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PubMed1989

Changes in size of motor axons in hereditary canine spinal muscular atrophy.

Hereditary canine spinal muscular atrophy (HCSMA), a dominantly inherited disorder of motor neurons, has three phenotypes: accelerated, intermediate, and chronic. In the accelerated and intermediate phenotypes, axonal sizes in ventral roots were smaller than in controls. Reductions in axonal size occurred primarily in large axons, and the frequency of small-caliber axons was increased. In HCSMA, nerve fiber shape, i.e., circularity, was reduced, and the relative thickness of the myelin sheath as a function of axonal caliber was decreased. The density of fibers in motor nerves was increased, making it unlikely that a selective loss of large-caliber axons explained the increased frequency of small-caliber axons. These observations suggest that, in HCSMA, changes in axonal size in motor nerves are associated with both growth arrest and axonal atrophy.

Age Factors↗
PubMed1987

Biochemical and immunocytochemical characterization and distribution of phosphorylated and nonphosphorylated subunits of neurofilaments in squid giant axon and stellate ganglion.

Monoclonal antibodies to squid neurofilament (aNFP) and intermediate filament (aIFA) proteins were used as probes for the biochemical and immunocytochemical analyses of neurofilament structure and distribution in the squid giant axon and stellate ganglion. On Western blots the aNFP antibody stained exclusively the 220 kDa and high-molecular-weight (HMW) components of neurofilaments in the giant axon, whereas the aIFA antibody primarily labeled the 60 kDa protein in the giant axon and the 60 and 65 kDa proteins in the stellate ganglion. Dephosphorylation of axoplasmic proteins by alkaline phosphatase resulted in a decrease in the molecular weights of both the 220 kDa and HMW neurofilament proteins and a concomitant loss of reactivity with the aNFP antibody on Western blots. This indicated that the aNFP antibody is specific for a phosphorylated epitope in the neurofilament. Increased dephosphorylation of the 220 kDa protein led to an enhanced immunostaining of the resultant 190 kDa polypeptide by the aIFA antibody, suggesting that the phosphorylated epitope may mask the conserved epitope recognized by aIFA. Light and electron microscopic immunocytochemical studies show intense labeling by the aNFP antibody in the giant axon. In contrast, the aIFA antibody labeled the glial cells around the giant axon intensely, while labeling of the giant axon itself was considerably less than that with the aNFP antibody. Since the 60 kDa protein in axoplasm is intensely stained by the aIFA antibody on Western blots, the relatively low amounts of labeling seen on semithin and thin sections of the giant axon by this antibody may be due to the masking of the 60 kDa protein by in situ fixed axoplasmic proteins. However, the aIFA antibody intensely labeled glial cells within the stellate ganglion and "islands" of filaments and nuclear membranes within ganglion cells. No reactivity for either antibody was seen in synapses. The aNFP antibody specifically labeled "beadlike" portions and cross-bridges on the axonal neurofilaments, suggesting that these components consist of the 220 kDa and HMW proteins. In contrast, the aIFA antibody labeled relatively smooth filaments in ganglion and glial cells. These data suggest that the 65 kDa protein represents the squid glial filament protein and that the 60 kDa protein found in axoplasm represents the low-molecular-weight subunit in the axonal neurofilament. The latter appears to be formed and/or organized in "islands" of filaments within ganglion cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Deposition and transfer of axonally transported phospholipids in rat sciatic nerve.

Radioactive glycerol, ethanolamine, or choline injected into the vicinity of the cell bodies of rat sciatic nerve sensory fibers is incorporated into phospholipid. Some newly synthesized ethanolamine and choline phosphoglycerides are subsequently committed to transport down the sciatic nerve axons at a rate of several hundred millimeters per day. Most labeled choline phosphoglycerides move uniformly down the axons; in contrast, the crest of moving ethanolamine phosphoglycerides is continually attenuated. These data, as well as differences in the clearance of these phospholipids distal to a nerve ligature, suggest that various classes of labeled phospholipids are differentially unloaded from the transport vector (possibly by exchange with unlabeled lipid in stationary axonal structures) during movement down the axons. The extent of unloading appears to be defined by the base moiety; both diacyl and plasmalogen species of ethanolamine phosphoglycerides exchange extensively with stationary axonal lipids, while most choline phosphoglycerides continue down the axons. Autoradiographic studies with 3H-choline and 3H-ethanolamine demonstrated that most unloaded phospholipid is initially deposited in axonal structures; some of this unloaded lipid is subsequently transferred to the axon/myelin interface (axolemma?) and then to myelin. Although transported ethanolamine phosphoglycerides exchange more extensively with lipids in stationary axonal structures than do choline phosphoglycerides, at early times more label from 3H-choline is found in myelin. A model to resolve this seeming discrepancy is proposed, wherein a differential topographic localization of phospholipid classes in the membrane of the transport vector allows for a preferential extensive exchange of transported ethanolamine phosphoglycerides with lipids in stationary axonal structures, while choline phosphoglycerides become available for rapid transfer to myelin by a process involving vesicle fusion with axolemma.

