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At least 19 recordsLinked to original sources
PubMed1987

Primary afferent projections to the central octavus nuclei in the elasmobranch, Rhinobatos sp., as demonstrated by nerve degeneration.

Nerve degeneration studies were performed to determine the central projections of the octavus nerve in the guitarfish. Rhinobatos sp. Most first-order octavus nerve afferents are confined to the ventral longitudinal column of the medulla, which consists of four octavus nuclei: the nucleus octavus anterior (NOA), nucleus octavus magnocellularis (NOM), nucleus octavus descendens (NOD); and nucleus octavus posterior (NOP). Central projections of the octavus nerve outside of the ventral octavus nuclear column are to the vestibulolateral lobe of the cerebellum, the large multipolar cells that lie deep to the cerebellar crest of nucleus intermedius, the reticular formation, and the nucleus octavolateralis efferens. In addition, the cytoarchitectural features of the four octavus nuclei have been analyzed: the NOA consists of large spindle-shaped neurons and medium-sized multipolar neurons; the NOM is a small nucleus consisting of very large multipolar neurons; the NOD contains several types of neurons including large spindle-shaped neurons, large multipolar neurons, and polymorphic small and medium-sized neurons; and the NOP contains small spherical and small multipolar neurons evenly distributed throughout the nucleus. On the basis of the morphology of the neurons, the NOA and NOD appear to have subdivisions suggesting a more complex organization of the octavus nuclear column than previously recognized.

Afferent Pathways↗
PubMed1998

Differentiation and apoptosis without DNA fragmentation in cultured Schwann cells derived from wallerian-degenerated nerve.

The Schwann cell cables provide particularly favorable sites for the growth of regenerating axonal sprouts. However, if they remain denervated, endoneurial fibrosis takes place with the Schwann cells atrophying and total Schwann cell number gradually decrease with time. Even when regenerating axonal sprouts invade into the cables, Schwann cells do not survive for long periods if they fail to make axonal contact. These observations strongly suggest the involvement of apoptosis in peripheral nerve degeneration and regeneration. So, we investigated the behavior of Schwann cells prepared from wallerian-degenerated adult rat sciatic nerve in vitro. The secondary cultured Schwann cells showed serial changes in morphology, mitotic activity and migratory activity as they do during Schwann cell cable formation in vivo. At the final stage of differentiation, the Schwann cells became rounded and detached from the flask with extensive blebbing. Electron micrographs clearly demonstrated typical cytoplasmic changes of apoptosis, but, nuclei of most of the cells retained their size and morphology with residual nucleolar structures. An agarose gel electrophoresis of DNA clearly demonstrated that there was not any DNA fragmentation up to 120 h after detachment. Results by in situ apoptosis detection assay did not show any DNA degradation despite the substantial decrease in Schwann cell number. In conclusion, during peripheral nerve degeneration and regeneration, supernumerary Schwann cells are removed by apoptosis, however, it lacks most of the nuclear events of usual apoptosis.

Journal Article↗
PubMed2004

Pre-degenerated nerve shows enhanced regeneration after incremental elongation in rats.

Following nerve degeneration, we investigated effects of linear elongation on subsequent nerve regeneration in a total of 92 Wistar rats (weight 380-430 g). The nerve was ligated at the midthigh and then elongated incrementally by a total of 15 mm by leg lengthening at a rate of 3 or 5 mm/day. Seven days after initiation of nerve elongation, the external fixator was removed and normal leg length was restored with internal fixation. Then a 10 mm nerve segment at the ligature site was excised, and the nerve was repaired with sutures (group D). At 2, 4, 6, and 8 weeks after nerve suturing, we examined transverse semi-thin nerve sections compared with group I (severed and repaired after leg lengthening without a nerve ligature) and control group (severed and repaired without leg lengthening). After lengthening at 3 mm/day, nerve regeneration in group D was enhanced at 4 weeks. After lengthening at 5 mm/day, nerve regeneration in group D also was enhanced at 6 and 8 weeks. Pre-degenerated nerve showed better regeneration after suturing than intact nerve. Elongation holds promise as an alternative to nerve grafting in treatment of nerve injury.

Animals↗
PubMed1984

Ca2+ dependence of the release of noradrenaline during nerve degeneration in the parotid gland.

