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PubMed1990

[Degeneration of articular cartilage of the ankle in cadavers studied by gross and radiographic examinations].

Eighty-two joints out of 41 cadavers were studied grossly in order to evaluate degenerative changes in talocrural articular cartilage with age. Cartilage degeneration was seen in 97.6% of joints. Cartilage degeneration associated with cartilage defects were seen at the age of 50 years. Thereafter, the severity of degeneration became more marked with aging. This severe cartilage degeneration was mainly found in medial and anterior regions in the talocrural joints. The anterior tibiofibular, deltoid, calcaneofibular and anterior talofibular ligaments of 40 joints of out 20 cadavers were grossly studied in order to establish the relationship between the degree of degeneration of these ligaments and that of articular cartilage. Grossly severe degeneration was present only in the anterior talofibular ligaments of 2 joints. Both joints presented severe cartilage degeneration in the medial region of the talocrural joint. Severe cartilage degeneration was present in 7 out of 30 joints (23%) whose ligaments were apparently normal upon gross observation. These cartilage degenerations were present in the medial and anterior regions of the talocrural joints.

Aged↗
PubMed1987

Ultrastructural analyses of afferent terminals in the subthalamic nucleus of the cat with a combined degeneration and horseradish peroxidase tracing method.

The synaptic organization of the feline subthalamic nucleus (STN) was studied electron microscopically. Following horseradish peroxidase (HRP) injections into the globus pallidus (GP) and electrolytic lesions of the nucleus tegmenti pedunculopontinus pars compacta (TCP) in the same cat, both degenerating and HRP-labeled terminals were found in the STN with abundant retrogradely HRP-labeled neurons. Degenerating terminals of TPC origin were medium-sized and characterized by asymmetric synaptic contacts. They synapsed widely on the STN neuronal surface, including the somata, dendrites of varying dimensions, dendritic spines and vesicle-containing processes. They formed 25.1%, 65.1%, 4.7%, and 4.7%, respectively, of all TPC efferent terminals. Some of the postsynaptic components were labeled with HRP. Occasionally both degenerating terminals and HRP-labeled terminals were in synaptic contact with the same HRP-labeled neuron: therefore, afferents of TPC and GP converge on the same STN projection neuron. In order to discover the origin of these HRP-labeled terminals, a mixed solution containing HRP and kainic acid was injected into the GP. Numerous degenerating terminals were observed to synapse with HRP-labeled STN neurons, but no HRP-labeled terminal was observed. These degenerating terminals were similar in appearance to the above-mentioned HRP-labeled terminals. They were characterized by their relatively large size, predominantly symmetric synapses, and preferential distribution on the somata and large or medium-sized dendrites. They formed 39.6%, 20.1%, and 31.1%, respectively, of all GP efferent terminals. Therefore, it became clear that both the HRP-labeled terminals of the first experiment and the degenerating terminals of the second experiment originated from the GP. Following surgical ablations of the primary sensorimotor cortex (Cx), some axon terminals in the STN showed degeneration. These degenerating terminals were small and formed asymmetric synapses mainly with dendritic spines, small dendrites and vesicle-containing processes. They formed 48.0%, 28.0%, and 12.0%, respectively, of all Cx efferent terminals. These electron microscopic investigations reveal the convergence of TPC and GP afferents and that STN projection neurons relay the TPC and pallidal inputs directly to the GP.

Afferent Pathways↗
PubMed1996

Reduced hyperalgesia in nerve-injured WLD mice: relationship to nerve fiber phagocytosis, axonal degeneration, and regeneration in normal mice.

