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PubMed1976

An electron microscopic study of lesion-induced synaptogenesis in the dentate gyrus of the adult rat. I. Magnitude and time course of degeneration.

Synapses in the rat dentate gyrus are rapidly lost after removal of the primary input from the entorhinal cortex. In this paper we describe the extent and time course of degeneration and in the subsequent paper the nature of the reinnervation processes. They synapses of entorhinal afferents are remarkably concentrated in their zone of termination. Unilateral removal of the rat entorhinal cortex results in the loss of about 86% of all synapses in the outer three-fourths of the molecular layer of the epsilateral dentate gyrus. Entorhinal synapses are all asymmetric (Gray type I) and terminate on dendritic spines. Analysis of the degeneration reaction provides a means to examine the characteristics of the loss of a relatively homogeneous afferent on a single cell type. The morphological characteristics of the the degenerating terminals showed some heterogeneity; both the electron lucent and electron dense types of degenerating terminals were identified. The electron lucent type was observed only at short survival times. The time course of the loss of degenerating terminals was resolvable into two components, each of which followed first order decay kinetics. Thus degenerating entorhinal terminals behaved as a population which disappeared randomly at a rate dependent on the fraction of terminals present at any time. The loss of degenerating terminals was accompanied by the loss of postsynaptic sites. At short survival times the majority of postsynaptic sites (defined by the presence of a postsynaptic density) had disappeared. There was also a loss of complex spines and some shrinkage of the molecular layer.

Animals↗
PubMed1990

3-Acetylpyridine results in degeneration of the extrapyramidal and cerebellar motor systems: loss of the dorsolateral striatal dopamine innervation.

3-Acetylpyridine (3-AP) administration to rats results in degeneration of the dopamine (DA) innervation of the striatum as well as degeneration of the olivocerebellar system. We now report that administration of this pyridine neurotoxin results in a decrease in striatal DA concentration which is restricted to the dorsolateral aspects of the caudatoputamen. 3-AP treatment did not alter DA levels in the ventromedial striatum, the nucleus accumbens, or the anteromedial prefrontal cortex. Both 3-AP and another pyridine neurotoxin, 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), potently inhibited in vitro MAOB activity and in contrast weakly inhibited MAOA activity. However, in vitro inhibition of MAOB by the selective inhibitor deprenyl did not prevent or attenuate 3-AP-induced striatal DA depletion. These data indicate that 3-AP administration to rats not only results in degeneration of the olivocerebellar system, but also effects degeneration of the DA innervation of the dorsolateral striatum, the striatal sector thought to subserve motoric and sensorimotor function. 3-AP-induced nigrostriatal degeneration differs from that elicited by MPTP in that the former is not prevented by deprenyl pretreatment. The 3-AP-induced degeneration of both extrapyramidal and cerebellar motor systems may offer insight into the mechanisms involved in degeneration of the two motor systems in certain strains of rodents (such as the Weaver mutant mouse), and suggests that the sequelae of administration of this pyridine may serve as a useful model for olivopontocerebellar atrophy-associated parkinsonism.

Animals↗
PubMed1994

The influences of age, retinal topography, and gender on retinal degeneration in the Fischer 344 rat.

The Fischer 344 (F344) rat is presently the animal of choice for age-related research. The existence of an age-related retinal degeneration was reported previously in the males of this strain, but a gender comparison has not been performed. In this study, histological and morphometric measurements of the retina related to age, retinal topography, and gender were made on 3- to 24-month-old animals. The thicknesses of the outer nuclear layer (ONL) and the photoreceptor layer (PRL) were measured from sagittal sections at six loci. Retinas of both sexes showed steady decline with age in the thicknesses of the ONL and PRL at all locations. An important finding was the presence, after 12 months of age, of a drastically accelerated rate of peripheral retinal degeneration seen only in male subjects. Females showed a less dramatic rate of peripheral degeneration which did not begin until after 18 months of age. In addition, two other forms of retinal degeneration were found--cystoid degeneration was found earlier and more frequently in the male, while a paving-stone type of degeneration was found in both sexes. These two types of lesions were preferentially, but not exclusively found in the peripheral retina. In conclusion, the F344 rat offers a convenient model to study a pattern of retinal degeneration affected by the combination of gender, regional and age-related factors.

