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At least 19 recordsLinked to original sources
PubMed1978

The internal structure of axons from rat sciatic nerve.

Sciatic nerves from rats were examined electron microscopically following fixation in 4% tannic acid in 2.5% glutaraldehyde, which allowed demonstration of a filamentous network between the usual intra-axonal organelles. The network appears to consist of longitudinal 10 nm in diameter filaments and cross-linking filaments of about 6 nm diameter. Exposure to cold caused disruption of microtubules, but not the filaments, and incubation at 37 degrees C following cold exposure resulted in reformation of the microtubules which again showed linking with the filaments. Exposure of the nerves to cold in the presence of D2O did not cause disruption of the microtubules but there did appear to be some loss of the fine filaments. These findings suggest that the finer cross-linking filaments are of a different nature than the longitudinal 10 nm filaments, and that there is a dynamic relationship between these filaments and microtubules since the cross-linkages reappear following microtubule disruption and reformation.

Animals↗
PubMed1979

Effects of nerve impulses on threshold of frog sciatic nerve fibres.

1. The firing thresholds of single myelinated fibres of frog sciatic nerves were monitored as a function of impulse activity in the fibre. The threshold was given by the number of coulombs in current pulses that excited a particular fibre half the time when delivered to the whole nerve. Threshold was tracked by a device that incrementally decreased the number of coulombs in the current pulse whenever the fibre responded and increased the pulse if it did not respond. 2. There was a pattern to the after-oscillations of threshold following activity. The fibres were briefly refractory, transiently superexcitable for about 1-1.5 sec and then entered a phase of raised threshold or 'depression' that lasted for many minutes. 3. Activity produced little change in the threshold curve during the refractory period. Strong depressions following prolonged activity prevented the threshold from returning to the base-line level within the time associated with the refractory period for the same fibre at rest. 4. After an impulse, superexcitability reached a maximum within 7-20 msec. This peak was larger as the number of impulses in a preceding burst increased and as the intervals between the impulses became briefer. Each successive impulse of a burst contributed less to the growth of superexcitability, and after the burst had 6-10 impulses additional impulses contributed nothing. 5. The depression phase was marked by the interaction between build-up, which depended on the activity rate, and recovery, which required as long as an hour or more for the threshold to be completely restored to resting level. These two mechanisms, one causing build-up and the other recovery, led to formation of dynamic equilibria. The threshold level at equilibrium increased monotonically with the activity rate. 6. The processes associated with superexcitability interact with those producing depression. In active fibres showing raised thresholds, impulses are followed by a relative superexcitability that persists for at least as long as an absolute superexcitability (with threshold below the resting level) can be measured in the same fibre at rest. 7. The duration of the superexcitable phase interpreted as a relative change in excitability was roughly the same regardless of the level of depression. 8. The magnitude of the oscillation in threshold was give to ten times larger than the grey region (the range of stimuli for which response is probabilistic). It is concluded that at regions of low conduction safety such as axonal branches, where weak forces can influence whether an impulse will pass, such pronounced and long-lasting after-effects of firing can be expected to modulate conduction of nerve impulses.

Action Potentials↗
PubMed1978

Isolation of a product from the trypsin-digested glycoprotein of sciatic nerve myelin.

When purified rabbit sciatic nerve myelin, whether lyophilized or not, is treated with low amounts of trypsin (25 microgram/ml) for 0.5, 3, or 24 h the resulting protein patterns viewed on sodium dodecyl sulfate (SDS) gel electrophoresis are similar. The most striking feature of the trypsinized myelin is the accumulation of a heavy band at the basic protein position, molecular weight 19 000, which is accounted for as a degradation product of the PO protein, referred to as the TPO protein. The PO protein, the major glycoprotein of sciatic nerve myelin, as well as the 23K and P2 proteins and albumin, an absorbed component, are all partially degraded; most high molecular weight bands are lost. The TPO protein, isolated by gel filtration in 2% SDS on an agarose column, like the PO protein, is highly insoluble in aqueous solvents. It is a glycoprotein (8% carbohydrate), staining with periodic acid-Schiff reagent; containing 3 mannose, 1 galactose, 3 N-acetylglucosamine, 1 sialic acid, and 1 fucose residues and is identical to the nonasaccharide of the parent PO protein. The amino acid composition of the TPO protein, is similar to the PO protein, but has a much higher content of hydrophobic residues and begins with NH2-methionine. This suggests that the PO protein is an amphipathic membrane protein in which its more polar character is confined to the first third of its NH2-terminus. This polar domain is probably positioned above the lipid leaflet where it is accessible to trypsin which cleaves a sensitive lysinyl (or argininyl)-methionine linkage. The more hydrophobic domain (the TPO protein) is buried in the myelin bilayer where it is protected from further tryptic attack. Thus trypsin can serve as a useful probe of myelin structure.

