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PubMed2005

Functional consequences of retinal degeneration in spatial orientation in C3H wild type and Lurcher mutant mice.

Lurcher mutant mice represent a model of genetically determined olivocerebellar degeneration. In the C3H strain there is also hereditary retinal degeneration. The aim of this work was to assess, whether the retinal degeneration influences spatial orientation and results of the spatial learning tasks. Two experiments in the Morris water maze were arranged. First, mice learned to find a platform position, which was linked to two labels on the periphery of the maze. In the second experiment the platform was removed and swimming velocity and preference of central or peripheral zone of the maze were assessed. Presence of the retinal degeneration was detected histologically. Both Lurcher mutant and wild type mice that exhibited long latencies in the first experiment were affected with the retinal degeneration, while animals that performed the trial well, had normal retina. Swimming velocity was not changed substantially. The maze exploration strategy was different in mice with and without the retinal degeneration.

Animals↗

PubMedDate not supplied

Glutathione S-transferase M1, T1, and P1 gene polymorphism in exudative age-related macular degeneration: a preliminary report.

PURPOSE: To elucidate whether the gene polymorphisms of glutathione S-transferase (GST) M1, T1, and P1 are associated with the development of exudative age-related macular degeneration. METHODS: The authors genotyped 35 white patients with exudative age-related macular degeneration and 159 healthy controls. Genomic DNA from peripheral blood was examined using polymerase chain reaction and defined for the genetic polymorphisms of GST. RESULTS: No association was observed between GSTM1, GSTT1, and GSTP1 polymorphisms and age-related macular degeneration risk (p>0.05). The frequencies of the combination of the GSTM1 (null) and GSTP1 (mutant), GSTM1 (null), and GSTT1 (null) genotype polymorphisms in patients with exudative age-related macular degeneration differed greatly from those of the control group (p=0.001 OR [95% CI]: 7.70 [2.28-25.98] and p=0.007 OR [95% CI]: 3.88 [1.51-10.02], respectively). CONCLUSIONS: The present study suggests that the GSTM1 (null) and GSTT1 (null), GSTM1 (null), and GSTP1 (mutant) combinations may be a genetic risk factor for the development of exudative age-related macular degeneration. However, the potential role of GST polymorphisms as a marker of susceptibility to age-related macular degeneration needs further studies in a larger number of patients.

Aged↗

PubMed2006

Neural functional and morphological consequences of retinal degeneration in C3H Lurcher mutant and wild type mice.

Lurcher mutant mice represent a model of olivocerebellar degeneration associated with the total functional elimination of the cerebellar cortex. The affected animals suffer from cerebellar ataxia and worsening of cognitive functions. Healthy littermates of Lurchers-wild type mice serve as controls. Except mentioned patterns some animals derived from the C3H strain exhibit signs of a hereditary retinal degeneration. The impact of the retinal degeneration on visuospatial abilities and on the neuronal morphology in visual projection of both C3H Lurcher mutant and wild type mice has been studied in this work. The Morrris water maze was used for examination of spatial learning when the animals learned to find a platform hidden under the water surface. Time of reaching the platform (escape latency) in individual experimental days as well as the swimming velocity was measured and the strategy of maze exploration was assessed. The presence of the retinal degeneration was proved histologically by means of classical hematoxillin-eosin method. The neurohistological examination of the superior colliculus and visual cortex was performed using a Ramón-Moliner modification of the Golgi method. The results obtained showed that retinal degeneration influenced the strategy of the maze exploration and caused generally worse results. The histological examination of eyes in animals with bad results confirmed presence of the retinal degeneration. The neurohistological examination of the brain visual projections of animals affected with the retinal defect showed most detectable changes in dendritic spines of the V1 cortex (lower density in general and less immature types).

Animals↗

PubMed1986

Induction of rat E and chicken A-I apolipoproteins and mRNAs during optic nerve degeneration.