Aging↗
PubMed1992

Signals that induce sprouting in the central nervous system: sprouting is delayed in a strain of mouse exhibiting delayed axonal degeneration.

This study evaluates whether CNS sprouting is initiated by signals related to the degeneration of presynaptic axons. We evaluate the time course of sprouting of cholinergic septohippocampal fibers after unilateral entorhinal cortex (EC) lesions in a substrain of mice carrying a mutation which leads to a substantial delay in the onset of Wallerian degeneration. We first verified that axonal degeneration resulting from EC lesions was delayed in mutant mice using silver-staining techniques (the Fink-Heimer method). Cholinergic sprouting was then evaluated using a histochemical technique for acetylcholinesterase (AChE) in mutant mice and normal controls. In normal control mice, both axonal degeneration and cholinergic sprouting occurred with a time course that was comparable to that described in rats. Argyrophilic degeneration debris was prominent by 4 days postlesion, and increases in AChE staining in the molecular layer of the dentate gyrus were well developed by 10 days. In mice carrying the "Ola" mutation, however, argyrophilic degeneration debris was not detectable at 4 or 6 days postlesion, began to appear in the dentate gyrus by 8 days postlesion, but did not become prominent until 12 days. Increases in AChE staining in the molecular layer of the dentate gyrus were not detectable even at 12 days postlesion, but developed gradually after 14 days. These results demonstrate that the signals which initiate at least one form of CNS sprouting are related to the degeneration of presynaptic axons.

Acetylcholinesterase↗
PubMed1992

Reciprocal retinal transplantation: a tool for the study of an inherited retinal degeneration.

The pathogenesis of retinal degeneration in rd mutant mice has been extensively studied, the gene responsible for the defect has been cloned, and the neural retina has been identified as the primary site for the degeneration. However, the possible contributory role of the ocular environment in this form of retinal degeneration remains undetermined. Retinal transplantation, which provides the opportunity to implant the neural retinal into a genetically defined intraocular environment, was used to examine this possibility. A reciprocal retinal transplantation paradigm was designed based on three experimental groups: (1) normal immature retina transplanted into rd/rd mutant eyes, (2) rd/rd immature retina transplanted into normal eye, and (3) normal immature retina transplanted into normal eyes. The rates of survival and histological characteristics of the grafts were compared between the three groups. At post-transplantation Day 3 (PTD 3), there were no differences between the three groups. Between PTD 10 and 15, the retinal grafts in group 1 showed degeneration. In contrast, the retinal grafts in groups 2 and 3 survived and developed well. At PTD 30, the retinal grafts in both groups 1 and 2 showed degeneration, but the retinal grafts in group 3 survived and remained differentiated well. These results suggest that the retinal degeneration of rd mice may be caused by both a deficit of the neural retina and intraocular environmental changes which are elicited either as a result of mutation or as a sequel to retinal degeneration.

Animals↗
PubMed2005

Fluoro-Jade C results in ultra high resolution and contrast labeling of degenerating neurons.

The causes and effects of neuronal degeneration are of major interest to a wide variety of neuroscientists. Paralleling this growing interest is an increasing number of methods applicable to the detection of neuronal degeneration. The earliest methods employing aniline dyes were methodologically simple, but difficult to interpret due to a lack of staining specificity. In an attempt to circumvent this problem, numerous suppressed silver methods have been introduced. However, these methods are labor intensive, incompatible with most other histochemical procedures and notoriously capricious. In an attempt to develop a tracer with the methodological simplicity and reliability of conventional stains but with the specificity of an ideal suppressed silver preparation, the Fluoro-Jade dyes were developed. Fluoro-Jade C, like its predecessors, Fluoro-Jade and Fluoro-Jade B, was found to stain all degenerating neurons, regardless of specific insult or mechanism of cell death. Therefore, the patterns of neuronal degeneration seen following exposure to either the glutamate agonist, kainic acid, or the inhibitor of mitochondrial respiration, 3-NPA, were the same for all of the Fluoro-Jade dyes. However, there was a qualitative difference in the staining characteristics of the three fluorochromes. Specifically, Fluoro-Jade C exhibited the greatest signal to background ratio, as well as the highest resolution. This translates to a stain of maximal contrast and affinity for degenerating neurons. This makes it ideal for localizing not only degenerating nerve cell bodies, but also distal dendrites, axons and terminals. The dye is highly resistant to fading and is compatible with virtually all histological processing and staining protocols. Triple labeling was accomplished by staining degenerating neurons with Fluoro-Jade C, cell nuclei with DAPI and activated astrocytes with GFAP immunofluoresence.