Amino Acids↗
PubMed1976

Peripheral nerve glycoproteins and myelin fine structure during development of rat sciatic nerve.

Developmental changes in relative amounts of peripheral nerve proteins and glycoproteins have been correlated with the degree of morphological myelination at various ages during the first 25 postnatal days in rat sciatic nerve. At birth there is virtually no major myelin glycoprotein (P0), but there is a protein which migrates to the same point on sodium dodecyl sulphate (SDS) polyacrylamide gels as the small myelin basic protein (P2). During the time myelin is being formed in the nerve, the P0 protein increases and the P2 protein appears to decrease in relative amount in the nerve. The accumulation of P0 protein in the nerve correlates extremely well with the degree of myelination in sciatic nerve. At 4-6 days postnatal, smooth membrane profiles are observed which are located within axons and in the inner Schwann cell cytoplasm. Such profiles are also observed to fuse with the axolemma-Schwann cell interface. The profiles may represent membrane material being added to or deleted from the axolemma or myelin during myelination.

Animals↗
PubMed1978

The topography of root fibres within the sciatic nerve trunk of the dog.

The architecture of the fibres in the sciatic nerve of the dog has been analysed by following the degeneration of fibres resulting from division of the individual spinal nerves which contribute to the sciatic nerve. A pattern has been demonstrated which varies in part with the size of the contribution to the sciatic nerve from each of the spinal nerves L6, L7 and S1. The redistribution of the fibres of each spinal nerve to form the various branches of the sciatic nerve is also described, and the significance of these arrangements is discussed.

Animals↗
PubMed1978

Abnormalities of the sciatic nerves of dystrophic mice with reference to the large U-axons.

A statistical study using regression analysis was used to evaluate the density of axonal organelles in dystrophic peripheral nerves. The slope of the density of neurotubules (NT) in myelinated (M-) axons was different from that in small unmyelinated (U-) axons. The slope of the density of NT in large U-axons (larger than 1.5 micron in diameter) was similar to that of the M-axons in both the dystrophic and control mice. There was a higher density of NT in the dystrophic M-axons than in the controls in the anterior, posterior and mixed nerves of the sciatic nerve. There was also a higher density of NT in the dystrophic small U-axons than in the controls. There was a higher density of neurofilaments (NF) of M-axons in the dystrophic mice than in the controls. On the contrary, the NF of small U-axons were lower in density in the dystrophic mice. These results were different from our previous reports, which were observed in the distal part, depending on when the groups of U-axons were divided (Okada, Mizuhira and Nakamura 1976a).

Animals↗
PubMed1979

Evidence that 4S RNA is axonally transported in normal and regenerating rat sciatic nerves.