The pathogenesis of neuropathic pain states is influenced by inflammatory factors associated with nerve injuries and may be mediated in part by the macrophage-dependent process of Wallerian degeneration. Macrophages play a dominant role in the Wallerian (axonal) degeneration that characterizes the painful chronic constriction injury model of neuropathy by liberating proinflammatory cytokines at the site of nerve injury. These cytokines directly affect the structural integrity of neural systems and have been implicated in the development of hyperalgesic states. We hypothesized that interference with the pathologic process of Wallerian degeneration would alter the development of the neuropathic pain state. To test this hypothesis, we studied the development of thermal hyperalgesia in the chronic constriction injury model of neuropathy using normal mice and mice of the WLD strain in which recruitment of macrophages to the site of nerve injury and Wallerian degeneration are delayed. We compared the onset and magnitude of the hyperalgesia with quantitative measures of nerve injury including the phagocytic cellular activity associated with Wallerian degeneration. In C57BL/6J (6J) mice, hyperalgesia peaked 3-10 days after placement of the ligatures, qualitatively matching the response previously reported for rats. In C57BL/WLD (WLD) mice, there was reduced hyperalgesia temporally associated with reduced numbers of phagocytic cells in the injured nerve. In injured WLD nerves there was a reduced rate of axonal degeneration compared to similarly injured 6J nerves. Regeneration was correspondingly delayed in the WLD animals. The results suggest that the process of Wallerian degeneration is a key factor in the pathogenesis of hyperalgesia. Continued development of mouse models of neuropathic pain will be important in exploring the molecular basis of neuropathic pain. Interference with the cellular mediators of Wallerian degeneration may be a useful therapeutic strategy that might modulate the onset and magnitude of hyperalgesia following nerve injury.

Animals↗
PubMed1989

Screening for mouse retinal degenerations. I. Correlation of indirect ophthalmoscopy, electroretinograms, and histology.

Mice with hereditary retinal degeneration have provided excellent models for human disease of the biochemical and physiological events occurring in retinal degeneration. Since a number of mouse models are available for other human conditions, more mouse retinal degenerations would be expected to be known; however, finding new models has proved difficult since the search has usually involved laborious histologic screening. We applied the clinical technique of indirect ophthalmoscopy to screen mice for retinal degeneration and then used electroretinography and histology to determine whether true retinal degeneration was present. A Dawson-Trick-Litzkow microfiber corneal electrode was used to record the electroretinogram since the fiber does not occlude the pupil in these small eyes. Normal control values were developed. As an example of the success of the technique, one strain, lethal spot (ls) on indirect ophthalmoscopy appeared to have a retinal degeneration, but these mice had a normal electroretinogram indicating a primary optic atrophy. Likewise, one ls heterozygote that was tested as a control animal and was not suspected of having a retinal degeneration had an abnormal electroretinogram and peripheral retinal degeneration.

Animals↗
PubMed1996

Microglial reactions to retrograde degeneration of tracer-identified thalamic neurons after frontal sensorimotor cortex lesions in adult rats.

Thalamic neuronal degeneration after neocortical lesions involve both anterograde and retrograde components. This study deals with the thalamic microglial response after neocortical aspiration lesions, using fluorogold fluorescent prelabeling, to identify retrogradely degenerating thalamocortical neurons, combined with histochemical or immunohistochemical staining of microglial cells. Adult male Wistar rats were injected with the retrograde fluorescent tracer fluorogold, in the right sensorimotor cortex (forepaw area) in order to retrogradely label thalamic neurons projecting to this area. After 1 week, the fluorogold injection site was removed by aspiration, axotomizing at the same time the thalamic projection neurons now retrogradely labeled with fluorogold. After 3, 7, 14, and 28 days the animals were killed and processed for nucleoside diphosphatase histochemistry or complement type 3 receptor immuno-histochemistry and class I and II major histocompatibility complex immunohistochemistry using OX42, OX18, and OX6 antibodies. The histological analysis showed a prominent and progressive nucleoside diphosphatase-, OX42-, and OX6-positive microglial cell response in the ventrolateral, posterior, and ventrobasal thalamic nuclei with ongoing retrograde and anterograde neuronal degeneration. Initially the reactive microglia had a bushy morphology and were succeeded by ameboid microglia and microglial cluster cells as the reaction progressed. However, in the reticular thalamic nucleus, which suffered exclusively anterograde neuronal degeneration, a different picture was seen with only bushy microglia. The neurons undergoing retrograde degeneration in the ventrolateral, posterior, and ventrobasal thalamic nuclei were retrogradely labeled by the fluorogold tracer. Individual nucleoside diphosphatase-, OX42-, or OX6-positive microglial cells extended long cytoplasmic processes surrounding fluorogold-labeled neurons and had in some cases apparently phagocytized these. Several microglial cells were thus double-labeled with nucleoside diphosphatase or OX42 and fluorogold. In addition, small nucleoside diphosphatase-positive, fluorogold-labeled perivascular cells were observed in the neocortex near the fluorogold-injected and ablated neocortical areas and in the ipsilateral thalamus. This study demonstrates: (1) that the microglial response to thalamic degeneration after neocortical lesion is graded with a limited reaction to the well-known massive anterograde axonal degeneration and a more extended reaction to the axotomy-induced retrograde cell death; and (2) that also perivascular cells and possibly macrophages may contribute to this reaction, as seen by uptake of fluorogold from axotomized neurons in the degenerating thalamic nuclei.