Animals↗
PubMed1988

Axon classes and internodal growth in the ventral spinal root L7 of adult and developing cats.

Internodal length, number of myelin sheath lamellae and axon diameter were estimated in samples of nerve fibres reconstructed from transverse sections (EM and LM) of the L7 ventral spinal root of adult cats, kittens and cat fetuses. The axon calibre spectrum was unimodal in the youngest fetuses, became bimodal at 47 days after mating, i.e. about 2 weeks before birth (63 days after mating) and trimodal at 1 week of postnatal age. Alpha-axons received myelin during the period 40-45 to 50-55 days after mating while gamma-axons became myelinated from 60-63 days after mating to 2-3 weeks of postnatal age. The mean length of the first completely myelinated internodes measured 139 microns and 209 microns in the alpha- and gamma-fibre group respectively. The adult mean values were 1390 microns and 640 microns respectively. The average internodal elongation was x 10 and x 3 in the two fibre groups, whereas the longitudinal growth of the whole ventral root was x 5.4 and x 3.5. A combined linlog function could be fitted to describe the regression between internodal length and axon diameter and was established from birth onwards. The separate alpha- and gamma-fibre samples were best described by linear functions, the alpha internodal length being independent of axon diameter while the gamma internodal length increased linearly with axon diameter. The amount of internodal myelin increased linearly with increasing mantle area of the internodal axon. The mean amount of internodal myelin of alpha-fibres showed two periods of intense growth; one from the start of myelination to 2 months postnatally and the other between 4 and 6 months of age. The mean length of the lamellar spiral forming the myelin sheath showed about the same increase per unit length of axon circumference (about 160:1) in both alpha- and gamma-fibre groups as long as longitudinal internodal growth persisted.

Age Factors↗
PubMed1980

Fast axonal transport in early experimental disc edema.

Previous work has documented impairment of slow axonal transport in papilledema, but the abnormalities in rapid transport were less certain. Therefore fast axonal transport was studied in 19 primate eyes subjected to ocular hypotony for 6 to 72 hr following surgical fistulization of the anterior chamber. Mild, irregular alterations in fast axonal transport were detected only after nerve head swelling was apparent. These changes in fast transport mechanisms in cases of nerve head edema occur after, and may be secondary to, impaired slow axoplasmic flow and the resultant axonal swelling. Furthermore, since prolonged complete interruption of axonal transport is theoretically inconsistent with the continued normal neuron function characteristic of papilledema and, moreover, since previous data shows a "slowdown" rather than complete blockade of axonal transport in papilledema, it is likely that in eyes with papilledema there does not exist a complete flock of axonal transport. Therefore we hypothesize that the swelling results when slow axoplasmic flow is locally slowed down but not totally stopped, with the axon distention producing secondary mild, irregular changes in fast axonal transport.

Animals↗
PubMed1984

The non-directional pattern of axonal changes in Wallerian degeneration: a computer-aided morphometric analysis.

Wallerian degeneration was investigated to determine whether axonal changes occur progressively in a somatofugal or somatopetal direction or simultaneously along the length of the axon. Microtubule density was used as a measure of the extent of axonal degeneration and was assessed by a computer-aided analysis of electron micrographs. The left sural nerves of ten rats were crushed and 30 hours later axonal areas and axonal microtubule numbers were recorded from a large sample of axons at two sites 1 cm and 3 cm distal to the crush. The same recordings were made from the right unoperated nerve at two comparable sites. Statistical analysis of all the data provided no evidence for a somatofugal or reverse direction of degeneration. It is concluded therefore that in Wallerian degeneration axonal changes, as indicated by microtubule dissolution, occur simultaneously along the length of the axon. It is proposed that to interpret the conflicting published data on the direction of fibre degeneration, Schwann cell changes (e.g. myelin ovoid formation) and axonal changes (e.g. microtubule dissolution) should be considered independently since they have different aetiological mechanisms which may account for the differing experimental results reported.

