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PubMed1993

A gene affecting Wallerian nerve degeneration maps distally on mouse chromosome 4.

When a nerve axon is cut or crushed, the nerve fibers in the distal part of the axon, separated from the cell body, undergo a form of spontaneous degeneration, known as Wallerian degeneration. A substrain of the mouse inbred strain C57BL, known as C57BL/Ola, carries a mutant form of a gene involved in Wallerian degeneration in the peripheral and central nervous systems, and in retrograde degeneration of retinal ganglion cells. Wallerian degeneration in this substrain is abnormally slow. Previously the defect had been shown to be due to an autosomal dominant gene. The locus has been given the name and symbol Wallerian degeneration Wld, with the mutant allele Wlds (Wallerian degeneration-slow). The Wld locus has now been mapped, by using conventional and molecular markers, to the distal end of chromosome 4, near the locus of pronatriodilatin (Pnd). The order of loci (with recombination distances in centimorgans, cM) is cen-D4Mit11-8.9 +/- 1.7 cM-Fuca-2.5 +/- 0.93 cM-Akp-2-3.2 +/- 1.1 cM-D4Mit48-3.5 +/- 1.1 cM-(Wld, Pnd, D4Mit49)-0.71 +/- 0.50 cM-(Eno-1, D4Mit33)-1.4 +/- 0.70 cM-D4Mit42-2.5 +/- 0.93 cM-D4Smh6b. The information on the position of the Wld locus should be valuable in further characterization of this gene involved in nerve degeneration and regeneration.

Animals↗
PubMed2003

Gradual loss of myelin and formation of an astrocytic scar during Wallerian degeneration in the human spinal cord.

Axons undergo Wallerian degeneration distal to a point of injury. Experimental investigations have documented many of the cellular and molecular events that underlie this behaviour. Since relatively little is known about such events in human CNS pathologies and current experimental intervention strategies indicate the possibility of significant axon regeneration along the original degenerated fibre tract, we performed an immunohistochemical investigation of the dynamics of Wallerian degeneration in post mortem spinal cords of patients who died 2 days to 30 years after either cerebral infarction or traumatic spinal cord injury. Neurofilament (NF) staining demonstrated a spatio-temporal pattern of axonal loss within degenerating descending nerve fibre tracts that could be detected close to the lesion as early as 12 days after injury and progressed to an almost complete loss of NF immunoreactivity at survival times of 1 year and longer. Immunohistochemistry for glial fibrillary acidic protein revealed a late astrocytic reaction starting at 4 months after injury in the degenerating tracts, leading to the long-term deposition of a dense astrocytic scar. These events were accompanied by the gradual reduction of myelin basic protein in affected nerve fibre tracts, leading to almost complete loss by 3 years after injury. Since the extracellular matrix molecule chondroitin sulphate proteoglycan (CSPG) is known to be strongly inhibitory for axonal regeneration and to be a major component of gliotic scar tissues, we investigated the possible deposition of CSPG within the degenerating nerve fibre tracts. Apart from a local up-regulation close to the lesion site, our results show no enhanced CSPG expression within degenerated tracts at any survival time. This suggests that despite the apparent lack of CSPG in Wallerian degeneration, the slow reduction of CNS myelin and the long-term deposition of a dense astrocytic scar may present an environment that is non-supportive for axon regrowth.

Adult↗
PubMed1980

Local and distant neuronal degeneration following intrastriatal injection of kainic acid.