Animals↗
PubMed2026

Transcriptome analysis of the pectoral fin degeneration in half-smooth tongue sole (Cynoglossus semilaevis).

Appendage degeneration is a notable morphological feature of some teleosts with specialized benthic lifestyles. The half-smooth tongue sole (Cynoglossus semilaevis) undergoes severe pectoral fin regression during metamorphosis. However, the molecular basis underlying rapid pectoral fin degeneration remains unclear. Here, we performed time-series transcriptome sequencing on pectoral fins at pre-metamorphosis, metamorphosis peak and post-metamorphosis to characterize the molecular changes associated with pectoral fin degeneration. Transcriptional dynamics and functional enrichment showed that no significant enrichment of classical apoptosis-related transcriptional pathways was detected during pectoral fin degeneration. Instead, sustained downregulation of twist1b, identified as a transcriptomic candidate, together with significant upregulation of ssh1, coupled with enrichment of lysosome and ubiquitin-proteasome system (UPS) pathways, suggested enhanced tissue remodeling during pectoral fin degeneration. Temporal expression clustering revealed heterochronic misalignment in the developmental gene expression: upstream initiator tbx5 was upregulated at early metamorphosis, while downstream maintenance signal fgf10 decreased synchronously. Distal patterning gene hoxd12a exhibited premature expression and rapid decay, losing sustained late-phase expression. Moreover, transient elevation of gli3 during metamorphosis may contribute to restricted distal fin growth. We conclude that pectoral fin degeneration in C. semilaevis is associated with heterochronic disruption of developmental signaling and extensive tissue remodeling. This study provides transcriptomic insights into pectoral fin degeneration in tongue soles and establishes a basis for future functional studies of appendage reduction in teleosts.

Animals↗
PubMed2000

Presence of apolipoprotein E immunoreactivity in degenerating neurones of mice is dependent on the severity of kainic acid-induced lesion.

Apolipoprotein E (apoE) is a major apolipoprotein in the central nervous system (CNS) that may play a role in various CNS disorders. ApoE is primarily localised in astrocytes, but neuronal apoE mRNA expression has been demonstrated in normal and diseased human brain, as well as in ischaemic rat brain. To obtain further insight into the role of apoE in neuronal degeneration in the CNS and conditions of neuronal apoE localisation, we have investigated in mice the distribution of apoE following neuronal injury induced by kainic acid (n=35, 25 or 35 mg kainic acid/kg BW). Consecutive series of brain sections were immunostained for apoE and markers for astroglia (GFAP) and microglia/macrophage cells (CR3). Degenerating neurones were identified with a silver-degeneration staining technique. The intensity and cellular distribution of apoE-immunoreactivity (apoE-ir) was dependent on the severity of neuronal injury. Mice that developed mild neuronal degeneration, restricted to a subset of neurones in the hippocampus, showed increased apoE-ir in astrocytes concomitant with increased GFAP-ir and mild microgliosis. In these mice, no neuronal apoE-ir was detected. In contrast, mice developing severe neuronal injury in the hippocampus - frequently also showing degeneration in other brain regions including cortex, thalamus, striatum and amygdala - showed intense apoE-ir in degenerating neurones. Surrounding the lesion, apoE-ir was increased in neuropil recurrently whereas GFAP-ir astrocytes disappeared. Thus, in mice apoE accumulates in degenerating neurones in conditions of severe neuronal injury putatively in association with disruption of the glial network.