Amylase secretion "in vitro" was used as an indication of the degeneration activity of sympathetically denervated parotid glands. Seventeen and a half hours after sympathetic denervation, slices of parotid gland released amylase into the incubation medium at a rate higher than that observed for non-denervated glands. The time course of amylase release from denervated glands followed a bell-shaped pattern similar to that observed in other denervated structures. Lowering extracellular Ca2+ to 0.25 mmol/l diminished significantly the release of amylase. Low Ca2+ however, did not decrease the amylase release in response to added noradrenaline. These results indicate that Ca2+ is required for the release of noradrenaline from degenerating nerve endings.

Amylases↗
PubMed2000

[The attractive effects of nerve regeneration chamber fluid and degenerated nerve segments on the growth and the migration of the cocultured dorsal root ganglion neuron].

OBJECTIVES: We intended in this study to investigate the neurotropic effects of regeneration chamber fluid (RCF) and the degenerated nerve segments from distal of the regeneration chamber on the dorsal root ganglion (DRG). METHODS: The capillary model was first tested for its reliability to form concentration gradient with a dye being contained in the capillaries. The tissue culture in RCF test was divided into two groups each with 8 DRGs implanted in 8 dishes. RCF was contained in capillaries inserted down to the bottom of the dishes with their lower ends at a distance of about 1 mm to the DRGs in the experimental group, and DMEM media was contained in the control group. Segments of degenerated sciatic nerve from distal of the regeneration chamber were implanted with DRGs at a distance of about 0.5 - 1 mm in the coculturing experiment. DRGs were observed for the direction of the growth of the cells and the fibres. RESULTS: While the capillary containing the dye was put down to the bottom of the culture dish coated with a piece of nylon pad, the red color slowly disseminated with heavier staining in the center and lighter staining in the peripheral portion. We believe this pattern of shade could simulate the concentration gradient of tropic factors in this model. There were significantly more nerve fibres growing from the DRGs towards the capillaries in 6 of the 8 dishes in the experimental group after 72 hours of culture. The tissue and nerve fibers grew evenly in the control group. 76.5% of all the nerve fibres were growing in the direction facing the degenerated nerve segments after 12 hours of coculturing, and only 33.3% of the nerve fibres growing in that direction in the control group. Cells from the DRGs migrated towards the degenerated nerve segments, yet they tended to avoid the normal nerve segments. The migration index of the cells was 0.98 in average in the coculturing experiment with the degenerated nerve segments, but only 0.43 in average with the normal nerve coculturing. CONCLUSION: The capillary model was effective in studying the chemotactic growth of nerve tissue. RCF and the degenerated nerve segments had definite neurotropic effects on DRGs tissue.

Animals↗
PubMed2000

MMP-2 and MMP-9 increase the neurite-promoting potential of schwann cell basal laminae and are upregulated in degenerated nerve.

Compared to degenerated nerves, the ability of normal adult peripheral nerve to support axonal regeneration is poor and may be attributed to the inhibition of endoneurial laminin by chondroitin sulfate proteoglycan (CSPG). In cryoculture assays, neuritic growth of neonatal and adult peripheral neurons was increased on sections of normal nerve by pretreatment with CSPG-degrading enzymes, including the matrix metalloproteinases MMP-2 and MMP-9. Axonal regeneration is known to occur within the Schwann cell basal laminae of degenerated nerve. Similarly, deconvolution microscopy revealed that neuritic growth on nerve tissue sections occurred principally on the lumenal surface of enzymatically modified basal laminae. Compared to normal nerve, there was a marked increase in the neurite-promoting activity of the degenerated nerve, and this activity was not increased significantly by subsequent MMP treatment. Additionally, the expression and activation of MMP-2 and MMP-9 were elevated in degenerated nerve, suggesting that degradation of inhibitory CSPG by the MMPs contributes to the growth-promoting properties of degenerated nerve.

Age Factors↗
PubMed2000

Repair of nerve gap with the elongation of Wallerian degenerated nerve by tissue expansion.