Apolipoprotein synthesis was measured in control optic nerves and optic nerves undergoing Wallerian degeneration. After short term organ culture with radiolabeled amino acid, optic nerve extracts were reacted with antiserum to rat or chicken apolipoproteins. Immunoprecipitates were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In the degenerating rat optic nerve, apo-E synthesis increased from 0.30 to 0.90% of newly synthesized protein and from 0.45 to 1.4% of secreted protein. A DNA-excess solution hybridization assay was constructed to measure the absolute amount of apo-E mRNA in control and degenerating optic nerves. Paralleling the increase in apo-E protein synthesis, the absolute amount of apo-E mRNA was elevated 3- to 4-fold after enucleation. Similar to rat apo-E, apo-A-I synthesis was increased in degenerating chicken optic nerve. Chicken apo-A-I represented 0.65 and 3.5% of newly synthesized protein from control and enucleated optic nerves, respectively. Apo-A-I increased from 0.85 to 5.5% of secreted protein following enucleation. Using in vitro translation to quantitate relative amounts of chicken apo-A-I mRNA, enucleated optic nerve apo-A-I mRNA content was increased 5-fold. These results suggest that local apolipoprotein synthesis may be involved in the mobilization of myelin cholesterol which occurs during Wallerian degeneration. The similar response of the rat and chicken to increase optic nerve apolipoprotein synthesis during degeneration supports the idea that avian peripheral apo-A-I and mammalian peripheral apo-E may be performing functions common to both classes of animals.

Animals↗

PubMed1987

Rod ERGs in retinitis pigmentosa and cone-rod degeneration.

Rod amplitudes as a function of retinal illuminance were analyzed by determining the parameters of the best fit Naka-Rushton function for 15 normal subjects, 25 patients with rod-cone degeneration, and 10 patients with cone-rod degeneration. Rod b-wave implicit times were analyzed by determining the best linear fit to log retinal illuminance. Retinal illuminances necessary for a criterion b-wave implicit time and for a half-maximum amplitude response (log k) were highly correlated indices of rod sensitivity. Both measures were normal or near normal in patients of all ages with cone-rod degeneration, but significantly elevated in patients with rod-cone degeneration. These results suggest that the underlying mechanisms of rod degeneration are fundamentally different in these two forms of hereditary retinal degeneration.

Adolescent↗

PubMed1995

Axotomy-induced axonal degeneration is mediated by calcium influx through ion-specific channels.

We examined the role of extracellular calcium entry, the possible involvement of axonal calcium channels, and the potential protective effect of calcium channel and calpain antagonists in axotomy-induced axonal degeneration using murine dorsal root ganglia in cell culture. We found that calcium entry is both necessary and sufficient to induce axonal degeneration after axotomy, and may be inhibited by cobalt, manganese, dihydropyridines, and bepridil. Tetrodotoxin and omega-conotoxin are ineffective in preventing axonal degeneration. The activation of calpains also appears to be necessary and sufficient for axonal degeneration to proceed, and can be blocked with membrane-permeant leupeptin analogs and the oxirane aloxistatin. Although other calcium-activated events may occur, it appears that inhibition of calpain is sufficient to preserve the axon at the light microscope level, and to prevent axonal cytoskeleton degradation as detected by immunofluorescent staining. Our results suggest that axonal degeneration after axotomy involves the following sequence of events: (1) a lag-period after axotomy prior to the onset of axonal degeneration, (2) entry of calcium into the axon through an intact axolemma via a calcium-specific ion transport mechanism, (3) activation of calcium-dependent effector molecules such as calpains, (4) degradation of the axonal cytoskeleton. The details of the second step require further elucidation, and are of particular interest because this step is a potential target for therapies directed towards peripheral neuropathies.

Animals↗

PubMed1996

Gene therapy in the adult primate brain: intraparenchymal grafts of cells genetically modified to produce nerve growth factor prevent cholinergic neuronal degeneration.