After intrastriatal injection, the neurotoxin, kainic acid, was cleared from the rat forebrain in a biphasic manner with 70% eliminated within 2 hours; by 24 hours after infusion, less than 1% of the kainic acid remained in the forebrain. The kainic acid diffused into adjacent brain structures, achieving mu molar concentrations in several regions ipsilateral to the injected striatum. At various times after intrastriatal injection of 9.3 nmoles of kainic acid, the brain was serially sectioned; the sections were stained for Nissl substance with cresyl violet or for degenerating neurons with the ammoniacal silver method. Neuronal degeneration spread unevenly into contiguous structures from the central sphere in the injected striatum and affected the ipsilateral pyriform cortex and amygdala, the deep layers of the overlying cerebral cortex, and the medial aspects of the bed nucleus of the stria terminalis and of the nucleus accumbens. In half of the rats, the pyriform cortex contralateral to the side of injection also underwent degeneration. A subpopulation of pyramidal cells in layer IV of the lateral neocortex and the CA3-CA4 pyramidal cells in the ipsilateral hippocampus were selectively affected, whereas adjacent neurons remained intact. The distribution of agyrophilic fibers and terminals in subcortical structures was consistent with the degeneration of neurons of origin in the affected striatal and extrastriatal regions. Brain sections stained by the gold sublimate technique from rats perfused 20 days after injection revealed an intense astrocytic response in all areas affected by acute neuronal degeneration. Extrastriatal damage could be markedly reduced by injection of lower doses of kainic acid (2.3 nmoles) with brief anesthesia; under these conditions, however, the subpopulation of large striatal neurons were relatively resistant, as compared to the Golgi II neurons. These studies demonstrate significant and variable neuronal degeneration beyond the primary site of the lesion after intracerebral injection of kainic acid; several factors affect the pattern of degeneration, including the amount of kainic acid injected, its biological activity, its diffusion, duration of anesthesia, and variable sensitivity of neurons. Consequently, care must be exercised in the use of this neurotoxin to determine the extent and selectivity of neuronal damage, particularly with reference to neuronal vulnerability beyond the central sphere of intrinsic neuronal degeneration.

Amygdala↗
PubMed2006

Retinal nerve fiber layer analysis in the diagnosis of glaucoma.

PURPOSE OF REVIEW: The detection of optic disc and retinal nerve fiber layer damage and change is the cornerstone of glaucoma management. Assessment of the retinal nerve fiber layer for localized and diffuse damage has been traditionally based on clinical examination, with documentation of change primarily qualitative. With the latest improvements in optical imaging instruments, objective and quantitative measurements of the retinal nerve fiber layer are now possible. This review summarizes the results from recent cross-sectional studies evaluating the discriminating ability of automated retinal nerve fiber layer measurements to detect glaucoma, and from longitudinal studies assessing the ability to predict and monitor glaucomatous changes. RECENT FINDINGS: Numerous cross-sectional studies have documented good diagnostic accuracy of a scanning laser polarimeter (GDx VCC), the optical coherence tomograph (Stratus), and the Heidelberg Retina Tomograph retinal nerve fiber layer measurements for differentiating between healthy and glaucoma eyes. There are only limited data available on the ability of these retinal nerve fiber layer measurements to document change over time. SUMMARY: It is essential that the clinician understand the specific strengths and weaknesses of each technique so that only good quality retinal nerve fiber layer information will be used in conjunction with careful clinical examination and visual function testing for glaucoma management decisions. Longitudinal studies are needed to evaluate the ability of these instruments to document retinal nerve fiber layer change over time.

Diagnostic Imaging↗
PubMed1995

The rate of Wallerian degeneration in cultured neurons from wild type and C57BL/WldS mice depends on time in culture and may be extended in the presence of elevated K+ levels.

Wallerian degeneration of severed axons is delayed in C57BL/WldS mice. We have examined this further in cultured sympathetic, sensory and CNS neurons using superior cervical ganglion (SCG), dorsal root ganglion (DRG) and cerebellar granule neurons respectively from neonatal mice. We found that the time taken for the neurites to degenerate depends upon the length of time in culture before cutting, reaching a maximum by approximately 7 days when C57BL/WldS neurites survive for > 6 days after axotomy. The onset of degeneration could also be extended in SCG and DRG neurites from wild type C57BL/6J mice. After 7 days in culture these neurites normally degenerate within approximately 12-16 h of axotomy, but in the presence of raised K+ (50 mM) degeneration often did not begin until a further 2 days had lapsed. Under similar conditions degeneration of neurites from C57BL/WldS mice was also found to be further delayed, extending survival from approximately 5-6 days to > 7 days. The L-type Ca2+ channel blockers nifedipine (5 microM) and verapamil (10 microM) both blocked the effect of raised [K+], although not completely. Thapsigargin, which raises cytoplasmic [Ca2+], and the cAMP analogue 8-(4-chlorophenyl-thio)cAMP were also able to delay degeneration, but only when added 24 h prior to axotomy. These results show that it is possible to influence the course of Wallerian degeneration and that increases in levels of cytoplasmic Ca2+ can protect neurites from its onset.