We have found previously that expansion of the Wallerian degenerated nerve was accompanied by accelerated Schwann cell proliferation. In this study, we investigated the usefulness of the elongation of Wallerian degenerated nerve for the repair of short nerve gap. Male Wistar rats were used. After the left sciatic nerve was transected the rats were divided into 4 groups. In the control group, nerve coaptation was not performed. In group 1, tensionless coaptation was performed immediately. In group 2, delayed tensionless coaptation was performed with the elongation of Wallerian degenerated nerve. In group 3, coaptation was performed immediately with autologous interposition nerve graft. The ideal tensionless nerve repair of group 1 was considered to produce the best result. Rats in group 2 showed functional recovery as good as rats in group 1. On histologic assessment, in group 2, a fibrous capsule that was very rich in vascularity was formed around the tissue expander. After 14 weeks, the capsule was diminished markedly in size, but the vascularity was rich around the sciatic nerve. We think that the excellent functional recovery seen in group 2 can be attributed to the increased activity of Schwann cell proliferation and increased vascularity.

Animals↗
PubMed1996

Peripheral nerve regeneration through short- and long-term degenerated nerve transplants.

The present study was designed to compare regenerative potential of normal and degenerated nerve grafts. Peripheral nerves in rats were induced to undergo in situ degeneration for a period of 6 weeks, 3, 6 and 12 months. During early phase of denervation the myelin and axons degenerated and were absorbed. With prolonged denervation (i.e. 12 months), such nerves were reduced in size and exhibited extensive fibrosis. A 2 cm long segment of the degenerated nerve was transplanted in an surgically created gap in the host peroneal nerve to evaluate their regeneration supporting ability. Regeneration of host axons occurred rapidly through nerves degenerated for a period up to 3 months. The extent of regeneration was compromised in 6-month degenerated nerve group, and was significantly reduced in the 12-month degenerated nerve grafts. These results show that with extended degeneration interval, the regeneration supporting ability of nerves is compromised. It is concluded that nerve repair should not be excessively delayed in order to compromise recovery.

Animals↗
PubMed1982

Delay by drugs of adrenergic nerve degeneration after proximal or distal sympathectomy of the submaxillary gland.

1. Degeneration of nerve terminals of the submaxillary gland of the rat proceeds at a faster rate after crushing adrenergic nerves close to the gland than after ganglionectomy. 2. Bretylium, pargyline, nialamide and clorgyline delayed degeneration to the same extent after either type of denervation. 3. Chlorpromazine and pentobarbitone also delayed adrenergic degeneration, effect related to the hypothermia induced by these drugs. 4. Colchicine applied on the nerve trunk innervating the right gland delayed not only degeneration of the ipsilateral nerve terminals but the contralateral gland as well. 5. From the data obtained it seems probable that the drugs tested delay adrenergic nerve degeneration at the levels of nerve terminals. This effect is not related to lysosomal stabilization.

Acid Phosphatase↗
PubMed1982

Peripheral nerve phospholipid composition: development in normal nerve and age-dependent changes in Wallerian degenerated nerve.

The phospholipid composition of normal peripheral nerve as a function of developmental age as well as that of Wallerian-degenerated nerve as a function of age at nerve transection and duration of Wallerian degeneration have been quantitated in rabbit sciatic nerve. During development, increases in the proportions of ethanolamine plasmalogen, sphingomyelin, and combined phosphatidyl serine plus phosphatidyl inositol and decreases in the proportions of phosphatidyl choline and phosphatidyl ethanolamine correlated well with the concurrent myelin accretion. During Wallerian degeneration, age-dependent changes in phospholipid composition were observed. The large and statistically significant increase in the proportion of phosphatidyl choline and decrease in the proportion of ethanolamine plasmalogen were manifest promptly in nerves transected at 2 weeks of age but in a delayed manner in nerves transected at 8, 12, and 20 weeks of age. The rate of loss of individual phospholipids was greater in nerves transected at younger ages. The findings from normal developing peripheral nerve may well serve as baseline data for subsequent studies of phospholipid composition in pathological peripheral nerve. The findings from Wallerian-degenerated peripheral nerve provide additional evidence for age-dependent chemical changes occurring in Wallerian-degenerated peripheral nerve that may be of significance in explaining the superior functional recovery from peripheral nerve injury observed in younger compared with older subjects.

Aging↗
PubMed1993

A comparison of the passage of regenerating axons through old degenerated nerve autografts and fresh nerve autografts in rats.

