting with Schwann cells from the PNS. This study will not only provide morphometric data on regenerated optic fibers but also shed light on possible factors in determining the fiber morphometry. METHODS: The optic nerves of rats aged 6 weeks were cut intra-orbitally and replaced with a autologous sciatic nerve. After a survival period of 9 months, the graft or "regenerated" nerves containing the regenerated optic axons and Schwann cells were processed for morphometric measurements. RESULTS: The mean myelinated axon diameter of regenerated nerve (1.8 +/- 0.2 micro m) was significantly (P < 0.05) greater than that of the optic nerve (0.9 +/- 0.03 micro m). However, unmyelinated regenerated optic axons had a smaller mean axon diameter (0.49 +/- 0.04 micro m) than normal myelinated optic axons. This may suggest that myelinating glial cells exert an influence on axon caliber and Schwann cells seem to have greater effect than oligodendrocytes. The mean g-ratio showing the relative myelin sheath thickness was found to be the highest in the optic nerve (0.78 +/- 0.003), least in the sciatic nerve (0.6 +/- 0.009) and intermediate in the regenerated nerve (0.68 +/- 0.01). The results indicated that Schwann cells myelinating the regenerated optic axons have produced a thinner myelin sheath. Intra-axonally, no significant difference was detected in the number of axonal microtubules and neurofilaments between the regenerated and optic nerves. Therefore the disposition of microtubules and neurofilaments into axon may be intrinsically determined. CONCLUSIONS: In this study, we have identified some of the extrinsic and intrinsic factors in determining the fiber morphometry of the regen-erated nerve. The axon-size and myelination by glial cells were determined through the external axon-glial interactions, whereas the number of axonal microtubules and neurofilaments were intrinsically determined.     

Quantitative studies on myelinated and unmyelinated nerve fibres in the interatrial septal region of aged rat hearts

Intracardiac nerve fibres from the interatrial septum were studied quantitatively and qualitatively by electron microscopy of transversely sectioned nerve bundles in male Wistar rats of 4 and 24 months. No significant changes were found in the myelinated fibre diameters, myelinated axon diameters, myelin sheath thicknesses, g ratios, myelinated fibre areas, unmyelinated axon diameters and unmyelinated axon areas. However, there was evidence of structural changes to the nerve fibres and Schwann cells at 4 and 24 months, increasing in prevalence with age: some myelinated fibres showed infolds, disruptions and clefts of the myelin sheath and accumulation of electron dense myelin-like fragments in the axoplasm. Unmyelinated axons showed fewer changes in structure but also contained similar fragments in the axoplasm. The numbers of neurotubules and neurofilaments per microm2 in unmyelinated intracardiac axons was significantly greater than in those in samples of the cervical vagal trunk. This may be an adaptation to the continuous mechanical stress experienced by these intracardiac nerves. It is concluded that there is little structural evidence to suggest that the conductive properties of intracardiac nerve fibres are adversely affected in aged rats.     

The penetration of fluorescein-conjugated and electrondense tracer proteins into Xenopus tadpole optic nerves following perineural injection.

The permeability of Xenopus tadpole optic nerves to macromolecules was studied in order to evaluate the usefulness of this system for studying mechanisms of serum-induced CNS demyelination in vivo. Single injections of either horseradish peroxidase (HRP), ferritin or fluorescein-conjugated human IgG were injected around the right optic nerve and tadpoles were then sacrificed between 15 min and 48 h. Each of the tracers had penetrated the nerve parenchyma by 30 min. Entry of HRP and ferritin occurred mainly via extracellular clefts between adjacent astrocytic endfeet in the glia limitans region. A similar mode of passage was suggested for IgG. Once within the nerve, the tracers became rapidly associated with myelinated axons. HRP was also seen in the periaxonal space but did not directly penetrate the myelin sheath. By 24 h, extracellular localization of tracer was virtually absent with nearly all of the tracer now being concentrated in vesicles within astrocytic processes and perikarya. The distribution of the tracers was not confined to the optic nerve on the injected side; some was seen in adjacent cranial peripheral nerves and surrounding extraocular musculature. Also, tracers eventually penetrated the pial sheath of the contralateral optic nerve. The results of this study indicate that tadpole optic nerves are permeable to a wide range of macromolecules. Furthermore, the distribution of these tracers to nearby cranial peripheral nerves may provide an important opportunity for testing the differential effect of various substances on central and peripheral myelin sheaths.     