Acid Anhydride Hydrolases↗
PubMed1995

Tenascin-C expression during wallerian degeneration in C57BL/Wlds mice: possible implications for axonal regeneration.

Schwann cells in the distal stumps of lesioned peripheral nerves strongly express the extracellular matrix glycoprotein tenascin-C. To gain insights into the relationship between Wallerian degeneration, lesion induced tenascin-C upregulation and regrowth of axons we have investigated C57BL/Wlds (C57BL/Ola) mice, a mutant in which Wallerian degeneration is considerably delayed. Since we found a distinct difference in the speed of Wallerian degeneration between muscle nerves and cutaneous nerves in 16-week-old C57BL/Wlds mice, as opposed to 6-week-old animals in which Wallerian degeneration is delayed in both, we chose the older animals for closer investigation. Five days post lesion tenascin-C was upregulated in the muscle branch (quadriceps) but not in the cutaneous branch (saphenous) of the femoral nerve in 16-week-old animals. In addition myelomonocytic cells displaying endogenous peroxidase activity invaded the muscle branch readily whereas they were absent from the cutaneous branch at this time. We could further show that it is only a subpopulation of axon-Schwann cell units (mainly muscle efferents) in the muscle branch which undergo Wallerian degeneration and upregulate tenascin-C at normal speed and that the remaining axon-Schwann cell units (mainly afferents) displayed delayed Wallerian degeneration and no tenascin-C expression. Regrowing axons could only be found in the tenascin-C-positive muscle branch where they always grew in association with axon-Schwann cell units undergoing Wallerian degeneration. These observations indicate a tight relationship between Wallerian degeneration, upregulation of tenascin-C expression and regrowth of axons, suggesting an involvement of tenascin-C in peripheral nerve regeneration.

Animals↗
PubMed1990

Histological and ultrastructural evidence that D-amphetamine causes degeneration in neostriatum and frontal cortex of rats.

D-Amphetamine sulfate, continuously administered for 3 days subcutaneously via an implanted minipump, induced neural degeneration in Long-Evans and Sprague-Dawley rats at doses between 20 and 60 mg/kg/day. Using Fink-Heimer silver staining, axonal degeneration was detected in the neostriatum and the dorsal agranular insular cortex and degenerating pyramidal cells were observed in portions of the somatosensory neocortex in both strains. In contrast, dense axonal degeneration largely confined to layers 2 and 3 of frontal motor areas (Fr1, Fr2 and Fr3 of Zilles36) with occasional degenerating cells was seen reliably in Long-Evans rats but rarely in Sprague-Dawley rats. In the electron microscope, cortical degeneration consisted mainly of disrupted cell bodies and dark processes, including axons making asymmetric synapses. Damage in all cortical areas represents damage to non-monoamine neurons and processes since tyrosine hydroxylase and serotonin immunolabeling were normal. In contrast, the damage in neostriatum probably includes damage to dopamine axonal terminals since tyrosine hydroxylase immunolabeling was patchy with many swollen and distorted labeled axons. Serotonin and Leu-enkephalin labeling were normal. Electron microscopy confirmed that the neostriatum contained many tyrosine hydroxylase-labeled axons that were swollen and disrupted, although other labeled processes made normal symmetric synapses onto spines and dendrites. Additional degeneration found only in amphetamine-treated rats included many dark, shrunken profiles. Some of these appeared to be astrocytic processes and a few were myelinated axons, suggesting that some non-monoamine, possibly cortical afferents, are also degenerating in the neostriatum. Since similar degrees of behavioral activation, weight loss and lethality were seen in both strains, a genetic predisposition constrain amphetamine-induced motor cortex damage but not neostriatal damage.