Gene therapy may be a useful means of delivering substances to the brain that are capable of preventing neuronal degeneration. In the present experiment, we determined whether intraparenchymal transplants of primary autologous cells genetically modified to produce nerve growth factor (NGF) would prevent injury-induced degeneration of cholinergic neurons. Cultured primary monkey fibroblasts were genetically modified to produce human NGF, and secreted 13.2 ng NGF/10(6) cells/h in vitro. Adult monkeys then underwent fornix transections to induce degeneration of basal forebrain cholinergic neurons, and received autologous grafts of either NGF-producing or control, beta-galactosidase-producing fibroblasts directly into the basal forebrain region. One month later, 61.7 +/- 8.9% of cholinergic neurons remained indentifiable in NGF-graft recipients compared to 26.2 +/- 5.0% in control graft recipients (P < 0.02). Neuronal protection correlated with the accuracy of graft placement: up to 92% protection from neuronal degeneration occurred when NGF-secreting grafts were accurately placed immediately adjacent to injured neurons. Thus, intraparenchymal NGF delivery to the adult primate brain by gene transfer can prevent the degeneration of basal forebrain cholinergic neurons. Gene therapy can target intraparenchymal brain sites for regionally specific neurotrophin delivery, thereby avoiding limitations imposed by diffusion of substances across the blood-brain barrier and through CNS parenchyma, while avoiding adverse effects of neurotrophic factors delivered in a non-directed manner to the central nervous system. The delivery of NGF by gene transfer to the brain merits further study as a means of preventing cholinergic neuronal degeneration in human disorders such as Alzheimer's disease.

Animals↗

PubMed1996

Age-dependent neuronal and synaptic degeneration in mice transgenic for the C terminus of the amyloid precursor protein.

The molecular basis for the degeneration of neurons and the deposition of amyloid in plaques and in the cerebrovasculature in Alzheimer's disease (AD) is incompletely understood. We have proposed that one molecule common to these abnormal processes is a fragment of the Alzheimer amyloid precursor protein (APP) comprising the C-terminal 100 amino acids of this molecule (APP-C100). We tested this hypothesis by creating transgenic mice expressing APP-C100 in the brain. We report here that aging (18-28 month) APP-C100 transgenic mice exhibit profound degeneration of neurons and synapses in Ammon's horn and the dentate gyrus of the hippocampal formation. Of the 106 transgenic mice between 8 and 28 months of age that were examined, all of those older than 18 months displayed severe hippocampal degeneration. The numerous degenerating axonal profiles contained increased numbers of neurofilaments, whorls of membrane, and accumulations of debris resembling secondary lysosomes near the cell body. The dendrites of degenerating granule and pyramidal cells contained disorganized, wavy microtubules. Cerebral blood vessels had thickened refractile basal laminae, and microglia laden with debris lay adjacent to larger venous vessels. Mice transgenic for Flag-APP-C100 (in which the hydrophilic Flag tag was fused to the N terminus of APP-C100) showed a similar degree of neurodegeneration in the hippocampal formation as early as 12 months of age. The 45 control mice displayed only occasional necrotic cells and no extensive cell degeneration in the same brain regions. These findings show that APP-C100 is capable of causing some of the neuropathological features of AD.

Age Factors↗

PubMed1997

Genistein, a protein tyrosine kinase inhibitor, ameliorates retinal degeneration after ischemia-reperfusion injury in rat.