Animals↗
PubMed1983

Embryonic development of the leech nervous system: primary axon outgrowth of identified neurons.

This paper describes the embryonic development of the leech nervous system and focuses on the differentiation of two identified pressure sensory (P) neurons, the PD and PV neurons. In the adult leech the P neurons have distinctive cell body locations in the central nervous system (CNS), different peripheral axon branching patterns, and different receptive field territories in the skin. The embryonic P neurons also have distinct and reproducible locations in the CNS and have been studied with recording and dye-filled microelectrodes from the time the first growth cones are projected from their somata. The peripheral axons of the P neurons are among the earliest peripheral axons to develop and may play an important role in the formation of peripheral nerves. The first or primary peripheral axons of the P neurons grow directly to their separate target territories. The specificity of the P neurons for their targets is probably not due to temporal differences in the outgrowth of their primary axons. Instead, the PD neuron seems to exhibit a preference early in embryogenesis for the target of its primary axon despite an apparent opportunity to occupy the target of the PV primary axon. It is hypothesized that the primary peripheral axons of the P neurons are among the first axons projected from the CNS and follow environmental cues to reach and innervate their target territories.

Animals↗
PubMed1983

[Ultrastructure of the synapses of the initial axonal segment of the pyramidal neuron].

Ultrastructure of the proximal part of the axon in the neurons, identified according to a number of morphological signs as pyramidal, has been studied in the layer III of the cat cerebral hemisphere sensomotor cortex. In sections, tangential to the cortical surface, in the initial axonal segment, a submembranous osmophilic layer and fasciculi of microtubules are revealed. On the initial segment spines are found, they contain cysterns resembling by their structure the spine system of the dendritic spines. Axonal terminals revealed along the axonal distribution are in contact both with the axonal trunk and with the spines. Regarding the initial segment, they are presynaptic, contain oval synaptic vesicles and form symmetric axo-axonal synapses only. In transversal sections axonal terminals are detected, arranging on the surface of the initial segment mostly as single ones, in longitudinal sections they are seen as clusters. Analysing the author's data and those from the literature, a conclusion is made that in intact animals the synaptic contacts at the initial segment of the axon are the only form of axo-axonal synapses in the neocortex.

Animals↗
PubMed1983

An analysis of axon caliber within the optic nerve of the cat: evidence of size groupings and regional organization.

Axon size in the optic nerves of three adult cats was measured using an accurate planimetric method. A sample of the axon complement was obtained from sets of more than 125 electron micrographs taken at each nerve. In contrast to previous reports, the distribution of axon diameter, as estimated from measurements of axonal cross-sectional area was clearly bimodal. The group of finest axons had a mode at approximately 1 micrometer, and the mode of the group of intermediate size axons was approximately 2 micrometers. Fibers with diameters larger than 3.5 micrometers formed the extensive tail of the distribution. The proportions of large, intermediate, and small axons were estimated to be 5%, 45%, and 50%. These groups probably correspond to the alpha, beta, and gamma classes of retinal ganglion cells. Regional distributions of axon caliber were also bimodal and, in a few instances, even trimodal. A peripheral crescent of each nerve contained a large number of fine fibers. Mean fiber diameter within discrete regions of the optic nerve varied inversely with the density of axon packing. The thickness of the myelin sheath was highly correlated with the inner fiber diameter, hence, myelin sheath width was also distributed in a bimodal manner. These results furnish the first clear evidence that the distribution of fiber caliber within the cat's optic nerve mirrors the principal classes of retinal ganglion cells.

Animals↗
PubMed1995

The growth of the axon is not dependent upon net microtubule assembly at its distal tip.

