SEARCH · PubMed Health

Results for “DEGENERATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources

PubMed1997

Degeneration of spermatocytes during meiotic divisions in the golden hamster testis.

The appearance and morphology of spontaneously degenerating meiotic spermatocytes was studied in late pubertal golden hamster testes by high resolution light and electron microscopy. While degeneration of primary spermatocytes during the long prophase of meiosis I is chiefly confined to midpachytene cells in stages VII-VIII of the seminiferous cycle, the subsequent meiotic phases (and their degenerative disorders) appear side by side in stage XIII of the cycle. Degeneration regularly concerns, in decreasing order of frequency, midpachytene primary spermatocytes (prophase I), metaphases I/II, telophases I/II, prophase II, and anaphases I/II. This closely corresponds to the apparent durations of these respective phases. In all meiotic phases studied, degeneration follows the same morphological pattern, including an initial vacuolar transformation of the cytoplasm and accumulation of densely staining material along membranes and microtubules, a progressive condensation of all nuclear and cytoplasmic structures, and the final cellular disintegration. In meta- and anaphase cells, meiotic spindle fibres are often perceivable even in advanced stages of degeneration. Both the morphological uniformity of spermatocyte degeneration and the constant susceptibility of meiotic phases to degeneration throughout meiotic divisions point to a generally similar mechanism underlying the physiological loss of meiotic spermatocytes.

Animals↗

PubMed1998

Relative increase of biglycan and decorin and altered chondroitin sulfate epitopes in the degenerating human intervertebral disc.

OBJECTIVE: Proteoglycans are major components of the extracellular matrix of the intervertebral disc. They are vital for the biomechanical properties of the tissue, and are subject to changes in disc degeneration. We aimed to further define these changes and their relationship to normal aging. METHODS: Normal discs (age 13-53 years, n = 6) were analyzed from 5 different sites across the sagittal anterior-posterior direction. Degenerated anterior annulus fibrosus was collected from 7 patients aged 39-46 years. Extracted proteoglycans were separated using agarose and polyacrylamide gel electrophoresis and detected with toluidine blue staining and Western blotting. RESULTS: The center of the disc showed the highest level of total proteoglycans, but lowest levels of decorin and biglycan. Western blots displayed reduced signal for both glycanated and nonglycanated biglycan and decorin after adolescence, while an increased signal of biglycan was observed in degenerated annuli. The 7D4(-) and 3B3(-) epitopes on native chondroitin sulfate chains were present in the large proteoglycans of intervertebral discs, but their signal intensity had no correlation to degeneration. Chondroitinase ABC digestion of the blots brought up 7D4(+) signal in the small proteoglycans of degenerated, but not in healthy tissue. Decrease or total loss of 2B6(+) epitope (indicating 4-sulfated stubs of chondroitin sulfate chains) were found in the large proteoglycans of all degenerated annuli. CONCLUSION: Human intervertebral disc degeneration involves the accumulation of decorin and biglycan relative to other uronic acid containing proteoglycans, the disappearance of 4-sulfated core region in aggrecan-like large proteoglycans, and the emergence of a core structure in the chains of small proteoglycans reacting with the 7D4 antibody; these findings indicate a fundamental alteration in matrix properties that may contribute to the pathogenesis of the disease.

Adolescent↗

PubMed1976

Rate of climbing fiber degeneration in rabbit cerebellum following parafloccular stalk and medullopontine lesions.