We have compared the passage of regenerating axons through old degenerated nerve autografts and fresh nerve autografts in two groups of Sprague Dawley rats. In one group the right sciatic nerve was divided and repaired with the graft taken from the distal segment of the left sciatic nerve, which had been severed 15 weeks before. In the other group the right sciatic nerve was repaired with the graft taken from the intact left sciatic nerve. Eight weeks later the myelinated axons were counted at three different locations in the grafted right sciatic nerve in both groups. The old degenerated nerve autografts were less effective in allowing the passage of regenerating axons than the fresh nerve autografts, but the difference was not great. This provides justification for the use of old degenerated nerve as an additional graft where a large number of autogenous nerve grafts are required, such as in the operative treatment of injuries to the brachial plexus.

Animals↗
PubMed1977

Degenerating nerve fiber products do not alter physiological properties of adjacent innervated skeletal muscle fibers.

Partial denervation of rat extensor digitorum longus and soleus muscles resulted in the appearance of denervated and innervated surface muscle fibers lying adjacent to one another. The denervated muscle fibers showed the typical signs of denervation while the innervated muscle fibers were similar to those of control muscles. We conclude that denervated fibers do not induce substantial physiological changes in adjacent innervated muscle fibers.

Action Potentials↗
PubMed1951

Loss and recovery of excitability by normal and by degenerating nerves deprived of sodium.

A study has been made of the loss of excitability in a sodium-free medium and of the recovery of excitability in Ringer's solution by A fibers of normal frog nerves and of nerves in advanced stages of Wallerian degeneration. With normal nerves that are being kept in a sodium-free medium the number of conducting fibers does not undergo a readily detectable decrease in less than 1 to 2 hours; inexcitability of all the A fibers does not develop in less than 7 to 8 hours. During the development of inexcitability the speed of conduction of the still conducting fibers undergoes a progressive decrease; in advanced stages the speed of conduction is not more than one-fifth of the normal speed. The nerve fibers lose the ability to conduct rhythmic trains of impulses earlier than the ability to conduct single impulses. The recovery of excitability in Ringer's solution duplicates in a reverse order the sequence of changes that have been previously observed during the development of inexcitability. The rate of the recovery of excitability in Ringer's solution is higher than the rate of the loss of excitability in the sodium-free medium. With degenerating nerves the effect of the lack of sodium develops qualitatively in the same manner in which it develops with normal nerves. Degenerating nerve fibers, however, become inexcitable in a sodium-free medium earlier than normal fibers. The recovery of the excitability in Ringer's solution takes place in much the same manner in normal and in degenerating nerve fibers. The loss of excitability during Wallerian degeneration is a process that develops simultaneously, or practically so, throughout the entire length of the fibers. The nerve fibers retain a great deal of functional ability throughout the several days which precede the onset of inexcitability and then suddenly become inexcitable.

Sodium↗
PubMed1980

Delay by bretylium of adrenergic nerve degeneration after sympathectomy of the submaxillary gland.

Administration of 24 mumol/kg of bretylium 10 h after ganglionectomy delayed the loss of endogenous norepinephrine and the impairment of neuronal uptake of 3H-metaraminol (3H-MA) that follow sympathetic denervation. This delay was evident 16 and 20 h after denervation. Twenty four h after ganglionectomy, when NE stores and uptake of 3H-MA were reduced to their lowest values in untreated rats, in bretylium-treated ones these values were approximately 40% of those in normal glands. The onset of degeneration secretion in treated rats was delayed by about 9 h. The development of prejunctional supersensitivity was also delayed. The subcellular distribution of NE in normal and 16 h denervated glands showed that denervation reduced the neurotransmitter to the same extent in the 3 fractions: coarse, supernatant and microsomal. Treatment with bretylium and pargyline prevented the loss of NE from the microsomal fraction. Previous administration of pargyline antagonized the protection of 3H-MA uptake seen in 28 h denervated rats treated with bretylium. However, this drug combination induced a greater retention of endogenous NE 24 h after denervation. Bretylium inhibited intraneuronal MAO by 40%. It is concluded that bretylium treatment can delay the degeneration of adrenergic nerve terminals separated from the cell bodies by a pharmacological effect probably not related to MAO inhibition or to its neurone blocking action.

Animals↗
PubMed1975

Enlargement of synaptic vesicles in degenerating nerve endings: a comparison between cat and monkey.

The synaptic vesicles of optic nerve endings in the lateral geniculate nucleus of cats and monkeys were measured following eye enucleation. A notable increase in the mean vesicle volume was found in both species. Increments in the values of standard deviation were also noted. Comparison of the results obtained indicate that changes are faster in cats than in monkeys. An explanation for difference is proposed.

Animals↗