PURPOSE: The authors sought to determine the effect of genistein, a naturally occurring protein tyrosine kinase inhibitor, in a model of ischemia-reperfusion injury in the rat retina. METHODS: Ischemia-reperfusion injury was induced by temporary optic nerve ligation. A dose of 0.034 mg, 0.34 mg, and 3.4 mg of genistein or dimethyl sulfoxide (DMSO) alone was injected intraperitoneally 1 hour before the ligation of the optic nerve and just after the start of reperfusion. After 48 hours of reperfusion, the effect of genistein on overall protein tyrosine phosphorylation in the retina was studied using Western blot analysis. After 168 hours, the effect of increasing doses of genistein on retinal degeneration was examined by quantitative morphometric analysis of histologic sections of the retina. RESULTS: The authors found that tyrosine phosphorylation was increased after 48 hours of reperfusion in the ischemia-reperfusion-injured eyes treated with DMSO alone. A severe inner retinal degeneration was observed in the animals treated with DMSO alone after 168 hours of reperfusion. The treatment with 3.4 mg genistein inhibited the increase in tyrosine phosphorylation and protected the eyes significantly from the induced ischemic retinal degeneration by morphometric analysis of the mean thickness of the inner limiting membrane to the outer limiting membrane, the inner plexiform layer, and the inner nuclear layer (P < 0.02). Treatments with lower amounts of genistein (0.034 mg and 0.34 mg) did not show a significant protection of retinal degeneration after the injury. CONCLUSIONS: Systemic administration of high dose of genistein, a dietary-derived isoflavone, can ameliorate an ischemia-reperfusion-induced retinal degeneration. Genistein may be useful to prevent neuronal degeneration in the inner retina as a result of ischemic injury.

Animals↗

PubMed1997

Neurochemical development of the degenerating rat retina.

The Royal College of Surgeons' (RCS) rat is an experimental model for a group of hereditary retinal diseases commonly called retinitis pigmentosa. We used postembedding immunocytochemistry to determine the localisation of glutamate, gamma-aminobutyric acid (GABA), glycine, aspartate, glutamine, taurine, and arginine in the RCS rat retina during postnatal development. In addition, we evaluated the uptake characteristics for the three dominant amino acid neurotransmitters, glutamate, GABA, and glycine. Whereas, cellular localisation of all amino acids was similar to control retinas, there were major changes in the level of immunoreactivity, even before eye opening, and well before the onset of visibly detectable photoreceptor degeneration. Two major patterns emerged. First, neurochemical changes evident before degeneration, involving the amino acids glutamate, GABA, aspartate, glutamine, and arginine. Second, neurochemical changes that become evident during photoreceptor degeneration involving the amino acids taurine and glycine. Anomalies in uptake characteristics also become evident during the degeneration phase and are likely to reflect changes in cellular function as a consequence of the degeneration process. Neurochemical changes evident before photoreceptor degeneration involve both glutamate and GABA manufacturing pathways. Müller's cells displayed elevated levels of glutamine and arginine from an early age, and the neuroblastic layer in the RCS retina showed high glutamate levels. Modified aspartate immunoreactivity began at postnatal day 11 and is consistent with altered metabolic activity. These results suggest that amino acid neurochemistry is different in the RCS rat retina from an early age, which may indicate an underlying metabolic defect affecting multiple cell classes.

Aging↗

PubMed1997

Ultrastructural pathology of degenerating "dark" granule cells in the hippocampal dentate gyrus of adrenalectomized rats.

Adrenalectomy-evoked delayed degeneration and death of granule cells in the hippocampal dentate gyrus (DG) of the rat brain were studied by means of electron microscopy and a recently elaborated silver method that selectively stains the "dark", collapsed neurons in a Golgi-like manner. At the light microscopic level, the silver technique revealed degenerating granule cells located exclusively in the dentate gyrus; other glucocorticoid receptor-containing regions of the brain were not affected. The silver-stained cell bodies were shrunken, most of the dendrites had a beaded appearance, and the stained axons could be traced along their route to the CA3 pyramidal neurons of the hippocampus. The analysis of 2.5 microns thick Epon-embedded sections stained with toluidine blue revealed hyperchromatic, dark granule neurons and their remains and a heavy glial activity in the vicinity of collapsing neuronal profiles. At the ultrastructural level, early and late stages of neuronal degeneration were observed. The early phase was characterized by markedly increased electron density, a massive shrinkage of the whole somato-dendritic domain, vacuolization of mitochondria, swelling of the nucleolus and condensation of the nuclear chromatin. In the late stage, subcellular organelles were hardly recognizable due to the extremely high electron density and dramatic shrinkage of the cytoplasm. These profiles exhibited disintegration of the cellular organelles and loss of their afferents. Concomitantly, disintegration of granule cell dendrites (clasmatodendrosis) and lifting of "dark" mossy fibers from cell bodies and dendrites of CA3 pyramidal neurons were observed. In the latter cells, this partial denervation caused no apparent signs of ultrastructural alterations. Proliferation of astrocytes and microglial cells was also obvious as they engulfed and eliminated the degenerating neuronal elements. Degenerating neurons frequently occurred adjacent neurons with normal morphology. These morphological features indicate that the delayed degeneration of hippocampal granule cells following adrenalectomy might proceed through a cytoskeletal collapse terminating in cell death.