Regenerative repair in the severed optic nerve of the newt (Triturus viridescens): Effect of nerve growth factor antiserum

At 14 days after transection those regenerating newt (Triturus viridescens) optic nerves receiving anti-nerve growth factor treatment were easily distinguished from regenerating controls. Quantitative analysis revealed that antiserum treatment significantly reduced nerve diameter and cross-sectional areas compared to the control groups. Quantitation from electron microscope montages of nerve cross sections revealed similar results. In addition, antiserum treatment significantly reduced the area of regenerating axon fascicles per nerve cross section compared to the control groups. Most significantly, the mean number of regenerating axons per nerve decreased more than 50% in the antiserum-treated group. Regenerating axons appeared normal in all three groups. Axons were filled with clear cytoplasm containing neurofilaments, neurotubules, and an occasional mitochondrion. Axon density was not significantly different among the three groups and axon diameters were similar from 0.1 to 0.8 μm. Distention of glial cell processes surrounding fascicles of axons and increased intra- and extracellular debris may indicate an alteration of glial cell activity in the antiserum group. Many of the 14-day antiserum-treated nerves have the appearance of an untreated transected optic nerve 6 to 10 days after lesion.     

Ultrastructural basis of impulse propagation failure in a nonbranching axon

The morphological basis of intermittent conduction failure in the excitor axon innervating the crayfish opener and stretcher muscles was investigated using the electron microscope. The connective tissue component of the sheath surrounding the axon was found consistently to be thinner in the region at which blocking occurs than in control regions located one cm either proximally or distally, at which blocking does not occur. Otherwise, in these regions differences in the width of the periaxonal spaces, the length or width of the mesaxons, the density of mitochondria, the width of the adaxonal glial cell layer, or the structure of the lamination of the sheath are not observed. Because of the thinner connective tissue component of the sheath in the joint region, neighboring axons are distributed more densely around the excitor, and the volume of the extracellular space is reduced. The possibility that the reduced extracellular space might allow excessive accumulation of potassium during repetitive discharge, causing conduction block, is discussed. Alternative mechanisms consistent with this morphology are also considered.     

Changes in extracellular space in optic nerves of regenerative and nonregenerative animals after hypertonic fixation: Implications for axon regeneration

The optic nerves of some regenerative and nonregenerative animals were compared using electron microscopy, after hypertonic perfusion. Optic axons and glial cell processes separated more readily in regenerative animals, creating large extracellular spaces. In mammals, cell processes remained in close proximity. These findings may indicate lesser adhesion between cell processes in optic nerves of regenerative animals, a characteristic that could allow “potential” space for axon regrowth after nerve injury.     

Remodeling of the proximal segment of crayfish motor nerves following transection

Transected crustacean motor axons consist of a soma-endowed proximal segment that regenerates and a soma-less distal segment that survives for up to a year. We report on the anatomical remodeling of the proximal segment of phasic motor nerves innervating the deep flexor muscles in the abdomen of adult crayfish following transection. The intact nerve with 10 phasic axons and its two branches with subsets of 6 and 7 of these 10 axons undergo several remodeling changes. First, the transected nerve displays many more and smaller axon profiles than the 6 and 7 axons of the intact nerve, approximately 100 and 300 profiles in the two branches of a preparation transected 8 weeks previously. Serial images of the transected nerve denote that the proliferation of profiles is due to several orders of axon sprouting primary, secondary, and tertiary branches. The greater proliferation of axon sprouts, their smaller size, and the absence of intervening glia in the one nerve branch compared with the other branch denote that sprouting is more advanced in this branch. Second, the axon sprouts are regionally differentiated; thus, although in most regions the sprouts are basically axon-like, with a cytoskeleton of microtubules and peripheral mitochondria, in some regions they appear nerve terminal-like and are characterized by numerous clear synaptic vesicles, a few dense-core vesicles, and dispersed mitochondria. Both regions possess active zone dense bars with clustered synaptic vesicles found opposite other sprouts, glia, hemocytes, and connective tissue, but because the opposing membranes are not differentiated into a synaptic contact, the active zones are extrasynaptic. Third, some of the transected axons display a glial cell nucleus denoting assimilation of an adaxonal glial cell by the transected axons. Fourth, within the nerve trunk are a few myocytes and muscle fibers. These most likely originate from adjoining and intimately connected hemocytes, because such transformation occurs during muscle repair. In a crustacean nerve, however, where muscle is clearly misplaced, its presence implies an instructive role for motor nerves in muscle formation.     