Animals↗
PubMed1984

Scanning electron microscopy studies of erythrocytes in spinocerebellar degeneration.

Spinocerebellar degeneration is a heredofamilial disease of unknown aetiology. The shape of erythrocytes as revealed by scanning electron microscopy was studied in this disease. Echinocytes I, as defined by Bessis, were seen more frequently in spinocerebellar degeneration than in age and sex matched controls (7.2 +/- 1.5% in spinocerebellar degeneration, 3.4 +/- 1.2% in controls, p less than 0.001), Parkinson's disease, motor neuron disease, myopathy, and Huntington's chorea. Erythrocyte deformability was impaired to a greater extent in spinocerebellar degeneration than in the controls when the pH was raised from 7.2 to 8.0; Echinocytes I in spinocerebellar degeneration increased from 8.4 +/- 0.6 to 15.4 +/- 2.4%, in the control group from 2.8 +/- 1.2 to 13.3 +/- 2.1%. In spinocerebellar degeneration no significant correlation was found between the level of serum low density lipoprotein and the number of Echinocytes I. In both groups there was a significant correlation between the occurrence of Echinocytes I and age, and the difference of Echinocytes I was greater in aged subjects in spinocerebellar degeneration. The data suggest that membrane abnormality in erythrocytes exists in spinocerebellar degeneration and may be accelerated with the advance of age.

Adult↗
PubMed1994

Extent of pontine pyramidal tract Wallerian degeneration and outcome after supratentorial hemorrhagic stroke.

BACKGROUND AND PURPOSE: Pyramidal tract Wallerian degeneration has been detected on magnetic resonance imaging (MRI) as T2-weighted high-intensity areas. We analyzed the relation between the extent of brain stem Wallerian degeneration and activities of daily living (ADL) after supratentorial hemorrhagic stroke. METHODS: Twenty-six patients with supratentorial hemorrhage were examined on the coronal T2-weighted image of the pons 3 months or later after stroke, and the percentage of Wallerian degeneration in the pons was calculated. The patients were divided into three groups. In group A (n = 6), MR films were taken 3 to 6 months from the onset, and the ADL assessment was done within 2 months from the MRI. In group B (n = 11), MR films were taken 3 to 6 months from the onset, and the ADL assessment was done within 10 months from the MRI (mean, 15.5 months from the onset). In group C (n = 9), MR films were taken after 10 to 17 months (mean, 12.0 months) from the ictus, and the ADL assessment was done simultaneously. Barthel Index score was used for quantitative ADL assessment. RESULTS: All patients showed various degrees of pontine pyramidal tract Wallerian degeneration associated with capsular involvement by the hematoma. In group A, the percentage of degeneration did not correlate with the Barthel Index score (r = .2101, P = .6895). An inverse relation between percentage of degeneration and Barthel Index score was seen in groups B (r = .7354, P = .0099) and C (r = .888, P = .0014). In groups B and C, Wallerian degeneration was higher in patients with Barthel scores less than 60 (P = .005). CONCLUSIONS: The extent of pontine Wallerian degeneration on MRI 3 months or later after the stroke correlated with the patient's Barthel Index score 1 year after the stroke.

Activities of Daily Living↗
PubMed2006

Truncation mutation in HRG4 (UNC119) leads to mitochondrial ANT-1-mediated photoreceptor synaptic and retinal degeneration by apoptosis.