Adrenal Glands↗

PubMed1997

A pathologic study of degeneration of the rod and cone populations of the rhodopsin Pro347Leu transgenic pigs.

PURPOSE: Transgenic pigs with rhodopsin (Pro347Leu) mutation exhibited rod-cone degeneration. We compared the pathologic characteristics of the rod degeneration versus those of the cone cells. METHODS: The posterior and peripheral retinas of these transgenic pigs of age 4, 6, 8, 12, 24 and 33 weeks and normal pigs of age 4 and 8 weeks were studied by light and EM and morphometry. RESULTS: The pathologic changes observed in the posterior and peripheral retinas of the transgenic pigs could be conveniently described in 3 phases: I) an initial phase of rapid and extensive degeneration of the rod cells in the first 6 weeks of age; II) an acute phase of cone cell degeneration involving approximately half of the population and lingering rod degeneration in the 6 to 12 weeks of age; and III) a partial cone recovery to be followed by a chronic degenerative phase of the remaining cones cells from 12 to 33 weeks of age. CONCLUSION: Our study showed that the degenerative changes of rod cells could be differentiated from those of the cone cells. Cone and rod populations degenerated along different time schedule with different pathologic features. Hence, treatment for retinitis pigmentosa might vary with the different stages of the disease.

Animals↗

PubMed1998

Retinal degeneration in the rd mouse in the absence of c-fos.

PURPOSE: Apoptosis is the final common death pathway of photoreceptors in light-induced retinal degeneration and in several animal models for retinal dystrophy. To date, little is known about gene regulation of apoptosis in the retina. The expression of the immediate early gene c-fos is upregulated concomitant with apoptosis in light-induced photoreceptor degeneration and in the rd mouse, an animal model for inherited retinal degeneration. In a recent study it was shown that c-Fos is essential for light-induced apoptosis of photoreceptors in vivo. To determine whether c-Fos is also involved in the apoptotic pathway of inherited retinal degeneration, rd/rd, c-fos -/- double-mutant mice have been generated. METHODS: Double-mutant mice (rd/rd, c-fos -/-) were crossbred from c-fos+/- mice and rd/rd mice. Their genotype was determined by polymerase chain reaction analysis of genomic DNA. Wild-type control mice and homozygous rd mice were killed at 2-day intervals from postnatal day (P)9 through P21. Double-mutant mice were killed at postnatal days P9, P11, P13, P15, and P21. To determine levels of apoptosis in the retina, eyes were enucleated and processed for light microscopy and in situ nick-end labeling. Total retinal DNA was extracted from isolated retinas for DNA fragmentation analysis. RESULTS: Morphologic, histochemical, and biochemical analyses showed that the time course of apoptosis and the outcome of photoreceptor degeneration in rd/rd, c-fos-/- double-mutant mice was indistinguishable from that in rd mice carrying functional c-fos. CONCLUSIONS: These data suggest that in contrast to its role in light-induced photoreceptor degeneration, c-Fos is not essential for apoptosis in the rd mouse.

Animals↗

PubMed1979

Terminal proliferation in the partially deafferented dentate gyrus: time courses for the appearance and removal of degeneration and the replacement of lost terminals.