Animals↗
PubMed1997

Systemic administration of MPTP induces thalamic neuronal degeneration in mice.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a known neurotoxicant primarily selective for catecholaminergic neurons, including those of the nigrostriatal dopaminergic system, thereby mimicking the pathology of Parkinson's disease (PD). In this study, serial transbrain sectioning, followed by staining with a newly developed fluorochrome (Fluoro-Jade) specific for degenerating neurons, was used to detect additional sites of MPTP-induced neuronal degeneration in mice. Male CD-1 mice received a single 50 mg/kg dose of MPTP intraperitoneally at room temperature or at a reduced temperature (6 degrees C), which has been shown to potentiate striatal dopamine depletion. Neuronal degeneration was observed in the substantia nigra pars compacta (SN), ventral tegmental area (VTA) and retrorubral field (RRF) of only animals dosed in the low temperature environment. Neuronal degeneration was also observed in other catecholaminergic nuclei in both treatment groups. In addition, degenerating cell bodies and fibers were detected in the midline and intralaminar thalamic nuclei of all dosed animals, regardless of the dosing environment. Pharmacological manipulations which prevented nigral degeneration (deprenyl and nomifensine pretreatment) also prevented the degeneration of thalamic neurons. MK-801 pretreatment, however, resulted in a disproportionate protection of the thalamic neurons. These findings confirm and extend our previous observations regarding the protective effect of hyperthermia in CD-1 mice and also suggest that regions of the thalamus may be relevant to the pathophysiology of PD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1997

Differences in the retinal GABA system among control, spastic mutant and retinal degeneration mutant mice.

Immunocytochemical methods were used to compare the GABA system in control mice and two mutant strains: spastic which has reduced glycine receptors and retinal degeneration mutant in which the photoreceptors degenerate and reportedly have increased GABA and GAD levels. We found that the spastic mutant retina had reduced GABA-immunoreactivity (IR) in the proximal retina, reduced staining for GAD-1440 in the OPL, and reduced GABAA receptor staining in the OPL, compared to control. The retinal degeneration mutant retinas had enhanced GABA-IR throughout the retina, particularly in Müller cells, bipolar cells and IPL, and enhancement of GABAA receptor staining in the OPL, compared to control. The distributions of GABA-IR, GAD-1440-IR and GABAA receptor-IR in retinas of spastic mutant mice that also expressed the retinal degeneration phenotype resembled those found in retinas of mice that expressed only the retinal degeneration phenotype rather than those that expressed only the spastic mutation. No differences were observed among the conditions for GAD-65, GAD-67 or GABA-T. Our results with the spastic and retinal degeneration mutant mice demonstrate that attenuation in the glycinergic system and photoreceptor degeneration, respectively, is accompanied by alterations in different aspects of the GABA system, giving impetus for caution in the interpretation of experiments involving genetic manipulation of complex phenotypes.

Animals↗
PubMed2002

Comparison of matrix metalloproteinase expression during Wallerian degeneration in the central and peripheral nervous systems.

The matrix metalloproteinases (MMPs) are a large family of zinc-dependent enzymes which are able to degrade the protein components of the extracellular matrix. They can be placed into subgroups based on structural similarities and substrate specificity. Aberrant expression of these destructive enzymes has been implicated in the pathogenesis of immune-mediated neuroinflammatory disorders. In this study we investigate the involvement of MMPs, from each subgroup, in Wallerian degeneration in both the central and peripheral nervous systems. Wallerian degeneration describes the process initiated by transection of a nerve fibre and entails the degradation and removal of the axon and myelin from the distal stump. A similar degenerative process occurs as the final shared pathway contributing to most common neuropathies. MMP expression and localisation in the peripheral nervous system are compared with events in the CNS during Wallerian degeneration. Within 3 days after axotomy in the peripheral nervous system, MMP-9, MMP-7 and MMP-12 are elevated. These MMPs are produced by Schwann cells, endothelial cells and macrophages. The temporospatial expression of activated MMP-9 correlates with breakdown of the blood-nerve barrier. In the CNS, 1 week after optic nerve crush, four MMPs are induced and primarily localised to astrocytes, not microglia or oligodendrocytes. In the degenerating optic nerve, examined at later time points (4, 8, 12 and 18 weeks), MMP expression was down-regulated. The absence of MMPs in oligodendrocytes and mononuclear phagocytes during Wallerian degeneration may contribute to the slower removal of myelin debris observed in the CNS. The low level of the inactive pro-form of MMP-9 in the degenerating optic nerve may explain why the blood-brain barrier remains intact, while the blood-nerve barrier is rapidly broken down. We conclude that the difference in the level of expression, activation state and cellular distribution of MMPs may contribute to the different sequence of events observed during Wallerian degeneration in the peripheral compared to the CNS.