PURPOSE: To characterize the time course of apoptosis and degeneration in a transgenic mouse model of retinal degeneration based on truncated mutant HRG4; to investigate the nature of binding of the mutant HRG4 to its target, ADP-ribosylation factor-like (ARL)2; to study its effects on the downstream molecules Binder-of-ARL2 (BART) and adenine nucleotide transporter (ANT)-1 and on the induction of apoptosis. METHODS: Saturation binding, microscopic morphometric, Western blot, immunofluorescence, and TUNEL analyses were used. RESULTS: Increased apoptosis did not occur until 20 months in the transgenic retina, consistent with the delayed-onset degeneration in this model. The truncated HRG4 protein exhibited approximately threefold greater affinity for ARL2 than the wild-type HRG4, likely resulting in nonfunctional sequestration of ARL2. A significant decrease in ARL2 was present by 20 months, accompanied by a 50% decrease in ANT-1 in the photoreceptor synaptic mitochondria, with evidence of mitochondrial dysfunction. Preapoptotic degeneration in the photoreceptor synapse was demonstrated with cytochrome c release and caspase 3 activation within the synapse-without evidence of TUNEL-positive apoptosis in the photoreceptor cell body-indicating an initial event in the synapse leading to apoptosis. Caspase 3 was activated in the accompanying secondary neuron, consistent with transsynaptic degeneration. CONCLUSIONS: The results support a novel mechanism of retinal degeneration in which preapoptotic degeneration starts in the photoreceptor synapse because of a deficiency in ANT-1 and spreads to the secondary neuron transsynaptically, followed by apoptosis and degeneration in the cell body of the photoreceptor.

Adaptor Proteins, Signal Transducing↗
PubMed2007

Retinal ischemia and reperfusion causes capillary degeneration: similarities to diabetes.

PURPOSE: Retinal neurons and vasculature interact with each other under normal conditions, and occlusion of the retinal vasculature can result in damage to retinal neurons. Whether damage to the neural retina will damage the vasculature, however, is less clear. This study was conducted to explore the relationship between vascular and nonvascular cells of the retina. The response of the retinal vasculature to an injury (ischemia and reperfusion; I/R) that is known to cause neuronal degeneration was studied. METHODS: I/R injury to the retinas was induced in Lewis rats and C57BL/6J mice by elevating intraocular pressure (IOP), and reperfusion was established immediately afterward. Some rats were pretreated with aminoguanidine (AMG, 50 mg/Kg BW in drinking water) before the procedure. Poly(ADP-ribose) polymerase (PARP) activity and expression of inducible nitric oxide synthase (iNOS), and cycloxygenase-2 (COX-2) were measured by Western blot analysis, and levels of TNF-alpha and intercellular adhesion molecule (ICAM)-1 mRNA were measured by qPCR at 2 and 7 days after the procedure. Also at 2 and 7 days after the I/R injury, apoptosis of retinal neural cells (demonstrated by TUNEL assay), density of cells in the ganglion cell layer, and thickness of retinas were quantitated, and the number of TUNEL-positive capillary cells and degenerated capillaries were assessed. Retinal neurodegeneration and capillary degeneration were also examined in C57BL/6J mice 2, 5, 8, and 14 days after I/R injury. RESULTS: As expected, loss of cells in the retinal ganglion cell layer was apparent 2 days after I/R injury in the rat and mouse models. In contrast, the retinal vasculature had essentially no pathology at this time in either model. Surprisingly, the number of degenerated capillaries increased greatly by 7 to 8 days after the injury. Administration of aminoguanidine significantly inhibited the I/R-induced capillary degeneration as well as neurodegeneration in the rat model. Retinal I/R caused increased PARP activity (detected by poly(ADP-ribosy)lated proteins), as well as upregulation of iNOS, COX-2, TNF-alpha, and ICAM-1 levels in rats, consistent with an inflammatory process. CONCLUSIONS: Capillary degeneration is an unrecognized component of acutely elevated IOP and develops only after neurodegeneration is severe. Thus, this finding raises the possibility that damage to the neural retina contributes to capillary degeneration. Aminoguanidine, a nonspecific inhibitor of iNOS, inhibited I/R-induced degeneration of both neuronal and vascular cells of the retina. The model of retinal ischemia and reperfusion will be a useful tool for investigating the relationship between neuronal damage and vascular damage in glaucoma and other diseases such as diabetic retinopathy.