Animals↗
PubMedDate not supplied

Unusual aspects of inflammation in the nervous system: Wallerian degeneration.

Wallerian degeneration in the PNS is accompanied by the rapid recruitment of monocytes, but monocytes do not invade CNS fibre tracts undergoing Wallerian degeneration. In recent years it has become apparent that the acute inflammatory response to cell degeneration in the CNS is unlike that in other tissues. We have been interested to learn why Wallerian degeneration does not provoke a typical inflammatory response. We investigated whether the vascular endothelial cells express adhesion molecules during Wallerian degeneration in PNS and CNS. We found that in the degenerating sciatic nerve there was upregulation of ICAM-1 and VCAM-1 expression on endothelial cells in the distal stump of the injured nerve as well as at the site of the lesion. However, in the degenerating optic nerve, the endothelium failed to upregulated these molecules in the distal stump of the nerve and ICAM-1 expression was only increased in the crush site. The lack of adhesion molecule expression on CNS endothelium molecules may be an explanation for the poor leukocyte recruitment during Wallerian degeneration in CNS when compared with PNS.

Animals↗
PubMed1990

Transganglionic degeneration of capsaicin-sensitive C-fiber primary afferent terminals.

Local treatment of rat peripheral nerves with capsaicin induces permanent impairment of afferent C-fiber functions and changes in the response properties of spinal dorsal horn neurons. In this study a new experimental approach, the "capsaicin gap" technique, has been utilized in an attempt to unravel pathomorphological alterations which commence in the domain of primary sensory neurons as a consequence of perineural treatment with capsaicin. The technique relies on the facts that peripheral nerves in the spinal dorsal horn are represented in a strict somatotopic manner, and on the observation that in the adult rat systemic injection of appropriate doses of capsaicin results in a selective degeneration of primary afferent fibers within Rexed's laminae I and II of the spinal cord. We have assumed that, if treatment of a peripheral nerve with capsaicin results in an irreversible destruction of primary afferent terminals related to that nerve, then the corresponding spinal projection areas will be free of degeneration following a subsequent systemic injection of capsaicin. The topographical distribution of degenerating axon terminals, induced by a systemic injection of capsaicin, was studied within the lumbar spinal cord of rats whose sciatic nerves had been treated with capsaicin or its vehicle one to three months previously. In the dorsal horn ipsilateral to the vehicle-treated nerve, axon terminal degeneration was found in the entire mediolateral extent of Rexed's laminae I and II. In contrast, in the dorsal horn ipsilateral to the capsaicin-treated nerve, virtually no degeneration was observed in areas which correspond to the projection territories of sciatic afferents. It is concluded that the central terminals of capsaicin-sensitive sciatic afferents underwent transganglionic degeneration as a result of prior perineural treatment with capsaicin, and a subsequent systemic injection of this neurotoxin therefore failed to cause axon terminal degeneration in somatotopic areas served by the treated nerve. Comparative quantitative morphometric analysis of cell populations of dorsal root ganglia related to capsaicin- or vehicle-treated nerves disclosed (1) a marked reduction in the proportion of small-sized neurons, (2) a fall of about 80% in the percentage of neurons which undergo degeneration after the systemic injection of capsaicin, and (3) a marked decrease in the total number of neurons in ganglia ipsilateral to the capsaicin-treated nerves. Quantitative electron microscopic studies on saphenous nerves treated perineurally with capsaicin revealed a 32% reduction in the number of unmyelinated axons as compared with the controls, whereas the number of myelinated fibers was unchanged.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed2003

Non-apoptotic neurite degeneration in apoptotic neuronal death: pivotal role of mitochondrial function in neurites.