To resolve inconsistencies in experimental studies which use reduced silver methods to detect cerebellar climbing fiber sources within the brain stem, an evaluation of the temporal course of degeneration was undertaken. The paraflocculus of the rabbit is uniquely situated within the temporal bone and connects with the corpus cerebelli via a stalk passing through a bony foramen. A unilateral electrolytic lesion deafferented the paraflocculus without disturbing blood supply or causing damage (18 animals). Comparatively, another group of unilateral lesions was placed at the dorsolateral pontomedullary junction, adding significantly to the cortical area deafferented (12 animals). Animals of each group were killed at successively longer intervals commencing at 18 hours, and a modified Fink-Heimer impregnation process was applied to the cerebellar cortex and opposite-sided controls. In parafloccular lesions, degeneration was detected at 24 hours in the climbing fibers of the molecular layer. At successively longer intervals, degeneration became increasingly evident in granule layer and white matter. Subsequent to dorsolateral pontomedullary lesions, climbing fiber degeneration was first observed in the molecular layer at 24 hours and was clearly evident there at 36 hours. By 72 hours degeneration had reached the white matter, meanwhile disappearing in the molecular layer where it was first seen. Using techniques of Nauta-Fink-Heimer to display secondary climbing fiber degeneration in cerebellar cortex, it was found that too long post-operative intervals could preclude its detection, since in both groups of animals it commenced earlier and disappeared sooner in the molecular layer.

Afferent Pathways↗

PubMed2006

Degeneration of neuronal cell bodies following axonal injury in Wld(S) mice.

The phenotype of Wld(S) ("slow Wallerian degeneration") mice demonstrates prolonged survival of injured axons. However, whether the Wld(S) mutation delays degeneration of the neuronal cell body following axonal injury is unclear. We used a retrograde model of axonal transport failure in Wld(S) mice to test whether the mutant Wld(S) protein has any beneficial effect on the neuronal cell body. Retrograde axonal transport was physically blocked by optic nerve crush and confirmed by the absence of Fluoro-Gold labeling in wild-type and in Wld(S) mice. After this axonal injury, there was marked protection of axonal degeneration in the Wld(S) phenotype, as confirmed by immunohistochemistry and electron microscopy. However, the Wld(S) protein, localized in the nucleus of retinal ganglion cells, did not prevent or delay degeneration of the retinal ganglion cell body, confirmed by TUNEL staining and Fluoro-Gold labeling. These results imply that, after axonal injury, Wallerian degeneration of axons and degeneration of the neuronal cell body have different mechanisms, which are autonomous and independent of each other. Although the Wld(S) phenotype can be used to demonstrate stable enucleate axons, the mutation is unlikely to protect neurons in neurodegenerative diseases in which there is failure of retrograde transport.

Analysis of Variance↗

PubMed1987

The spatio-temporal pattern of Wallerian degeneration in the rhesus monkey optic nerve.

Three patterns of degeneration were distinguished in the Rhesus monkey optic nerve following eye enucleation. A traumatic zone, extending for 1 to 2 mm from the site of transection and characterized by a rapid infiltration of haematogenous macrophages, the rapid degeneration and removal of all neural elements and the formation of astrocytic scar tissue within 35 days. A conical zone, closely associated with the central retinal blood vessels, in which the pattern of degeneration was similar to the traumatic zone except that the onset was delayed and the removal of debris was slower. There was extensive vesiculation of myelin sheaths in these two zones which was indicative of haematogenous cell infiltration. The remainder of the nerve underwent classical Wallerian degeneration in which endogenous cells slowly phagocytosed the degenerating nerve fibres. These observations are considered relevant to the controversy concerning the identification of the macrophage involved in Wallerian degeneration; many studies have described the macrophage within the area of trauma rather than the macrophage involved at some distance from the site of trauma.

Animals↗

PubMed1982

Patterns of Wallerian degeneration of myelinated fibres in short and long peripheral stumps and in isolated segments of rat phrenic nerve. Interpretation of the role of axoplasmic flow of the trophic factor.