Animals↗
PubMed2002

An electron microscopic study of neuronal degeneration and glial cell reaction in the retina of glaucomatous rats.

The present investigation was focused on the ultrastructural changes in the neurons and glial cells in the retina of rats with experimentally-induced glaucoma. An experimental glaucoma model was created by limbal-derived vein cauterization. Animals were sacrificed at 1, 3 weeks and 3 months post-operation. Retinae were dissected and processed for electron microscopy. Neuronal degeneration was observed in all the different layers of the retina at both 1 and 3 weeks post-operation. Some degenerating neurons were found in the ganglion cell layer (GCL), inner nuclear layer (INL) and outer nuclear layer (ONL). And the dying neurons presented apoptotic-like more than necrotic neurons. Many degenerating axons and axon terminals were observed between neurons in the GCL, inner plexiform layer (IPL), INL, and outer plexiform layer (OPL). Activated astrocytes and microglial cells were present in close association with degenerating neurons and axons. The Müller cells in the INL also presented longer and darker processes with more microfilaments than in normal cells. Degenerating neuronal debris, degenerating axonal profiles and electron-dense bodies were often found in the cytoplasm of macrophages. The results suggest that both microglial cells and astrocytes are activated in the process of neuronal degeneration in the retina of experimentally-induced glaucomatous rats. It is hypothesized that they may play a protective role in removing degenerating neuronal elements in the retina after the onset of glaucoma.

Animals↗
PubMed1990

Observations on the pattern of sensorineural degeneration in the human cochlea.

Cochlear sensory and neural degeneration was examined in nine pairs of human temporal bones fixed by perilymphatic perfusion, using phase-contrast and electron microscopy. Four pairs, three from females, had only slight sensorineural degeneration, limited to the very basal end of the cochlea. A predominantly neural degeneration was identified in a 54-year-old male. The process was bilateral, asymmetrical, uneven, and involved the entire length of the cochlea with several circumscribed areas of severe nerve degeneration. One case had mild, diffuse sensorineural degeneration in the lower half of the basal turn characteristic of presbyacusis. The other three pairs, all from males, revealed sensorineural degeneration patterns associated with noise injury and were remarkably similar to or almost identical with cochleas described previously. There was a good correlation between the presence of supporting cells and the survival of nerve fibres in the osseous spiral lamina in the corresponding area. In one cochlea, however, the degeneration of only inner hair cells in a small area was associated with complete nerve degeneration in the corresponding sector of the spiral lamina. Giant cilia were frequently seen in the apical turn.

Adult↗
PubMed1980

Experimental studies of mechanisms involved in methods demonstrating axonal and terminal degeneration.

Factors influencing the consistency and specificity of the staining of neuronal degeneration products were studied in brain sections by varying systematically the composition of solutions used in the steps which are common to the degeneration methods. The formation of nuclei of metallic silver was determined either by physical development of 110Ag, after dissolving reducible silver by acetic acid. In degenerating axons metallic silver nucleic are formed by their own reducing groups in the first (acid) and in the second (alkaline) impregnating bath. The first impregnation turned out to be sufficient to produce complete staining of degenerating axons. The reducing capacity of normal axons and myelin can be suppressed by oxidation or by lowering the pH of the impregnating solution. Degenerating axon terminals are not able to reduce silver ions in either of the impregnating baths. Rather, the metallic silver nuclei initiating their staining are formed in the Nauta reducer by interaction of its reducing agent (formol) with silver ions which had been trapped in the tissue during the impregnation. Thus the nuclei are enlarged to microscopic visibility by a nonstandardized physical developer coming about from the Nauta reducer and the silver ions transferred with the sections. In this reaction catalytic sites in degenerating terminals as well as ammonium ions and the alkali reserve of the tissue play an important role. On the basis of the present results it was possible to stabilize the conditions for staining degenerating axons and degenerating axons terminals in two separate staining procedures detailed in following papers.