The time courses for the appearance and removal of degenerating terminals and the loss and reappearance of intact terminals were investigated in the partially denervated inner molecular layer of the dentate gyrus of the adult rat. Dense degeneration was evident in the neuropil within 26 hours following contralateral hippocampectomy. These profiles increased rapidly in number until the maximal degree was reached at two to three days postlesion, after which the degenerating terminals were quickly removed from the neuropil. A more rapid rate of removal occurred during the 3-to 5-day survival period than from 6 to 50 days postlesion. The intact terminal population dropped 35% within two days of the lesion and remained at this level until six to eight days postlesion when the number began to steadily increase. The time course for this reappearance can be divided into two phases: a period of rapid terminal addition from 6 to 15 days followed by a phase of slower acquisition. This recovery continued until the normal synaptic density was regained by 50 to 65 days postlesion. These results indicate that a substantial proportion of degenerating endings are removed well in advance of the time at which terminal proliferation begins, suggesting that certain changes other than merely the removal of competitive inputs must take place prior to growth of new terminals. Possible explanation suggested by the present results for the delay in the onset of sprouting include: (1) an absence of appropriate postsynaptic targets during the 2-to 5-day postlesion period and (2) inhibition of axonal growth by the glial cells which are phagocytizing the degenerating products. Beyond the sixth postlesion day the rate at which new terminals appear does correlate with the rate at which degeneration is removed. This suggests that once underway the time course for sprouting may be determined by the avaiabliity of postsynaptic sites.

Afferent Pathways↗

PubMed1983

Retrograde and anterograde-transneuronal degeneration in the parabigeminal nucleus following tectal lesions in developing rats.

Degenerative effects in the parabigeminal nucleus were studied in adult rats that had received lesions of the superior colliculus at different postnatal ages. Unilateral lesions lead to complete degeneration of the dorsal and ventral divisions of the parabigeminal nucleus, which connect reciprocally with the damaged tectum, and produce effects on the middle division which receives afferents from the ipsilateral and projects to the contralateral tectum. On the side contralateral to the lesion there was a reduction in the cross-sectional area of the division as a consequence of retrograde degeneration, except in rats operated on at birth or when adults; ipsilateral to the lesion there was a reduction in the cross-sectional area of the division as a result of anterograde-transneuronal degeneration, except in animals operated on when adults. The reduction in cross-sectional area is partly due to a decrease in the number of neurones in the middle division. The maximal effects in both cases occurred in animals operated on at 10 days after birth, and the sensitivity to retrograde degeneration follows a U-shaped curve. Bilateral tectal lesions performed at birth or 5 days after birth produce virtually complete degeneration of the whole parabigeminal nuclei. Anterograde radioautographic tracing showed that all parabigeminal divisions received topographically organized projections from the ipsilateral superior colliculus. Ipsilateral projections from the dorsal and ventral divisions and crossed projections from the middle division were identified in the tectum of newborn rats with fluorescent retrograde tracers. Possible explanations for the cases in which tectal lesions failed to produce an effect on the architecture of the middle division include increased resistance to axonal damage and regulative processes over natural neuronal death. The results also indicate that the two forms of degeneration are additive with regard to the whole population of developing parabigeminal neurones.

Age Factors↗

PubMed2006

Effect of aging and degeneration on disc volume and shape: A quantitative study in asymptomatic volunteers.