The topographical level of nerve transection influences the time of appearance of Wallerian degeneration in the peripheral stump. After transection made in the distal portion of the nerve, degeneration appears earlier and is, for equal times, stronger than that observed under similar conditions after transection made near the beginning of the nerve. In nerves transected in the proximal part, the spatial pattern of degeneration along the peripheral stump depends on the time after neurotomy. A time span exists, different for each size class of fibres, within which the degree of degeneration decreases linearly with increasing distance from the site of transection. Within this time span, at increasing hours, the intercepts of calculated regression lines increase but the slopes change only slightly, so that an array of quasi-parallel lines is obtained. Departures from linearity occur at early times when some degree of degeneration has already appeared in the proximal part of the stump, whereas in its distal part all fibres still look normal. Another type of departure from linearity appears at late times (over 34 h). In isolated nerve segments the degeneration is weaker than in the peripheral stumps remaining in continuity with the nerve terminals and the longitudinal pattern of changes is strikingly altered. A unitary interpretation of these phenomena in terms of redistribution of the trophic factor by the bidirectional axoplasmic transport is proposed.

Animals↗

PubMed1990

Thalamic retrograde degeneration following cortical injury: an excitotoxic process?

Traumatic or stroke-like injuries of the cerebral cortex result in the rapid retrograde degeneration of thalamic relay neurons that project to the damaged area. Although this phenomenon has been well documented, neither the basis for the relay neuron's extreme sensitivity to axotomy nor the mechanisms involved in the degenerative process have been clearly identified. Physiological and biochemical studies of the thalamic response to cortical ablation indicate that pathological overexcitation might contribute to the degenerative process. The responses of thalamic projection neurons, protoplasmic astrocytes, and inhibitory thalamic reticular neurons in adult mice were examined from one to 120 days following ablation of the somatosensory cortex as part of an investigation of the role of excitotoxicity in thalamic retrograde degeneration. The responses of thalamic neurons to cortical ablation were compared with those produced by intracortical injection of the convulsant excitotoxin kainic acid, since the degeneration of neurons in connected brain structures distant to the site of kainic acid injection is also thought to occur via an excitotoxic mechanism. Within two days after either type of cortical injury, protoplasmic astrocytes in affected regions of the thalamic ventrobasal complex and the medial division of the posterior thalamic nuclei became reactive and expressed increased levels of immunohistochemically detectable glial fibrillary acidic protein. Within the affected regions of the ventrobasal complex an increased intensity of puncta positive for glutamate decarboxylase immunoreactivity, presumably due to an increase in its content within the terminals of the reciprocally interconnected thalamic reticular neurons, was also evident. These immunohistochemically detectable alterations in the milieu of the damaged thalamic neurons preceded the disappearance of the affected relay neurons by at least two days following cortical ablation and by seven to 10 days following intracortical kainic acid injection. Regions of the thalamus containing reactive astrocytes corresponded very closely to the regions undergoing retrograde degeneration. Protoplasmic astrocytes in these areas remained intensely reactive up to 60 days after cortical injury. Levels of glutamate decarboxylase were only transiently elevated in the degenerating regions of the ventrobasal complex following cortical ablation and returned to normal by 14 days. Increased glutamate decarboxylase immunoreactivity was transiently seen through the entire ventrobasal complex following intracortical kainic acid injection but was markedly more intense in degenerating regions. These patterns of labeling did not return to normal until 50 days after intracortical kainic acid injection, well after the death of the relay neurons. Cortical ablation and intracortical kainic acid injection produce similar alterations in thalamic neuronal and glial populations.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

Multiple system atrophy with retinal degeneration in a young child.

A 4-year-old girl with multiple system degeneration and retinal degeneration was presented. There was onset of an ataxic gait at two years and rapid progression of retinal degeneration, myoclonus and cranial nerve palsy. Neuropathological examination revealed severe degeneration of the cerebellar cortex and the pathways of auditory and deep sensation, as well as degeneration of the cerebellar efferent fibers, the striatonigral system, the cerebellar afferent fiber system and lower motor neurons. Cases of young children with spinocerebellar degeneration have been reported in several families of olivopontocerebellar atrophy (OPCA), but degenerative changes in our case were more widespread than those in OPCA cases. The multiple system lesions in the central nervous system and retina of this child are different from those of any other previously reported cases.