Studies in regenerating goldfish optic nerves indicate that RNA may be axonally transported during optic nerve regeneration14,18,19. The present study was performed to determine if the axonal migration of RNA could be demonstrated during regeneration of the rat sciatic nerve. Rats, which had only the left sciatic nerve crushed 10 days earlier, were injected bilaterally with [3H]uridine into the spinal cord at segmental levels L5 and L6, thus labeling ventral horn cells giving rise to the sciatic nerve. Six, 14 and 20 days later rats were sacrificed by cardiac perfusion of saline followed by 10% formaldehyde. Formaldehyde-precipitable radioactivity, identified as [3H]RNA, was 4--5 times greater in the regenerating sciatic nerve compared to the normal nerve and moved without impediment beyond the point of the crush into the regenerating portion of the nerve. The axonal migration of free unincorporated labeled RNA precursors was also demonstrated, raising the possibility that the distribution of [3H]RNA along the sciatic nerve might be entirely extra-axonal; i.e., free [3H]uridine is taken up by Schwann cells from the axon where it is incorporated into [3H]RNA. This interpretation of the data would also result in the appearance of a proximodistal distribution of RNA associated radioactivity. To determine whether any sciatic nerve [3H]RNA was due to axonal transport, rats which had only the left sciatic nerve crushed 10 days earlier were injected bilaterally with [3H]uridine into the spinal cord. Fourteen days after injection, rats were sacrificed and radioactivity present in the nerve was confirmed as RNA by SDS polyacrylamide gel electrophoresis. Radioactivity in the various RNA species 14 days after intraspinal injection showed the following distribution: 28 + 18S RNA--normal 39.3% +/- 2.1; regenerating 45.4% +/- 1.6; 4S RNA--normal 43.0% +/- 1.3; regenerating 46.8% +/- 2.7. Similar characterization of sciatic nerve RNA 1 or 3 days following the intravenous administration of [3H]uridine gave the following distribution: 28 + 18S RNA--normal 72.4% +/- 3.0; regenerating 75.0% +/- 3.6; 4S RNA--normal 7.7% +/- 1.3; regenerating 10.7% +/- 0.8. The intraspinal injection of [3H]uridine would label Schwann cell RNA and, in addition, any species of intra-axonal RNA, while intravenous injections would label Schwann cell RNA and not axonal RNA. If 4S RNA is in the axon, one would predict relatively more labeled 4S RNA following intraspinal injections than following intravenous injections. The data demonstrate an enrichment of 4S RNA in both normal and regenerating rat sciatic nerve following the intraspinal but not following the intravenous injection of labeled precursor. Therefore, we suggest that 4S RNA migrates axonally in both normal and regenerating sciatic nerves of rats.

Animals↗
PubMed1976

Tumour of the sciatic nerve.

A malignant neurilemmoma of the sciatic nerve is described. The requisites for making this diagnosis are discussed. It is pointed out that such tumours are commonly misdiagnosed as lumbar intervertebral discs and that local examination of the leg along the course of the sciatic nerve should be carried out on every patient complaining of sciatica.

Adult↗
PubMed1978

Chemical and structural changes of neurofilaments in transected rat sciatic nerve.

The sequence of changes occurring in transected rat sciatic nerve was examined by electron microscopy and by sodium dodecyl sulfate (SDS) polyacrylamide disc gel electrophoresis. Representative segments of transected nerves were processed for ultrastructural examinations between 0 and 34 days after the transection of sciatic nerves immediately below the sacro-sciatic notch. The remainder of the transected nerves and the intact portions of sciatic nerves were desheathed and immediately homogenized in 1 percent SDS containing 8 M urea and 50 mM dithioerythritol. Solubilized proteins were analyzed on 12 percent gels at pH 8.3 in a discontinuous electrophoretic system. Initial changes were limited to the axons of transected nerve fibers and were characterized by the loss of microtubules and neurofilaments and their replacement by an amorphous floccular material. These changes became widespread between 24 and 48 h after transection. The disruption of neurofilaments during this interval occurred in parallel with a selective loss of 69,000, 150,000 and 200,000 mol wt proteins from nerve homogenates, thus corroborating the view that these proteins represent component subunits of mammalian neurofilaments. Furthermore, the selective changes of neurofilament proteins in transected nerves indicate their inherent lability and suggest their susceptibility to calcium-mediated alterations. Electrophoretic profiles of nerve proteins during the 4-34-day interval after nerve transection reflected the breakdown and removal of myelin, the proliferation of Schwann cells and the deposition of endoneurial collagen. A marked increase of intermediate-sized filaments within proliferating Schwann cell processes was not accompanied by the appearance of neurofilamentlike proteins in gels of nerve homogenates.

Animals↗
PubMed1976

[Pharmacological studies on degeneration and regeneration of the peripheral nerves. (2) Effects of methylcobalamin on mitosis of Schwann cells and incorporation of labeled amino acid into protein fractions of crushed sciatic nerve in rats].