The length and thinness of neurites render them greatly susceptible to a variety of insults. Accumulating evidence suggests that neurite degeneration is not a passive, but an active and causative, event in some neurodegenerative diseases. Nonetheless, the mechanisms underlying neurite degeneration remain largely unknown. To elucidate the relevant mechanisms, we employed a mutant C57BL/Wld mouse with a unique phenotype of resistance to Wallerian degeneration, and separately analyzed the destruction of cell soma and neurites following treatment with vinblastine, a microtubule-disrupting agent, in superior cervical ganglion neurons. Vinblastine induced macromolecular synthesis-dependent cell death, which was indistinguishable between the wild-type and mutant mice. Evidence for a loss of mitochondrial cytochrome c, caspase activation, and nuclear fragmentation, has indicated that this type of cell death is entirely apoptotic. Consistent with this, the ATP level in the cell soma was well maintained and indistinguishable between wild-type and mutant mice. In neurites of wild-type neurons, vinblastine induced an early loss of mitochondrial membrane potential (MMP) and ATP depletion preceding caspase-independent degeneration, suggesting that this type of neurite degeneration is principally non-apoptotic. In contrast, neurites of mutant neurons were markedly resistant to vinblastine-induced degeneration, and both the MMP and the ATP content in the neurites were well maintained. Exposure of mutant neurons to carbonyl cyanide m-chlorophenyl-hydrazone, an uncoupler, caused extreme neurite degeneration following rapid MMP loss. Collectively, our findings suggest that: 1) neurite degeneration is regulated through a non-apoptotic process achieved by mitochondrial dysfunction in neurites; 2) the mitochondrial functional status is controlled separately in neurites and in the neuronal soma.

Adenosine Triphosphate↗
PubMed2000

Genetic association of manganese superoxide dismutase with exudative age-related macular degeneration.

PURPOSE: To elucidate whether any polymorphic genes for xenobiotic-metabolizing and antioxidant enzymes are associated with the development of exudative age-related macular degeneration. METHODS: A hospital-based case-control study was performed on a consecutive series of 102 Japanese patients with the exudative form of age-related macular degeneration who were recruited between 1993 and 1998 in the Kagoshima University Hospital. Controls were 200 systemically healthy individuals who had no senescent ocular disorders and were over 50 years of age. There was no evidence of age-related macular degeneration in the 200 controls. Genomic DNA from peripheral bloods was examined using polymerase chain reaction and defined for the genetic polymorphisms of cytochrome P-450 1A1, glutathione S-transferases, microsomal epoxide hydrolase, and manganese superoxide dismutase. RESULTS: We found a significant association of manganese superoxide dismutase gene polymorphism, valine/alanine polymorphism at the targeting sequence of the enzyme, with age-related macular degeneration. The patients had an increased frequency of alanine allele and alanine/alanine genotype (odds ratio = 10.14, 95% confidence interval = 4.84 to 2.13; P =.0005 after Bonferroni correction). We also observed a weak association of microsomal epoxide hydrolase exon-3 polymorphism with age-related macular degeneration (odds ratio = 2.20, 95% confidence interval = 4. 02 to 1.20; P =.020 after Bonferroni correction). Cytochrome P-450 1A1, glutathione S-transferases, and microsomal epoxide hydrolase exon-4 were polymorphic, but their genotype frequency distributions did not show a statistically significant difference between the patients and controls. CONCLUSIONS: The results suggest that manganese superoxide dismutase gene polymorphism is associated with exudative age-related macular degeneration. Microsomal epoxide hydrolase is another enzyme that may be associated with the disease. The exudative form of age-related macular degeneration may have genetic risk factors against oxidative stress and/or effects of xenobiotics. Further association studies in other polymorphic genes for xenobiotic-metabolizing enzymes are needed to elucidate the environmental-genetic interaction in the underlying cause of age-related macular degeneration.

Aged↗
PubMed1995

A twin study of age-related macular degeneration.