Brain Stem↗

PubMed1981

The fate of axonal debris in Wallerian degeneration of rat optic and sciatic nerves. Electron microscopy and immunofluorescence studies with neurofilament antisera.

Immunofluorescence demonstrated that axonal debris reacting with neurofilament antisera persist up to 4 months in rat optic nerves undergoing Wallerian degeneration. Antisera used in this study allowed the isolation of the 72,000- and 150,000-dalton neurofilament polypeptides from rat spinal cord by immunoaffinity chromatography. After 2 weeks of degeneration, proteins co-migrating with these neurofilament polypeptides were no longer identifiable in rat optic nerves, which suggests that immunofluorescent structures persisting in the nerves after this period contained neurofilament degradation products of different molecular weight. Additional evidence as to the persistence of axonal debris in degenerated optic nerves was obtained by electron microscopy. Two distinct types of axonal degeneration were observed in rat optic nerves by this method, floccular swelling and increased electron density of the axoplasm. In both types of degeneration, axoplasmic filaments and tubules were not identifiable. Although floccular material disappeared after 2 weeks of degeneration, so that only empty myelin sheaths remained, electron-dense axons persisted longer and were probably phagocytosed together with their myelin sheaths. In sciatic nerves, cross-reaction with neurofilament antisera had almost completely disappeared 10 days after transection. The same was true for nerves which had been tightly ligated to prevent axonal growth and to squeezed nerves which showed vigorous regeneration. A few scattered, brightly immunofluorescent fragments which persisted in nerves up to 2 weeks after transection were exception to these findings.

Animals↗

PubMed1976

Ageing and degeneration in the macular region: a clinico-pathological study.

Clinical and pathological examination was performed on 378 eyes from 216 patients aged 43 to 97 years. This series represented eyes in which the fundi were normal or showed various manifestations of senile macular degeneration. The eyes were divided into six groups according to the histological appearance of a linear deposit at the base of the retinal pigment cells. Groups I and II were considered to represent normal ageing, Groups III and IV the progressive development of senile macular degeneration and Groups V and VI the end-results. Group I showed no basal linear deposit. Thickening and hyalinization of Bruch's membrane was noted as early as the fifth decade. Group II showed patchy development of the basal linear deposit in relation to thickened or basophilic segments of Bruch's membrane, or over intercapillary hyalinization extending to the level of the outer surface of the choriocapillaris. Almost all eyes in these two groups retained a normal fundus appearance but visual acuity declined with age even in the absence of other causes. In Group III the basal deposit formed a thin continuous layer associated with moderate degeneration of the retinal pigment epithelium. More than half the eyes had developed a clinical disturbance of pigmentation and in most vision was reduced. Group IV was characterized by thickening of the deposit and more pronounced disturbance of the pigment epithelium. Clinically most eyes showed coarse pigmentary changes and vision was in the order of 6/24. 14-3 per cent of eyes in this group showed early neovascularization from the choroid. In Group V the pigment epithelium disappeared to produce circumscribed areas of depigmentation. The basal linear deposit could be traced throughout the depigmented area in most eyes. Thin fibrovascular sheets were found beneath the pigment epithelium in 41-7 per cent of eyes. Group VI represented disciform degeneration. The basal linear deposit could often be demonstrated as a disrupted hyalinized layer incorporated into the scar. Disciform degeneration was an alternative end-result to geographical atrophy. In each group the clinical and histological findings may be modified by the presence of drusen or by atrophy of the choroid. The basal linear deposit consisted of banded fibres embedded in granular material lying between the plasma infoldings and the basement membrane of the retinal pigment epithelium. This deposit seems to be a manifestation of gradual failure of the pigment epithelium and proved to be the most suitable criterion by which to study the natural history of senile macular degeneration.

Adult↗

PubMed1984

Wallerian degeneration demonstrated by magnetic resonance: spectroscopic measurements on peripheral nerve.