Animals↗
PubMed2002

Retinal cAMP levels during the progression of retinal degeneration in rhodopsin P23H and S334ter transgenic rats.

PURPOSE: To test whether high levels of cAMP promote apoptosis and shorten the life of retinal rod photoreceptors, the changes in cAMP levels during retinal degeneration were analyzed in two transgenic rat models that express rhodopsin P23H and S334ter mutations. METHODS: Dark- and light-adapted heterozygous P23H (lines 1 and 3; P23H-1 and -3), S334ter line 4 (S334ter-4), and Sprague-Dawley (control) rats were studied at 4 to 8 weeks by cAMP enzyme competitive immunoassay and by cAMP immunocytochemistry. RESULTS: In control animals retinal cAMP content reached a steady state level at 30 days of age. Dark-adapted control retinas had up to 97% higher cAMP content than light-adapted retinas, and photoreceptor cells were the major source of this increase. Dark-adapted photoreceptors in all three lines of transgenic rats at advanced stages of retinal degeneration had cAMP content different from that of the control. In rats that express mutant rhodopsin, the number of photoreceptor cells was progressively reduced, because of retinal degeneration, but dark-adapted cAMP levels did not decline accordingly. P23H transgenic animals of both lines had higher levels of cAMP per photoreceptor cell count than control animals. This elevation was more pronounced as degeneration progressed. S334ter animals showed smaller cAMP elevation than P23H rats at a similar stage of retinal degeneration, but at a point when S334ter rats were undergoing rapid retinal degeneration, whereas in P23H rats retinal degeneration was slowing down. CONCLUSIONS: All three lines of transgenic rats carrying rhodopsin mutations show an increase in dark-adapted photoreceptor cAMP levels. A complex relationship exists between cAMP levels and the rate of cell death in the retina. Although initially higher levels of cAMP may promote cell survival and slow down retinal degeneration, ultimately, elevated cAMP levels may become toxic and may contribute to retinal cell death.

Animals↗
PubMed1992

Lattice degeneration of the retina and retinal detachment.

Lattice retinal degeneration is considered the most significant peripheral retinal disorder potentially predisposing to retinal breaks and retinal detachment. Lattice degeneration affects the vitreous and inner retinal layers with secondary changes as deep as the retinal pigment epithelium and perhaps the choriocapillaris. Variations in clinical appearance are the rule; geographically, lattice lesions favor the vertical meridians between the equator and the ora serrata. Lattice degeneration begins early in life and has been reported in sequential generations of the same family. Along with its customary bilateral occurrence, lattice shares other characteristics of a dystrophy. The association between the vitreous and retina in lattice lesions may be responsible for the majority of lattice-induced retinal detachments. The tumultuous event of posterior vitreous separation in the presence of abnormally strong vitreoretinal adherence is the trigger for a retinal tear that, in turn, may lead to retinal detachment. Although retinal holes in young patients with lattice degeneration may play a role in the evolution of retinal detachment, the clinical course of lattice degeneration seems to be one of dormancy rather than of progressive change. This discussion outlines the pathophysiology of lattice retinal degeneration and the relationship of pathophysiology to clinical presentation. The epidemiology of lattice degeneration is summarized, as are the possible precursors to retinal detachment. A clinical characterization of the natural history of lattice degeneration is offered, and interventions for complications are described. To conclude, management strategies from a primary-care standpoint are reviewed.

Cataract Extraction↗
PubMed1988

Reciprocal connections between the claustrum and the auditory cortical fields in the cat. An experimental study using light- and electron microscopic anterograde degeneration methods, and the horseradish peroxidase retrograde axonal transport.