PURPOSE: To determine the importance of genetic factors in age-related macular degeneration by using a twin study to compare the concordance of age-related macular degeneration in monozygotic and dizygotic twin pairs. METHODS: We prospectively examined 134 consecutive twin pairs and two triplet sets for age-related macular degeneration. The zygosity was determined by genetic laboratory tests. RESULTS: The concordance of age-related macular degeneration was 100% (25 of 25) in monozygotic and 42% (five of 12) in dizygotic twin pairs. The other twins or triplets had no macular changes of age-related macular degeneration. CONCLUSIONS: The statistically significant higher concordance of age-related macular degeneration in monozygotic than in dizygotic twin pairs and the clinical heterogeneity of age-related macular degeneration strongly suggest the importance of genetic and nongenetic factors, respectively, in age-related macular degeneration.

Adult↗
PubMed1998

Presumed macular choroidal watershed vascular filling, choroidal neovascularization, and systemic vascular disease in patients with age-related macular degeneration.

PURPOSE: To investigate the possible association of presumed macular choroidal watershed vascular filling (PMWF), choroidal neovascularization, and systemic vascular disease in patients with age-related macular degeneration. METHODS: In a retrospective study, we evaluated 74 randomly selected indocyanine green videoangiograms of 74 patients with age-related macular degeneration. We also reviewed the charts of 20 randomly selected, age-matched control patients without age-related macular degeneration, initially referred for uniocular conditions, and subsequently performed indocyanine green videoangiography on their normal fellow eyes. We evaluated these videoangiograms for the presence of PMWF, manifesting as characteristic early choroidal hypofluorescence and its relation to choroidal neovascularization when present. Additionally, the incidence of hypertension, coronary artery disease, peripheral vascular disease, and diabetes mellitus was determined. RESULTS: Forty-one (55.4%) of 74 patients with age-related macular degeneration vs three (15.0%) of 20 normal control patients exhibited PMWF on indocyanine green videoangiography (P = .0014). Of the 61 patients with age-related macular degeneration and choroidal neovascularization, 36 (59.0%) exhibited PMWF on videoangiography. Associated choroidal neovascularization arose from the PMWF zone in 33 (91.7%) of these cases. Hypertension was observed in 24 (58.5%) of 41 patients with age-related macular degeneration and PMWF vs nine (27.3%) of 33 patients with age-related macular degeneration who did not exhibit PMWF (P = .007). CONCLUSIONS: An increased incidence of PMWF occurs in patients with age-related macular degeneration with a possible predisposition for the development of associated choroidal neovascularization. Additionally, PMWF may be accentuated by associated hypertensive choroidal microvascular insult.

Aged↗
PubMed2003

Participation of neurofilament proteins in axonal dark degeneration of rat's optic nerves.

Neurofilaments (NF) are neuronal intermediate filaments formed by three different subunits: high (NF-H), medium (NF-M) and light (NF-L). They are responsible for the determination and maintenance of axon caliber. Accumulation of NF or their immunoreactive products are components of several neurodegenerative disease lesions, such as neurofibrillary tangles, Lewy bodies and the spheroids of amyotrophic lateral sclerosis. Also, cytoskeletal breakdown is one of the first ultrastructural changes occurring after nerve crush or section. In the present study, Wistar rats were subjected to bilateral enucleation to induce Wallerian degeneration of optic nerve fibers and perfused 24 h, 48 h and 1 week later. Optic nerve segments were processed for electron microscopy (EM), light microscopy immunofluorescence (LM) and immunoelectronmicroscopy (IEM) for NF subunit detection. LM for NF of control nerves showed a slightly different pattern and intensity for each subunit, with more intense staining of NF-M and NF-H and less intense staining of NF-L. This reaction did not change considerably at 48 h, but was severely reduced 1 week after enucleation. Results of EM showed fibers in: (1) partial cytoskeleton degeneration or (2) watery degeneration or (3) dark degeneration. The number of dark degenerating axons was statistically higher at the latest time-interval studied. Neurofilament clumping areas and dark degenerating axons showed positive immunostaining for the three neurofilaments subunits when examined by IEM. These results suggest that dark degenerating axons develop from areas of neurofilament aggregation. We may also conclude that NF proteins participate in the process of axonal dark degeneration.

Animals↗
PubMed1996

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

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

Animals↗
PubMed1990

Retinal degeneration in the dog and cat.