Wallerian degeneration of rat sciatic nerves was induced by nerve section. Fifteen days later the degenerated nerves were compared with the intact contralateral nerves from the same animal. Histological sections showed the changes typical of wallerian degeneration: axonal degeneration and secondary demyelination. The freshly dissected nerves were analyzed by magnetic resonance (MR) spectroscopy at 10 MHz, and the water content was determined by dehydration. In the degenerated nerves there was a marked prolongation of both T1 and T2 relaxation times, accompanied by an increase of water content. The results demonstrate the sensitivity of MR for detection of secondary demyelination and disintegration of nerve structures. These results suggest that it should be possible to detect wallerian degeneration in MR images; this will have an important impact on neuropathological diagnosis of central and peripheral nervous system lesions.

Animals↗

PubMed1997

Differential effects of acrylamide on the degeneration and regeneration of myelinated fibers between C57BL/Ola and C57BL/6J mice after crush injury.

To investigate differences in the pathologic processes between mutant C57BL/Ola (Ola) and normal C57BL/6J (6J) mice, the effect of acrylamide (ACR) on the degeneration and regeneration of myelinated fibers after crushing the sciatic nerve was morphometrically evaluated. Both Ola and 6J mice were treated with either ACR (subcutaneous injection of 50 mg/kg every other day for 13 days, n = 6) or physiological saline (n = 6). Morphometric evaluation of myelinated fibers of the sciatic nerve 5 mm distal to the proximal end of the crush site was performed systematically on day 14 of the crushing for each mouse. In Ola mice treated with either saline or ACR, large and small myelinated fibers remained without obvious progression of Wallerian degeneration, and degeneration of myelinated fibers was slower than in 6J mice. On the other hand, in 6J mice treated with either saline or ACR, many small myelinated fibers regenerated after degeneration and loss of both large and small myelinated fibers. In Ola mice, no statistically significant difference in the morphometric parameters was found between saline-treated and ACR-treated groups. Therefore, ACR did not have a significant effect on Wallerian degeneration of myelinated fibers in Ola mice. However, in 6J mice regenerated myelinated fibers were fewer in those receiving ACR than in those receiving saline. Therefore, ACR suppresses regeneration of myelinated fibers after crushing in 6J mice. A delay or partial failure of axonal sprouting and elongation may be responsible for the lower numbers of regenerated myelinated fibers. This study demonstrates the importance of the substrain differences in the degeneration and regeneration of myelinated fibers which may have implications for understanding the different susceptibilities to various neuropathies in man.

Acrylamide↗

PubMed1990

The macular photostress test in diabetic retinopathy and age-related macular degeneration.

We propose the macular photostress test for the evaluation of macular function in the office setting. Eighty eyes were tested and divided into four diagnostic categories: background diabetic retinopathy, diabetic macular edema, age-related macular degeneration, and normal. The recovery times for the eyes with age-related macular degeneration were longer than for eyes with macular edema (P = .03). Age-matched patients with age-related macular degeneration had longer recovery times than did those without age-related macular degeneration (P = .0001). A possible explanation is that the prolonged recovery time in the eyes with age-related macular degeneration reflects that the anatomic lesion is located in the retinal pigment epithelium-photoreceptor complex. In comparison, the eyes with macular edema, whose lesion is in the inner retina and not the retinal pigment epithelium, show a less-prolonged recovery time than the eyes with age-related macular degeneration.

Adolescent↗

PubMed2001

Interventions for asymptomatic retinal breaks and lattice degeneration for preventing retinal detachment.