Axon-glia transfer of a protein and a carbohydrate

We have investigated the transfer of a fluorescent protein, the fluorescein isothiocyanate derivative of bovine serum albumin (FITC-BSA), and a fluorescent carbohydrate, FITC-dextran, from the crayfish medial giant axon (MGA) to the periaxonal glial cells. The dialyzed tracer was injected into one of the two MGAs, and, after a transfer period of 15-60 min, the tissue was fixed for histological examination of fluorescence distribution. With each tracer, the periaxonal sheath of the injected MGA was specifically labeled. Similar results were obtained with several different fixatives. During the transfer period, there was no appreciable change in the resting potential or conducted action potential of the MGA or in the resting potentials of the adaxonal glial cells. Polyacrylamide gel electrophoresis indicated that the axoplasmic and sheath fluorescence was produced by the intact tracers. These results suggest that "foreign" macromolecules can be exchanged from crayfish axons to glia under physiological conditions. Such transfers may indicate a substantial intercellular traffic of molecules or a means whereby neurons can eliminate waste materials.     

Morphometric effects of vincristine on nerve regeneration in the rat

Administration of vincristine (200, 100 or 50 micrograms/kg/week) for 6 months during regeneration of the sciatic nerve after crush injury caused a dose-dependent reduction in nerve fibre size and failure of removal of myelin debris. Successfully regenerating neurites showed an unusual amount of shape distortion. The ratio of myelin sheath thickness to axon circumference was reduced, but the ratio of myelin sheath thickness to axon area was normal. Microtubule concentration was diminished in axons, but neurofilament density was unaffected. Unmyelinated axons were reduced in number but their axon diameter distribution was not affected. Fibres on the non-crushed side appeared normal. The toxicity of vincristine to regenerating nerves is probably related to increased blood-nerve permeability occurring both at the site of crush and along the degenerating nerve.     

Prior Collateral Sprouting of Sensory Axons Delays Recovery of Pain Sensitivity after Subsequent Nerve Crush

Regeneration of motor axons is enhanced if they have sprouted prior to nerve injury. We examined whether sensory axon regeneration and recovery of pain response was affected by previous collateral sprouting. In the experimental group of rats, the right saphenous, tibial, and sural nerves were transected and ligated. The peroneal nerve was left to sprout into the adjacent denervated skin. Two months later, the axons of the peroneal nerve were crushed in the sciatic nerve. In the control group, the right sciatic nerve was crushed at the same time that the saphenous, tibial, and sural nerves were transected. Recovery of pain response in the foot was determined by the skin pinch test. Sensory axon elongation rate was measured by the nerve pinch test. The number of myelinated axons was determined in nerve cross sections stained by Azur blue. Recovery of pain sensitivity in the animals of the experimental group was delayed for 2–3 weeks in comparison to the control group. Moreover, the spatial pattern of pain response in the experimental group was irregular, displaying residual regions of insensitive skin which were not present in controls. The elongation rate of regenerating sensory axons in the experimental group was not decreased, and the number of myelinated axons in the peroneal nerves was even about 10% higher than in the control group. Therefore, we assume that the terminal arborization of the neurilemmal tubes pertaining to the former axon sprouts delayed regrowth of sensory axon terminals in the skin.     

Heat-shock proteins in axoplasm: High constitutive levels and transfer of inducible isoforms from glia