The reciprocal connections between the claustrum and the auditory cortical fields AI, AII and Ep were investigated by means of Nauta and Fink-Heimer selective silver impregnation procedures, electron microscopic identification of degenerated axons and synaptic boutons, and with the Mesulam horseradish peroxidase retrograde tracing technique. The course and termination of degenerating corticoclaustral axons were investigated following circumscript lesions of the AI, AII and Ep areas in 19 cats. The greatest amount of degeneration debris was observed following destruction of the AII area. The central third of the claustrum (stereotaxic level A13-A15) is filled with degenerating terminals (d. t.), with greatest concentration in the lateral wedge of the nucleus, and along its inferolateral border. Rostrally and caudally the density of degeneration diminishes but scattered d. t. were observed up to the rostral pole, and a moderate number - up to the caudal pole of the claustrum. Slightly lesser amount of d. t. was observed following Ep destruction. The caudal portion of the claustrum is filled with d. t. In the central third the degeneration field occupies mainly the ventrolateral zone of the nucleus. The rostral pole of the claustrum is free of degeneration. The projection from the AI field is considerably more moderate, and is diffusely organized. A substantial number of d. t. is encountered only in the lateral parts of the central claustral third. The crossed corticoclaustral connections mirror the ipsilateral ones but are far more modest. The AII area projects mainly to the central claustral third, the Ep area--to the caudal third. The projection of the AI area to the contralateral claustrum is very weak. The electron microscopic examination of the claustrum following auditory cortex destruction in 9 cats revealed an appreciable number of degenerating synaptic boutons. They undergo dark and more rarely light degenerative changes. The cortical terminals are classified in two types: "small round" (SR), comprising approximately 70 to 75% of the corticoclaustral boutons, and "large round" (LR)-25-30%, resp. The SR boutons measure 0.6-1.2 micron, contain tightly packed round synaptic vesicles (380-420 A), and form asymmetrical axodendritic contacts. The LR boutons measure 1-2.5 microns, contain round vesicles (400-500 A) and form asymmetrical axodendritic and (far more rarely) axosomatic contacts. The claustrocortical connection was investigated in 13 cats with selective injections of 30% HRP in the three subdivisions of the auditory cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

[Neuropathological background of spinocerebellar degeneration--with special reference to autonomic nervous system lesions in olivopontocerebellar atrophy, Shy-Drager syndrome and multiple system atrophy].

For elucidation of actual status of olivopontocerebellar atrophy (OPCA) in nosological relation to Shy-Drager syndrome (SDS) and multiple system atrophy (MSA), neuropathological examination with morphometric survey on the intermediolateral column of the spinal cord was performed. The materials were 13 cases registered in our laboratory. Clinically, they consisted of 9 sporadic OPCA including 2 cases with prominent autonomic failure, and 4 hereditary spinocerebellar degeneration. In the autonomic nervous system of CNS, degeneration of the intermediolateral column was found in the sporadic cases without exception, irrespective of presence or absence of orthostatic hypotension, while the hereditary cases showed neither orthostatic hypotension nor neuronal loss in the nucleus. The autonomic centers in the brain-stem and cerebellum were systematically affected in both the sporadic and the hereditary cases. It was particularly remarked that the fastigial nucleus, tractus and nucleus solitarius, which have been suggested to be related to cardiovascular control, was severely affected. The locus coeruleus, on the other hand, was less severely affected in the hereditary cases. The most remarkable finding was that there was no case with neuropathological change restricted only to the olivo-ponto-cerebellar (OPC) and/or autonomic nervous systems. The sporadic cases had OPC system degeneration with striato-nigral degeneration (SND) and autonomic nervous system degenerations, irrespective of differences in clinical features from case to case. It should be emphasized that the actual neuropathological status of our sporadic cases could be regarded as a multisystemic degeneration inevitably combined with OPC system degeneration, apart from whether such cases are designated as MSA or not. Finally it was remarked that the hereditary cases were different from the sporadic cases in that there occurred far less severe involvement of the locus coeruleus and intermediolateral column, and primary degeneration of the substantia nigra different obviously from SND.