Animals↗
PubMed2003

Involvement of the ubiquitin-proteasome system in the early stages of wallerian degeneration.

Local axon degeneration is a common pathological feature of many neurodegenerative diseases and peripheral neuropathies. While it is believed to operate with an apoptosis-independent molecular program, the underlying molecular mechanisms are largely unknown. In this study, we used the degeneration of transected axons, termed "Wallerian degeneration," as a model to examine the possible involvement of the ubiquitin proteasome system (UPS). Inhibiting UPS activity by both pharmacological and genetic means profoundly delays axon degeneration both in vitro and in vivo. In addition, we found that the fragmentation of microtubules is the earliest detectable change in axons undergoing Wallerian degeneration, which among other degenerative events, can be delayed by proteasome inhibitors. Interestingly, similar to transected axons, degeneration of axons from nerve growth factor (NGF)-deprived sympathetic neurons could also be suppressed by proteasome inhibitors. Our findings suggest a possibility that inhibiting UPS activity may serve to retard axon degeneration in pathological conditions.

Amino Acids↗
PubMedDate not supplied

Morphological characterization of the retinal degeneration in three strains of mice carrying the rd-3 mutation.

Retinal development in 3 strains of rd-3/rd-3 mutant mice, previously shown to have different rates of degeneration, was studied using light, electron, and immunofluorescence microscopy. The time course and phenotype of the degeneration as well as details on the mechanism of massive photoreceptor cell loss are compared with other known retinal degenerations in mice. Up until postnatal day (P) 10, the retinas of all three strains (RBF, 4Bnr, In-30) develop similarly to those of pigmented and nonpigmented controls. TUNEL-positive cells appear in the outer nuclear layer (ONL) by P14, and reach a maximum in all three mutant strains around P21. Scattered rods and cones form a loose, monolayered ONL by 8 weeks in the albino RBF strain, by 10 weeks in the albino 4Bnr strain, and by 16 weeks in the pigmented In-30 strain. Though the initial degeneration begins in the central retina, there is no preferred gradient of cell death between central and peripheral photoreceptors. Rods and cones are present at all ages examined. During development, stacks of outer segments (OS) form in all three strains though they never achieve full adult lengths, and often have disorganized, atypical OS. Rod opsin is expressed in the developing OS but is redistributed into plasma membrane as OS degeneration proceeds. Retinal pigment epithelial (RPE) cells of all mutant strains contain packets of phagocytosed OS, and their apical processes associate with the distal ends of the OS. At their synaptic sites, photoreceptor terminals contain ribbons apposed to apparently normal postsynaptic triads. As photoreceptors are lost, Müller cells fill in space in the ONL but they do not appear to undergo significant hypertrophy or migration, though during the degeneration, glial fibrillary acidic protein (GFAP) expression is gradually upregulated. Macrophage-like cells are found frequently in the subretinal space after the onset of photoreceptor apoptosis. As OS disappear, the RPE apical processes revert to simple microvilli. Late in the degeneration, some RPE cells die and neighboring cells appear to flatten as if to maintain confluence. In regions of RPE cell loss that happen to lie above retina where the ONL is gone, cells of the inner nuclear layer (INL), wrapped by Müller cell processes, may front directly on Bruch's membrane.

Aging↗
PubMed2001

Enrofloxacin-associated retinal degeneration in cats.