Debate continues on the effect of disc degeneration and aging on disc volume and shape. So far, no quantitative in vivo MRI data is available on the factors influencing disc volume and shape. The objective of this MRI study was to quantitatively investigate changes in disc height, volume, and shape as a result of aging and/or degeneration omitting pathologic (i.e., painful) disc alterations. Seventy asymptomatic volunteers (20-78 years) were investigated with sagittal T1- and T2-weighted MR-images encompassing the whole lumbar spine. Disc height was determined by the Dabbs method and the Farfan index. Disc volume was calculated by the Cavalieri method. For the disc shape the "disc convexity index" was calculated by the ratio of central disc height and mean anterior/posterior disc height. Disc height, disc volume, and the disc convexity index measurements were corrected for disc level and the individuals age, weight, height, and sex in a multilevel regression analysis. Multilevel regression analysis showed that disc volume was negatively influenced by disc degeneration (p < 0.001) and positively correlated with body height (p < 0.001) and age (p < 0.01). Mean disc height and the disc convexity index were negatively influenced by disc degeneration but not by gender, weight, and height. Disc height was positively correlated with age (p < 0.01). From the results of this study, it can be concluded that disc degeneration generally results in a decrease of disc height and volume as well as a less convex disc shape. In the absence of disc degeneration, however, age tends to result in an inverse relationship on disc height, volume, and shape.

Adult↗

PubMed2001

Dopamine cell degeneration induced by intraventricular administration of 6-hydroxydopamine in the rat: similarities with cell loss in parkinson's disease.

In an attempt to find a convenient rat model to study cell vulnerability in Parkinson's disease, we have investigated the cell-loss profile in different midbrain dopaminergic nuclei and subnuclei of rats injected with 6-hydroxydopamine (6-OHDA) in the third ventricle. Following administration of different doses (5-1000 microgram) of 6-OHDA, motor behavior was evaluated and tyrosine hydroxylase-immunostained neurons were counted in the A8 group and different subdivisions of A9 and A10 groups. Animals developed hypokinesia, repetitive chewing movements, and catalepsia. Signs of cell degeneration were evident from the first day after injection, reaching the definitive pattern at the end of the first week. There was a similar degeneration in both brain sides, the A9 group showing the highest degree of cell-loss, followed by A8 and A10 groups. In the A9 group, the degeneration mostly affected those subgroups located in its ventral, lateral, and posterior regions. In the A10 group the degeneration mainly affected the parabrachial pigmented nucleus, the paranigral nucleus and the ventral tegmental area. This topographic pattern of degeneration is very similar to that previously described in Parkinson's disease, suggesting that this model may be a useful tool in the study of the cell vulnerability mechanisms in this neurodegenerative disorder. In addition, our results also showed that small dopaminergic neurons are more resistant to degeneration than the large ones. In some DA subgroups, the cells that contained calbindin but not calretinin were less vulnerable to the neurotoxic effect of 6-OHDA.

Animals↗

PubMed1980

[Fasciola haptica L.: the parthenitae in degeneration or without development in Lymnaea truncatula müller (author's transl)].

The authors describe several types of parthenitae in degeneration or without development in infested snails showing the same parasitic phase (phase E 1, characterized by the presence of the first independent cercariae in the visceral cavity of the snail). The influence of three factors, snail-breeding temperature, body volume of the snail host, drying of ground, is analyzed on the quantitative variations of these parthenitae. In nonstarved snails, captive rediae within snail gonad and independent rediae without embryos do not develop. In all cases of snails, the rediae and cercariae can present three types of degeneration: (a) types DE 1 and DE2 (without cellular reaction of the snail) showing nuclear pycnosis (type DE1) or caryolysis (type DE 2); (b) type DE 3 showing nuclear pycnosis with the participation of the snail amebocytes and fibroblastlike cells. In nonstarved snails, the dengeration of rediae - type DE 1 especially - increases noticeably at higher breeding temperatures; on the other hand, the captive rediae are most numerous at low temperatures. In nonstarved snails breeded at the same temperature (20 degrees C), the body volume of the host has more effect upon the location of these rediae in the snail cavity than upon their total number. In starved snails, the degeneration - types DE 1 and DE 2 - first affects all rediae of generations 1 and 2; second, the cercariae degenerate later and the rediae of generation 3 are relatively unaffected by this process. The degenerating rediae in type DE 3 are few in number and only exist in these starved snails. The significance of the degeneration of these parthenitae is discussed.

Animals↗