Although there is agreement that the net addition of new microtubule polymer to the axon is required for its growth, controversy exists concerning the principal site in the neuron where this occurs. Some models hold that microtubule polymer is assembled within the cell body and translocated down the axon, while others hold that the net addition of polymer occurs at the distal tip of the axon. The foundation for the latter idea was a study in which anti-microtubule drugs were applied topically for 30 min to discrete regions of cultured sensory neurons (Bamburg et al., 1986). The axon continued to grow when the drugs were applied to the cell body, but stopped growing when the drugs were applied to the distal tip of the axon. Assuming that the sole action of the drug was to inhibit microtubule assembly, many workers have interpreted these findings as indicating that the growth of the axon requires net microtubule assembly at its distal tip. We repeated these experiments using a broader range of drug treatments, and evaluated using electron microscopy the effects of these treatments on microtubule levels. Our results indicate that the previous drug treatments went beyond inhibiting microtubule assembly, and also caused substantial microtubule disassembly. When the drug regime was altered so as to induce lower levels of microtubule disassembly in the distal region of the axon, the axon continued to grow. These results indicate that the growth of the axon is not dependent upon net microtubule assembly at its distal tip.

Animals↗
PubMed1995

The immunosuppressant FK506 increases the rate of axonal regeneration in rat sciatic nerve.

The axonal regenerative properties of the new immunosuppressant drug FK506 (tacrolimus) are further explored in this continuing study. In an initial report (Gold et al., 1994a), we described the ability of FK506 to reduce the time until return of function in the hind feet of rats following a sciatic nerve crush. In the present study, we examined the morphological correlate underlying this enhancement of functional recovery. In rats receiving daily subcutaneous injections of FK506 (1.0 mg/kg) for 18 d following a sciatic nerve crush the regenerating axons appeared larger in size compared to saline-injected control animals. Morphometric analysis of axonal calibers in the soleus nerve demonstrated that mean axonal areas for the largest 30% of axons were increased over axotomized control values by 93% in the FK506-treated animals. Next, the rate of axonal regeneration was determined by radiolabeling the L5 dorsal root ganglion (DRG) at 9 and 14 d following axotomy. Regression analysis of the outgrowth distances for sensory axons between 10 and 15 d revealed a 16% increase in regeneration rate. Electron microscopy of intramuscular nerve branches in the interosseus muscles confirmed that the axons in the FK506-treated animals were further advanced toward their targets; in some instances, axons were shown to reinnervate muscle spindles. The results are discussed in terms of the known ability of FK506 to inhibit the activity protein phosphatase 2B (calcineurin).

Animals↗
PubMed1994

The L2/HNK-1 carbohydrate is preferentially expressed by previously motor axon-associated Schwann cells in reinnervated peripheral nerves.

The carbohydrate epitope L2/HNK-1 (hereafter designated L2) is expressed in the adult mouse by myelinating Schwann cells of ventral roots and muscle nerves, but rarely by those of dorsal roots or cutaneous nerves. Since substrate-coated L2 glycolipids promote outgrowth of cultured motor but not sensory neurons, L2 may thus influence the preferential reinnervation of muscle nerves by regenerating motor axons in vivo. In the present study, we have analyzed the influence of regenerating axons on L2 expression by reinnervated Schwann cells by directing motor or sensory axons into the muscle and cutaneous branches of femoral nerves of 8-week-old mice. We observed that regenerating axons from cutaneous branches did not lead to immunocytochemically detectable L2 expression in muscle or cutaneous nerve branches. Axons regenerating from muscle branches led to a weak L2 expression by few Schwann cells of the cutaneous branch, but provoked a strong L2 expression by many Schwann cells of the muscle branch. Myelinating Schwann cells previously associated with motor axons thus differed from previously sensory axon-associated myelinating Schwann cells in their ability to express L2 when contacted by motor axons. This upregulation of L2 expression during critical stages of reinnervation may provide motor axons regenerating into the appropriate, muscle pathways with an advantage over those regenerating into the inappropriate, sensory pathways.

Animals↗
PubMed1993

The innervation of intradermal nevi. On the nevus-axon relations.