OBJECTIVE: The objective of this study was to evaluate the possible relationship between the administration of parenteral and/or oral [corrected] enrofloxacin and the onset of acute retinal degeneration in cats. The animals studied included 17 cats that received systemic enrofloxacin and developed retinal degeneration soon thereafter. PROCEDURES: In this retrospective clinical study, cats that received parenteral and/or oral [corrected] enrofloxacin and developed acute blindness were identified. Parameters recorded included breed, age, sex, enrofloxacin dosage (daily dose and number of days administered), medical condition for which the antibiotic had been prescribed, ophthalmic signs, examination results, and the visual outcome. Fundus photographs were obtained in seven cats, and electroretinography was performed in five cats. Histopathology was performed on two eyes from one cat (case 1) that received enrofloxacin 5 months previously and developed retinal degeneration. RESULTS: All cats were the domestic shorthair breed; seven were females (one neutered) and ten were males (seven castrated). Ages ranged from 3 to 16 years old (mean +/- SD; 8.8 +/- 4.6 years). The medical disorders for which enrofloxacin was administered ranged from lymphoma and pancreatitis to otitis and dermatitis, and eight cats had urinary diseases. The daily and total dosage of enrofloxacin and number of days of administration were also highly variable. Presenting clinical signs were most often mydriasis and acute blindness. All cats had diffuse retinal degeneration as evidenced by increased tapetal reflectivity and retinal vascular attenuation. Absence of recordable electroretinographic responses suggested diffuse and extensive outer retinal disease. Vision returned in a few cats, but the retinal degeneration persisted or even progressed. Histopathology of two eyes revealed primarily outer retinal degeneration, with diffuse loss of the outer nuclear and photoreceptor layers, and hypertrophy and proliferation of the retinal pigment epithelium. CONCLUSION: Parenteral and/or oral [corrected] enrofloxacin is potentially retinotoxic in some cats, and may result in acute and diffuse retinal degeneration. Blindness often results, but some cats may regain vision. Practitioners should adhere closely to the manufacturer's current enrofloxacin dosage recommendation (5 mg/kg q 24 h), and continue clinical observations for this drug toxicity in cats.

Acute Disease↗
PubMed2002

Dynamic changes of status epilepticus-induced neuronal degeneration in the mediodorsal nucleus of the thalamus during postnatal development of the rat.

PURPOSE: Status epilepticus (SE) was previously found to induce damage in the mediodorsal nucleus of the thalamus (MD) in both adult and immature rats. This study was designed to describe age-related changes of SE-induced neuronal degeneration in this part of the brain. METHODS: SE was induced by LiCl/pilocarpine in five age groups of rats (P12-P25). Distribution of degenerating neurons was studied at various time intervals from 4 h up to 1 week using Fluoro Jade B (FJB) staining. For P12 and P25 rats, an interval of 3 months was added. RESULTS: Damaged neurons were found in all age groups during a 1-week period after SE. Patterns of neuronal degeneration, however, changed in an age-related manner. In animals at P12 and P15, FJB-labeled neurons were located in the central and lateral segment of the MD. In the P18 group, degenerating neurons occurred in all three segments of the MD, with a prevalence in central and lateral subdivisions. In contrast, in P21 and P25 rats, FJB-labeled neurons were predominantly located in the central and medial segments. Degenerating neurons were still present 3 months after SE in the medial segment in P25 animals, whereas no labeled neurons were detected in the P12 group at this time. CONCLUSIONS: Our data demonstrate that the pattern of neuronal degeneration in MD is mainly related to age at SE onset. In addition to damage occurring during the acute phase of SE, a population of degenerating neurons was detected in P25 animals during the chronic period 3 months after SE.

Aging↗
PubMed2006

Pre-wallerian degeneration in the neonatal brain following perinatal cerebral hypoxia-ischemia demonstrated with MRI.

AIM: Pre-Wallerian degeneration was studied in term and near-term neonates with hypoxic-ischemic brain injury, and related to neurodevelopmental outcome. SUBJECTS: Thirty-nine surviving patients with hypoxic-ischemic encephalopathy or seizures and MRI-documented brain abnormalities were included. Patients were grouped according to the MRI findings: group 1 (n = 23), ischemic stroke or watershed infarcts; group 2 (n = 8), lesions of the basal ganglia; group 3 (n = 8), predominantly white matter lesions. METHODS: Cranial MRI, including diffusion-weighted MRI, was performed between 1 and 10 days after birth. ADC maps were created, and presence or absence of pre-Wallerian degeneration in the cerebral peduncles was assessed. RESULTS: Of the 15 neonates with pre-Wallerian degeneration, 14 had permanent abnormalities of motor development, whereas 1 had a transient asymmetry. Six neonates with a poor outcome had no pre-Wallerian degeneration, which may be contributed to the timing of the MRI in 2. Eighteen neonates had no pre-Wallerian degeneration and a normal motor development. CONCLUSION: Pre-Wallerian degeneration of the cerebral peduncles in neonates with hypoxia-ischemia is almost invariably associated with a poor motor development. In neonates with abnormalities of the basal ganglia or white matter and a poor outcome, pre-Wallerian degeneration is less common than in neonates with stroke or watershed infarcts and a poor motor outcome.