BACKGROUND: Asymptomatic retinal breaks and lattice degeneration are visible lesions that are risk factors for later retinal detachment. Retinal detachments occur when fluid in the vitreous cavity passes through tears or holes in the retina and separates the retina from the underlying retinal pigment epithelium. Creation of an adhesion surrounding retinal breaks and lattice degeneration, with laser photocoagulation or cryotherapy, has been recommended as an effective means of preventing retinal detachment. This therapy is of value in the management of retinal tears associated with the symptoms of flashes and floaters and persistent vitreous traction upon the retina, because such symptomatic retinal breaks are associated with a high rate of progression to retinal detachment. Retinal tears and holes unassociated with acute symptoms and lattice degeneration are significantly less likely to be the sites of retinal breaks that are responsible for later retinal detachment. Nevertheless, treatment of these problems is frequently recommended, in spite of the fact that the effectiveness of this therapy is unproven. OBJECTIVES: The purpose of this review is to evaluate the effects of interventions for asymptomatic retinal breaks and lattice degeneration. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register - CENTRAL (which includes the Cochrane Eyes and Vision Group specialized register), MEDLINE and EMBASE. Textbooks regarding retinal detachment and the reference lists of relevant reports were reviewed in an effort to find additional study reports. Experts in the field were contacted for details of other published and unpublished studies. SELECTION CRITERIA: This review was designed to include randomised controlled trials in which one treatment for asymptomatic retinal breaks and lattice degeneration was compared to another treatment or to no treatment. DATA COLLECTION AND ANALYSIS: One reviewer assessed the search results and collected relevant studies. Since no studies met the inclusion criteria, no studies were assessed for methodological quality. No data were extracted and no meta-analysis could be performed. MAIN RESULTS: No trials were found that met the inclusion criteria for this review. REVIEWER'S CONCLUSIONS: No conclusions could be reached about the effects of surgical interventions to prevent retinal detachment in eyes with asymptomatic retinal breaks and/or lattice degeneration. Some current recommendations for treatment, based upon a consensus of expert opinion, are contradicted by the best available evidence.

Humans↗

PubMed2005

Interventions for asymptomatic retinal breaks and lattice degeneration for preventing retinal detachment.

BACKGROUND: Asymptomatic retinal breaks and lattice degeneration are visible lesions that are risk factors for later retinal detachment. Retinal detachments occur when fluid in the vitreous cavity passes through tears or holes in the retina and separates the retina from the underlying retinal pigment epithelium. Creation of an adhesion surrounding retinal breaks and lattice degeneration, with laser photocoagulation or cryotherapy, has been recommended as an effective means of preventing retinal detachment. This therapy is of value in the management of retinal tears associated with the symptoms of flashes and floaters and persistent vitreous traction upon the retina in the region of the retinal break, because such symptomatic retinal tears are associated with a high rate of progression to retinal detachment. Retinal tears and holes unassociated with acute symptoms and lattice degeneration are significantly less likely to be the sites of retinal breaks that are responsible for later retinal detachment. Nevertheless, treatment of these problems is frequently recommended, in spite of the fact that the effectiveness of this therapy is unproven. OBJECTIVES: The purpose of this review is to evaluate the effectiveness of interventions for asymptomatic retinal breaks and lattice degeneration. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials - CENTRAL (which includes the Cochrane Eyes and Vision Group Trials Register) on The Cochrane Library (Issue 3 2004) MEDLINE (1966 to July 2004) and EMBASE (1980 to August 2004). Textbooks regarding retinal detachment and the reference lists of relevant reports were reviewed for additional study reports. Experts in the field were contacted for details of other published and unpublished studies. SELECTION CRITERIA: This review was designed to include randomised controlled trials in which one treatment for asymptomatic retinal breaks and lattice degeneration was compared to another treatment or to no treatment. DATA COLLECTION AND ANALYSIS: One reviewer assessed the search results and collected relevant studies. Since no studies met the inclusion criteria, no studies were assessed for methodological quality. No data were extracted and no meta-analysis could be performed. MAIN RESULTS: No trials were found that met the inclusion criteria for this review. AUTHORS' CONCLUSIONS: No conclusions could be reached about the effectiveness of surgical interventions to prevent retinal detachment in eyes with asymptomatic retinal breaks and/or lattice degeneration. Some current recommendations for treatment, based upon a consensus of expert opinion, are contradicted by the best available evidence.