In the study of the histogenesis of intradermal nevi, the nevus cell-Schwann cell relationship has been a matter of long debate. We have demonstrated a dense axonal supply in the intradermal nevi by protein gene product 9.5 (PGP 9.5) immunohistochemistry. There were small nerve bundles between nevus cell nests and numerous individual axons in the nests of all the intradermal nevi studied. The distribution of these axons was more dense in the deeper and middle portions than in the superficial portion of the nevi. The significance and morphogenesis of this rich axonal supply in the intradermal nevi remain obscure, but this nevic neurotropism suggests an intimate mutual interaction between nevus cells and axons: possibly, some activities of nevus cells stimulating axonal proliferation, or nevus cell migration into the preexisting nerves. The presence of the proliferated axons may have some influences upon Schwannian transformation of the nevus cells. The mode of contact between nevus cell and axon, the presence of true Schwann cells surrounding the proliferated axons and the demonstration of myelin structure should be investigated by further electron microscopic study.

Adult↗
PubMed1996

Restoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cells.

Although remyelination of demyelinated CNS axons is known to occur after transplantation of exogenous glial cells, previous studies have not determined whether cell transplantation can restore the conduction properties of demyelinated axons in the adult CNS. To examine this issue, the dorsal columns of the adult rat spinal cord were demyelinated by x-irradiation and intraspinal injections of ethidium bromide. Cell suspensions of cultured astrocytes and Schwann cells derived from neonatal rats transfected with the (beta-galactosidase) reporter gene were injected into the glial-free lesion site. After 3-4 weeks nearly all of the demyelinated axons were remyelinated by the transplanted Schwann cells. The dorsal columns were removed and maintained in an in vitro recording chamber; conduction properties were studied using field potential and intra-axonal recording techniques. The demyelinated axons exhibited conduction slowing and block, and a reduction in their ability to follow high-frequency stimulation. Axons remyelinated by transplantation of cultured Schwann cells exhibited restoration of conduction through the lesion, with reestablishment of normal conduction velocity. The axons remyelinated after transplantation showed enhanced impulse recovery to paired-pulse stimulation and greater frequency-following capability as compared with both demyelinated and control axons. These results demonstrate the functional repair of demyelinated axons in the adult CNS by transplantation of cultured myelin-forming cells from the peripheral nervous system in combination with astrocytes.

Animals↗
PubMed1996

Retroviral misexpression of engrailed genes in the chick optic tectum perturbs the topographic targeting of retinal axons.

We have investigated the role of the homeodomain transcription factor genes En-1 and En-2, homologs of the Drosophila segment polarity gene engrailed, in regulating the development of the retinotopic map in the chick optic tectum. The En proteins are distributed in a gradient along the rostral-caudal axis of the developing tectum, with highest amounts found caudally. Previous evidence suggests that En-1 and En-2 may regulate the polarity of the rostral-caudal axis of the tectum and the subsequent topographic mapping of retinal axons. We have tested this hypothesis by using a recombinant replication-competent retrovirus to overexpress the En-1 or En-2 genes in the developing tectum. Anterograde labeling with the axon tracer Dil was used to analyze the topographic mapping of retinal axons after the time that the retinotectal projection is normally topographically organized. Overexpression of either En-1 or En-2 perturbed the topographic targeting of retinal axons. In En-infected tecta, nasal retinal axons form an abnormally diffuse projection with numerous aberrant axons, branches, and arbors found at topographically incorrect locations, colocalized with domains of viral infection. In contrast, temporal axons did not form a diffuse projection or discrete aberrant arbors; however, many temporal axons were stunted and ended aberrantly rostral to their appropriate TZ, or in other cases either did not enter the tectum or formed a dense termination at its extreme rostral edge. These findings indicate that En-1 and En-2 are involved in regulating the development of the retinotopic map in the tectum. Furthermore, they support the hypothesis that En genes regulate the polarity of the rostral-caudal axis of the tectum, most likely by controlling the expression of retinal axon guidance molecules.

Animals↗
PubMed1996

The influence of predegenerated nerve grafts on axonal regeneration from prelesioned peripheral nerves.