Adult↗
PubMedDate not supplied

Seminiferous tubule degeneration in human cryptorchid testes.

Two types of degenerating seminiferous tubules were found in cryptorchid testes with Sertoli cell hyperplasia of children and adults: 1) tubules with central degeneration, and 2) tubules with total degeneration. Central degeneration begins with degenerative changes in germ cells that accumulate in the lumen of the seminiferous tubule. Some Sertoli cells may also be affected. Degenerated cells finally disappear, and the remaining tubule is composed of only a cuboidal epithelium, which consists mainly of Sertoli cells and occasional germ cells surrounding a wide lumen. Total degeneration is principally seen in tubules with severe germinal hypoplasia. All the seminiferous epithelium cells degenerate and lose their characteristic distribution, forming a disorganized Sertoli cell nodule surrounded by a thickened basement membrane. Lastly, Sertoli cells disintegrate, and the seminiferous epithelium disappears. Tubular degeneration might be related to the thickening of the basement membrane, which hinders metabolic interchange between the seminiferous epithelium and the interstitium.

Adolescent↗
PubMed2004

Correlation of radiographic and MRI parameters to morphological and biochemical assessment of intervertebral disc degeneration.

UNLABELLED: Degenerative disc disease (DDD) is a common finding in MRI scans and X-rays. However, their correlation to morphological and biochemical changes is not well established. In this study, radiological and MRI parameters of DDD were assessed and compared with morphological and biochemical findings of disc degeneration. Thirty-nine human lumbar discs (L1-S1), age 19-86 years, were harvested from eight cadavers. Within 48 h postmortem, MRIs in various spin-echo sequences and biplanar radiographs of intact spines were obtained. Individual discs with endplates were then sectioned in the mid-sagittal plane and graded according to the morphological appearance. Samples from the nucleus of each disc were harvested for biochemical analysis including water and proteoglycan contents. On MRIs, T2-signal intensity, Modic changes, disc extension beyond the interspace (DEBIT), nucleus pulposus shape, annular tears, osteophytes and endplate integrity were graded. On radiographs, an independent observer classified the parameters disc height, endplate sclerosis, osteophytes, Schmorl's nodes, intradiscal calcifications and endplate shape. General linear-regression models were used for statistical analysis. Backward elimination with a 10% significance cut-off level was used to identify the most significant parameters, which then were summed to create composite scores for radiography, MRI and the combination of both methods. The grading was performed by three observers, and a reliability analysis using Cronbach's alpha model was used to control interobserver agreement. The three radiographic parameters height-loss, osteophytes and intradiscal calcifications correlated significantly with the morphological degree of degeneration (p<0.001, R2=642). Significant differences of even one morphological grade could also be differentiated in the composite radiological score (p<0.05), except at the extremes between grades 1 and 2 and grades 4 and 5. All MRI parameters correlated significantly with the morphological grade (p<0.05); however Modic changes, T2-intensity and osteophytes accounted for 83% of the variation in the data. T2-signal intensity correlated significantly with H2O and proteoglycan content (p<0.001), and was best for detecting highly degenerated discs. Regression showed that the combined score was better correlated with the morphological grade (p<0.001, R2=775) than either the composite radiographic (p<0.001, R2=642) or composite MRI (p<0.001, R2=696) alone. Based on the combined score, a backwards elimination of the regression was performed, in which the parameters Modic changes, and T2-intensity loss (MRI) as well as calcifications (X-ray) accounted for 87% of the variability. The interobserver validation showed a high correlation for all three scores (Cronbach's alpha values ranging from 0.95 to 0.97). CONCLUSION: Selective imaging parameters and a newly created scoring scheme were found to correlate with disc degeneration as determined in a morphological manner. Surprisingly, radiographic parameters were able to distinguish different stages of degeneration, whereas MRI could only detect advanced stages of disc degeneration. We conclude that X-rays may remain a cost-effective, non-invasive in vivo-grading method to detect early disc degeneration, and, combined with MRI, correlate best with morphological and biochemical assessment of disc degeneration.

Adult↗