Diffusion Magnetic Resonance Imaging↗
PubMed2003

NMDA-antagonist MK-801-induced neuronal degeneration in Wistar rat brain detected by the Amino-Cupric-Silver method.

The neurotoxic effect following a single intraperitoneal injection of MK-801 (10 mg/kg) in adult female Wistar rats at different survival times was studied with the 1994 version of de Olmos' Amino-Cupric-Silver (A-Cu-Ag) technique for detection of neural degeneration. In addition to the well documented somatodendritic degeneration observable in cortical olfactory structures, dentate gyrus, retrosplenial and sensory cortices, we detected this type of neuronal degeneration also in the main olfactory bulb, motor and anterior cingulate cortices, thalamus and cerebellum. Terminal degeneration, not reported by previous authors, was detected in cortical olfactory structures, hippocampal formation, sensory, infralimbic, prelimbic, agranular insular, ectorhinal, perirhinal and lateral orbital cortices. These results demonstrate that the A-Cu-Ag procedure is more efficient than other silver methods for detecting the degeneration induced by MK-801. In fact, the use of the A-Cu-Ag method has made it possible to infer the connectional relations between the damaged cell bodies and corresponding terminal degeneration. Our results also indicate that the A-Cu-Ag technique may be a suitable method for the staining of neurons undergoing apoptotic-like degeneration. The probable degenerative mechanism of MK-801 in the main olfactory system is discussed.

Animals↗
PubMed1997

Proton magnetic resonance spectroscopic imaging in progressive supranuclear palsy, Parkinson's disease and corticobasal degeneration.

We used proton magnetic resonance spectroscopic imaging (1H-MRSI) to assess the in vivo cortical and subcortical neuronal involvement in progressive supranuclear palsy, Parkinson's disease and corticobasal degeneration. This technique permitted the simultaneous measurement of compounds containing N-acetylaspartate (NA), choline (Cho), creatine-phosphocreatine (Cre) and lactate, from four 15-mm slices divided into 0.84-ml single-volume elements. The study included 12 patients with progressive supranuclear palsy, 10 with Parkinson's disease, nine with corticobasal degeneration and 11 age-matched normal control subjects. Regions of interest were selected from the brainstem, caudate, thalamus, lentiform nucleus, centrum semiovale, and from frontal, parietal, precentral, temporal and occipital cortices. Progressive supranuclear palsy patients, compared with control subjects, had significantly reduced NA/Cre in the brainstem, centrum semiovale, frontal and precentral cortex, and significantly reduced NA/Cho in the lentiform nucleus. Corticobasal degeneration patients, compared with control subjects, had significantly reduced NA/Cre in the centrum semiovale, and significantly reduced NA/Cho in the lentiform nucleus and parietal cortex. There were no significant differences between Parkinson's disease patients and control subjects, or between patients groups in any individual region of interest. In the parietal cortex of corticobasal degeneration patients, NA/Cho was significantly reduced contralateral to the most affected side. There were statistically significant group differences in the regional pattern of NA/Cre and NA/Cho reduction, comparing normal control subjects with all patient groups, Parkinson's disease with corticobasal degeneration, and Parkinson's disease with progressive supranuclear palsy. Although the occurrence of significant groups differences does not imply that it is possible to differentiate between individual patients using 1H-MRSI in progressive supranuclear palsy and corticobasal degeneration, detection of specific cortical and subcortical patterns of neuronal involvement is possible with this technique. We suggest that this regional pattern of neuronal involvement found in progressive supranuclear palsy and corticobasal degeneration may help in the diagnostic evaluation of affected individuals.

Aged↗