Humans↗

PubMed2001

The WldS protein protects against axonal degeneration: a model of gene therapy for peripheral neuropathy.

The WldS mouse is a spontaneous mutant that is characterized by the phenotype of delayed degeneration of transected nerves (slow Wallerian degeneration). Molecular genetic analysis identified a mutation in this animal that codes for a unique protein expressed in brain tissue of WldS mice. We asked whether the WldS phenotype, in addition to delaying axonal degeneration after axotomy, might provide neuroprotection against toxic neuropathy. In dorsal root ganglia (DRG) cultures, neurites from WldS transiently exposed to vincristine not only resisted axonal degeneration but resumed growth after withdrawal of the toxin. Neurites from wild type mice died rapidly and did not recover. To prove that the identified mutation and its protein product are responsible for the WldS phenotype, we used an adenoviral gene transfer system to deliver the WldS to rat DRG neurons. Rat neurons expressing the WldS protein were resistant to vincristine-induced axonal degeneration, confirming the functional significance of the identified gene mutation. These data provide evidence that the WldS protein can be neuroprotective against vincristine neuropathy, and possibly other disorders characterized by axonal degeneration. In addition, delivery of this gene to wild type cells can transfer the WldS phenotype, providing the possibility of "gene therapy" for peripheral neuropathy.

Adenoviridae↗

PubMed1980

Ascending projections of the dorsal column in a garter snake (Thamnophis siritalis): a degeneration study.

Ascending axons in the dorsal column of garter snakes were examined following hemisection of the spinal cord at segment levels 2, 3, 4, 11, 13, and 31. After postoperative survival periods of 11 to 28 days, sections of the spinal cord and brain were processed with a silver method to demonstrate degenerated axons and preterminals. The study demonstrated that most ascending degenerated axons are located in the outer half of the dorsal column. The somatotopic pattern of ascending fibers is evident, whereby dorsomedial fibers are primarily of caudal origin and the more dorsolateral axons are from rostral cord segments. Rostral to segment 31, all spinal segments appear to project to a strip of dorsal column adjacent to the dorsal median septum. From the septum, axons descend to terminate somatotopically on cells of the nucleus of Bischoff located caudal to the obex of the medulla. Dorsal column degeneration ascends to the level of the dorsal column nuclei, where most fibers terminate. Degeneration from caudal cord segments terminates on caudo-medial cells of the dorsal column nuclei, while rostral cord segments project to rostro-lateral cells. The dorsal column nuclei consist of an expanded lateral part between tractus descendens trigemini and the vago-solitary complex, and a contiguous, thin medial lamina of cells dorsal and medial to the vagal nuclei. The somatotopic pattern of degeneration in the dorsal column nuclei, probably of dorsal root origin, follows the mammalian organization, which suggests that the garter snake has primitive nuclei gracilis and cuneatus. Other terminal sites of degenerating fibers, although probably of spinal gray origin, are nucleus commissura infima, nucleus descendens vestibuli, and area postrema.

Animals↗

PubMed1992

Role of macrophages in peripheral nerve degeneration and repair.

A cut or crush injury to a peripheral nerve results in the degeneration of that portion of the axon isolated from the cell body. The rapid degeneration of this distal segment was for many years believed to be a process intrinsic to the nerve. It was believed that Schwann cells both phagocytosed degenerating axons and myelin sheaths and also provided growth factors to promote regeneration of the damaged axons. In recent years, it has become apparent that the degenerating distal segment is invaded by monocytes from the blood. We will review the evidence that these recruited macrophages play a role in both degeneration and regeneration of peripheral nerve axons after injury and consider whether the slow degeneration and poor monocyte recruitment in the central nervous system may contribute to the poor regeneration there.

Animals↗