Retinal degenerations in the dog and cat are an important cause of blindness in these species. Particularly in the dog, many retinal degenerations, collectively called progressive retinal atrophy, seen in clinical practice are inherited. The clinical signs, electrophysiological findings, pathology, and underlying biochemical defects in the retina vary from breed to breed. Specific categories of inherited retinal degeneration are now recognized, and classified into early onset photoreceptor dysplasias, late-onset retinal degenerations, or retinal degenerations secondary to primary RPE dystrophy. As new inherited retinal degenerations are reported in different breeds they can generally be assigned to one these categories. Other causes of retinal degeneration include nutritional deficiencies, glaucoma, inflammation, ischemia, and toxins. Idiopathic retinal degeneration occurs in the dog with some frequency.

Animals↗
PubMed1990

Rescuing neurons from trans-synaptic degeneration after brain damage: helpful, harmful, or neutral in recovery of function?

Certain instances of neuronal degeneration secondary to brain damage might be functionally beneficial, and steps taken to protect against such degeneration may adversely affect behavioural outcome. After unilateral damage to the intrinsic neurons of the striatum, which includes GABAergic striatonigral projections, delayed trans-synaptic degeneration occurs in the ipsilateral substantia nigra pars reticulata (SNr). This degeneration was prevented by a 2-week regimen of muscimol delivered intraventricularly via osmotic minipumps. Muscimol is a direct-acting GABA agonist that presumably substituted for the absent GABA at the interface between the degenerating striatonigral GABAergic terminals and the GABAergic receptors located on SNr neurons. Sensorimotor asymmetry tests sensitive to unilateral striatal damage were carried out for 4 weeks to determine the functional consequences of the sparing of SNr neurons. Recovery of function was not improved. Instead, tactile extinction and hemiplegia were exaggerated in the contralateral forelimb. Other impairments were unaffected by the muscimol. The experiment was repeated using diazepam, rather than muscimol, to address the possibility that the disruptive effects of muscimol might reflect a more general disruptive influence on recovery processes. Diazepam, which has been shown in our lab to disrupt recovery of function after cortical lesions and to potentiate lesion-associated atrophy in remote subcortical structures, is an indirect-acting GABAergic agonist that requires GABA for its mechanism of action. Because GABAergic terminals at the SNr were destroyed, diazepam (as expected) failed to prevent SNr degeneration. Although diazepam presumably enhanced GABAergic synaptic activity in other brain regions, diazepam had no significant effect on postoperative behavioural function. Apparently, in the first experiment, the prevention of SNr degeneration per se was instrumental in the detrimental effects of muscimol. The rescued SNr neurons may have contributed to dysfunction because they lacked inhibitory GABAergic control. Transsynaptic degeneration secondary to brain damage was discussed as it might relate to release phenomena and their treatment by surgery or transmitter blocking agents in the clinical literature.

Animals↗
PubMed1986

[Can the use of infrared photography give evidence of the prognosis of hereditary macular degeneration?].

The question as to whether infrared photography can help determine the prognosis of hereditary macular degeneration cannot be answered simply in the affirmative or negative. Changes in the retinal surface layers are not detected by infrared photography. Therefore, no statement can be made regarding the prognosis of these types of macular degeneration. As far as macular degenerations of the deeper layers of the fundus are concerned, it cannot be stated as a general rule that severe changes in the infrared photograph imply a worse prognosis. Rather, one has to differentiate on the basis of the form and limitations of the defects. Infrared photography furnishes prognostic information by facilitating differential diagnosis between the prognostically favorable central areolar choroidal atrophy and the unfavorable progressive diffuse atrophy of the choroid. Further pointers to the prognosis can be obtained by differentiation between Stargardt's macular degeneration and diseases with favorable prognoses, which appear similar at the fundus, namely central areolar choroidal atrophy and dominant macular degeneration, which has a relatively benign course. In Stargardt's macular degeneration infrared photography seems to provide the following prognostic information: whether the degeneration is limited to the macula; whether flavimaculatus spots appear, or whether diffuse chorioatrophic degeneration will occur.

Atrophy↗