To characterize heat-shock proteins (HSPs) of the 70-kDa family in the crayfish medial giant axon (MGA), we analyzed axoplasmic proteins separately from proteins of the glial sheath. Several different molecular weight isoforms of constitutive HSP 70s that were detected on immunoblots were approximately 1–3% of the total protein in the axoplasm of MGAs. To investigate inducible HSPs, MGAs were heat shocked in vitro or in vivo, then the axon was bathed in radiolabeled amino acid for 4 hours. After either heat-shock treatment, protein synthesis in the glial sheath was decreased compared with that of control axons, and newly synthesized proteins of 72 kDa, 84 kDa, and 87 kDa appeared in both the axoplasm and the sheath. Because these radiolabeled proteins were present in MGAs only after heat-shock treatments, we interpreted the newly synthesized proteins of 72 kDa, 84 kDa, and 87 kDa to be inducible HSPs. Furthermore, the 72-kDa radiolabeled band in heat-shocked axoplasm and glial sheath samples comigrated with a band possessing HSP 70 immunoreactivity. The amount of heat-induced proteins in axoplasm samples was greater after a 2-hour heat shock than after a 1-hour heat shock. These data indicate that MGA axoplasm contains relatively high levels of constitutive HSP 70s and that, after heat shock, MGA axoplasm obtains inducible HSPs of 72 kDa, 84 kDa, and 87 kDa from the glial sheath. These constitutive and inducible HSPs may help MGAs maintain essential structures and functions following acute heat shock. J. Comp. Neurol. 396:1–11, 1998. © 1998 Wiley-Liss, Inc.     

Early neuron differentiation in the mouse of olfactory bulb. I. Light microscopy

The relation between the growth of axons and the development of their myelin sheaths was determined in rats for normal, myelinating sciatic nerves, and for an experimental model allowing to retard or accelerate axon growth. Axon caliber was measured, and sheath development was determined from measurements of thickness (light microscopy), from counts of the number of turns of myelin lamellae (electron micrographs), and from the rate of the incorporation of acetate-H³ into ether-ethanol extractable lipids. An excellent correlation between changes in sheath thickness and acetate-H³ incorporation was obtained for all experiments. For the myelinating nerves the changes in the rate of acetate-H³ incorporation were related specifically to the rate with which new length of myelin leaflet was added to the existing turns of sheath. The rate of axonal growth was manipulated by applying a snug ligature around the nerve by the fourteenth day, allowing the nerve to compress itself by its own growth. Most axons passed the constriction without interruption, but they were markedly hypoplastic distal to the constriction. After removal of the ligature these axons regrew to their normal caliber ranges. Examination of myelin sheath development in this model showed that retardation of axon growth retarded sheath growth, while acceleration of axon growth accelerated sheath growth. Thus, the rate of axon growth appeared to be the factor controlling the rate of myelin formation by the sheath cells. An appendix describes a model consisting of two interrelated feedback mechanisms by which expansion of the axon may directly control the number of turns of myelin lamellae formed by the sheath cell. The model correspons on all points to established features in the fine structure of fibers.     

Receptor protein tyrosine phosphatase sigma inhibits axon regrowth in the adult injured CNS

Recently, receptor protein tyrosine phosphatase-sigma (RPTPsigma) has been shown to inhibit axon regeneration in injured peripheral nerves. Unlike the peripheral nervous system (PNS), central nervous system (CNS) neurons fail to regenerate their axons after injury or in disease. In order to assess the role of RPTPsigma in CNS regeneration, we used the retinocollicular system of adult mice lacking RPTPsigma to evaluate retinal ganglion cell (RGC) axon regrowth after optic nerve lesion. Quantitative analysis demonstrated a significant increase in the number of RGC axons that crossed the glial scar and extended distally in optic nerves from RPTPsigma (-/-) mice compared to wild-type littermate controls. Although we found that RPTPsigma is expressed by adult RGCs in wild-type mice, the retinas and optic nerves of adult RPTPsigma (-/-) mice showed no histological defects. Furthermore, the time-course of RGC death after nerve lesion was not different between knockout and wild-type animals. Thus, enhanced axon regrowth in the absence of RPTPsigma could not be attributed to developmental defects or increased neuronal survival. Finally, we show constitutively elevated activity of mitogen-activated protein kinase (MAPK) and Akt kinase in adult RPTPsigma (-/-) mice retinas, suggesting that these signaling pathways may contribute to promoting RGC axon regrowth following traumatic nerve injury. Our results support a model in which RPTPsigma inhibits axon regeneration in the adult injured CNS.     

Regeneration of rat optic axons into peripheral nerve grafts

The regenerative response of myelinated axons of the mammalian central nervous system was investigated by inserting peripheral nerve grafts in the vicinity of traumatized rat optic axons. Peroneal nerve grafts were inserted into crushed optic nerves and assessed for the ability to support optic axon regeneration. Regenerating axons of retinal origin were present in the peripheral nerve grafts several weeks later. Horseradish peroxidase studies indicated that retinal ganglion cells were a source for regenerating nerve fibers.