Male Wistar rats (140 to 150 g) in which the unilateral sciatic nerve had been crushed were treated consecutively with methylcobalamin (5, 50 and 500 mug/kg/day i.p.) or saline immediately after the nerve-crush. Thereafter, they were periodically sacrificed for biochemical and histological examinations. At different intervals after the nerve-crush, L-leucine-4,5-T (20 mu Ci/100g, specific activity 15 mCi/m mole) or L-leucine -14C(U) (15 muCi/100g, specific activity 270 mCi/m mole) was given i.p. to some rats of each group and 3 hr later they were sacrificed to determine the rate of leucine incorporation into protein fractions of the crushed nerve and the denervated muscles. The nerve and muscles of the contralateral side served as control. Longitudinal sections of proximal and distal stumps of the sciatic nerve were prepared and stained with hematoxylin and eosin. As compared with saline group, repeated injections of 5, 50 and 500 mug/kg/day of methyl-cobalamin caused a significant increase of the in vivo incorporation of radioactive leucine into the protein fraction of the crushed sciatic nerve 5 to 7 days after the crush. In contrast, a recovery of the increased incorporation of leucine into the crushed nerve was more rapid in methylcobalamin groups than in the saline group. On the other hand, methylcobalamin (5 approximately 500 mug/kg/day i.p.) had no significant effect on the leucine incorporation into the denervated muscles (m. gastrocnemius, m. tibialis anterior and m. soleus). In addition, consecutive injections of methylcobalamin (5 approximately 500 mug/kg/day) did not affect the mitosis of Schwann cells during the period of Wallerian degeneration of the crushed sciatic nerve. These results suggest that methylcobalamin possesses a stimulating effect on proteosynthesis in Schwann cells at the initial stage of axon regeneration and it may facilitate neural regeneration.

Animals↗
PubMed1977

[Variation in the number and size of myelinated nerve fibers regenerated after repeated localized freezing of the sciatic nerve of rats].

The number and size of myelinated fibres have been determined in the nerve to medial head of the gastrocnemius muscle of Rats in which the sciatic nerve had been frozen locally 1 to 5 times at monthly intervals. The contralateral nerve was used as a control. When the measurements were made one month after the last freezing, the number of fibres increased progressively until the 3rd freezing, reaching about 220% of the normal value. No higher values were observed after 4 or 5 freezings. The mean diameter of fibres decreased with the number of operations. When the measurements were made 3, 6, 12 or 18 months after the 3rd freezing, the number of fibres decreased by about 30% between the 1st and the 3rd month and then stabilized. The mean diameter of fibres increased progressively. However, at the 18th month, the size of the myelinated fibres had not reached the normal value.

Animals↗
PubMed1976

[Pharmacological studies on degeneration and regeneration of peripheral nerves. (1) Effects of methylcobalamin and cobamide on EMG patterns and loss of muscle weight in rats with crushed sciatic nerve].

Experiments were performed to investigate the effects of Vitamin B12, i.e., methylcobalamin and cobamide, on the neural degeneration and regeneration. Male Wistar rats (140 to 150 g) under conditions of experimental unilateral sciatic nerve crushing were treated consecutively with methylcobalamin (50 and 500 mug/kg/day i.p.), cobamide (50 and 500 mug/kg/day i.p.) or saline. EMG recordings were periodically carried out and rats of each group were sacrificed to determine the weight-loss of denervated muscles 1, 2, 3 and 4 weeks after crush. Neither methylcobalamin nor cobamide exerted any significant effect on body-weight gain of the nerve-crushed rats with a daily injection of 50 and 500 mug/kg i.p.. The EMG pattern of the denervated biceps femoris muscle showed a total lack of fibrillation for 2 days after the nerve-crush. Thereafter, the fibrillation appeared and continued for 10 to 14 days until the nerve had regenerated, as evidenced by the appearance of a complex NMU voltage. The occurrence of fibrillation voltage was slightly delayed in methylcobalamin group (500 mug/kg/day) as compared with the saline control group. The re-appearance of normal NMU voltage was more rapid in the methylcobalamin 500 mug/kg group than in controls and other experimental groups. Neither methylcobalamin nor cobamide had any significant effect on the weight-loss of the gastrocnemius and tibialis anterior muscles following crush of the sciatic nerve. However, a daily injection of 500 mug/kg of methylcobalamin produced a significant increase in the weight of the soleus muscle which recovered to the extent of being the same weight of the contralateral 4 weeks after the nerve-crush. These results suggest that methylcobalamin may have an inhibitory effect on Wallerian degeneration and also a facilitatory effect on the neural regeneration of the crushed sciatic nerve of rats.

Animals↗