Recent in vitro work has indicated that predegenerated segments of peripheral nerve are more capable of supporting neurite growth from adult neurons than fresh segments of nerve, whereas previous in vivo studies which investigated whether predegenerated nerve segments used as grafts are capable of enhancing axonal regeneration produced conflicting results. We have reinvestigated this question by using predegenerated nerve grafts in combination with conditioning lesions of the host nerve to determine the optimal conditions for obtaining the maximal degree of regeneration of myelinated axons. The sciatic nerve of adult Dark Agouti rats were sectioned at midthigh level, and the distal portion was allowed to predegenerate for 0, 6 or 12 d in situ. 10-15 mm lengths of these distal nerve segments were then syngenically grafted onto the central stumps of sciatic nerves which had themselves received a conditioning lesion 0, 6, and 12 d previously, making a total of 9 different donor-host combinations. The grafts were assessed histologically 3 or 8 wk after grafting. Axonal regeneration in the 9 different donor-host combinations was determined by counting the numbers of myelinated axons in transverse sections through the grafts. All grafts examined contained regenerating myelinated axons. The rats given a 3 wk postgrafting survival period had an average of between 1400 and 5300 such axons. The rats given an 8 wk postgrafting survival period had between about 13,000 and 25,000 regenerating myelinated axons. Analysis of variance revealed significant main effects for both the Donor and Host conditions as well as Weeks (i.e. survival period after grafting). These results indicate that both a conditioning lesion of the host neurons and the degree of predegeneration of peripheral nerve segments to be used as grafts are of importance in influencing the degree of axonal regeneration. Of these 2 factors the conditioning lesion of the host appears to have the greater effect on the final number of regenerating myelinated axons.

Animals↗
PubMed1997

Clustering of voltage-sensitive sodium channels on axons is independent of direct Schwann cell contact in the dystrophic mouse.

The distribution of voltage-sensitive sodium channels on axons in the dorsal and ventral spinal roots of the dystrophic mouse 129/ReJ-Lama2dy was determined via immunocytochemistry. In these nerves there are regions in which Schwann cells fail to proliferate and myelinate axons in a normal manner, leaving bundles of closely packed large-diameter amyelinated axons. We have identified discrete and focal concentrations of sodium channel immunoreactivity on these axons by both confocal immunofluorescence and immunoelectron microscopy, using a peptide-derived polyclonal antibody. In addition, simultaneous labeling with an antibody recognizing neuronal-specific ankyrinG revealed a distinct colocalization with the sodium channels on both normal and amyelinated axons. The presence of patches of sodium channels along with their anchoring protein on amyelinated axons in the absence of intervening Schwann cells demonstrates that axons can form and maintain independently these initial aggregations. This confirms that direct contact between Schwann cell and axon is not required for the formation of sodium channel patches of nodal dimensions and density. Furthermore, this strongly suggests that local transfer of sodium channels from Schwann cells to axons is not required for this process.

Animals↗
PubMed1997

The relevance of axonal swellings and atrophy to gamma-diketone neurotoxicity: a forum position paper.

Traditionally, gamma-diketone neuropathy is classified as a distal axonopathy and has been characterized by giant axonal swellings in CNS and PNS tissues. These swellings contain neurofilamentous masses and are associated with thinning and retraction of the myelin sheath. It has been proposed that this axonopathy is caused by direct gamma-diketone modification of neurofilaments (NFs) involving pyrrolation of epsilon-amino groups on NF lysyl residues and possibly secondary autoxidation of the pyrrole rings with creation of covalent NF-NF crosslinks. Neurofilaments are thought to undergo chemical modification as they progress along the axonal axis and, eventually, accumulate at distal nodes of Ranvier where their proximodistal movement is impeded. Development of swelling presumably initiates axonal degeneration and subsequent functional deficits. However, other research suggests that axonal swellings are a non-specific effect related to subchronic gamma-diketone exposure. Such evidence draws into question the mechanistic relevance of these swellings. In contrast, research conducted over the past decade indicates axonal atrophy is a specific morphologic component of gamma-diketone neuropathy which might have both functional and mechanistic importance. In this overview, the potential neurotoxicological significance of both axonal swellings and atrophy are evaluated critically. Based on the evidence to be presented, we propose that axonal atrophy is the morphological consequence of the molecular mechanism of gamma-diketone neuropathy. Accordingly, several mechanistic scenarios related to the development of atrophy will be discussed. It is hoped that this Forum will stimulate scientific debate and initiate laboratory investigations which will either confirm or refute the involvement of axonal atrophy in gamma-diketone neurotoxicity. Investigating gamma-diketone atrophy might provide insight into the mechanism of other toxic axonopathies which are also associated with reduced axon caliber; e.g., acrylamide and carbon disulfide neuropathies.

Animals↗