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PubMed1989

Changes in neuronal cell bodies in N. laminaris during deafferentation-induced dendritic atrophy.

N. laminaris dendrites begin to atrophy almost immediately after they are deafferented. Accompanying this rapid change in shape is a loss of microtubules and neurofilaments at the base of the dendrite, and a decrease in the density of the dendritic cytoplasm. However, degenerative changes in the dendritic plasma membrane were not evident until 2 days after deafferentation. Thus it was unknown what happened to the volume and membrane lost from the atrophying dendrites before this time. The soma was investigated in this study as a possible recipient of the volume of the atrophying dendrite. Soma size increased significantly by 2 hours after deafferentation and continued to increase for 1-8 days after deafferentation. The nucleus, which is normally concentric with the soma, moved continuously to the dorsal pole of the soma, toward the innervated side of the cell. The cytoplasm on the ventral side of the soma showed a decrease in density and loss of cytoskeleton similar to what was found in the initial portion of the ventral primary dendrites in the accompanying paper. These changes are interpreted as indicative of a rapid resorption of the ventral dendrite back into the soma following deafferentation.

Animals↗

PubMedDate not supplied

Clinical nursing implications for the recovery of atrophied skeletal muscle following bed rest.

Atrophied skeletal muscle is a common clinical manifestation of bed rest that occurs primarily because of a lack of weight-bearing activity on the muscle. Findings from several studies using an animal model to simulate the effects of bed rest on muscles indicate that when atrophied muscle is used again for weight-bearing activity, it undergoes a series of physiological changes, such as muscle fiber (myofiber) damage, death, and regeneration. Also, in the recovering muscle, the inflammatory white blood cells, called macrophages, accumulate and shift in type in relation to the ongoing myofiber changes. Similar processes may occur in the muscles of a patient resuming normal physical activity following bed rest. The authors briefly describe the physiological changes related to atrophied muscle recovery and the implications for nursing care. Nursing measures for the recovery period may include (a) assessing for symptoms associated with muscle injury, decreased strength, and fatigue; (b) encouraging sufficient protein intake and maintaining normal metabolic demands to ensure muscle repair; and (c) temporarily avoiding the use of immunosuppressive therapy, if possible, to ensure adequate macrophage function.

Bed Rest↗

PubMedDate not supplied

Late-onset X-linked recessive spinal and bulbar muscular atrophy.

A family is described in which five males have late-onset facial weakness, dysarthria, dysphagia, and slowly progressive proximal weakness. Electrodiagnostic studies and muscle biopsy were compatible with spinal muscular atrophy. This family appears quite similar to several previously reported families with late-onset X-linked recessive spinal and bulbar muscular atrophy. Because of the relative homogeneity of this particular phenotype of spinal muscular atrophy, a single metabolic derangement was sought. Three obligate carriers were studied, and no abnormality was detected. A further family with this condition is briefly discussed.

Aged↗

PubMedDate not supplied

A possible role for glucocorticoids in denervation atrophy.

Skeletal muscle atrophies after denervation. Glucocorticoids also cause skeletal muscle to atrophy. The data presented in this report demonstrate that after denervation there is a significant increase in the number of glucocorticoid receptors in the cytosol of skeletal muscle of rats. The results are consistent with the hypothesis that a skeletal muscle atrophies after denervation because it becomes hypersensitive to glucocorticoids.

Animals↗

PubMed1993

Atrophy and degeneration of ganglion cells in central retina following loss of postsynaptic target neurons in the dorsal lateral geniculate nucleus of the adult cat.

Selective degeneration of neurons in the dorsal lateral geniculate nucleus (dLGN) of the adult cat was produced by in situ injection of kainic acid. This rapid degeneration mimics the loss of lateral geniculate neurons seen after neonatal visual cortex ablation. Following survivals of 2, 4, or 6 months, the geniculate was injected with horseradish peroxidase (HRP) and the retinas were examined for the presence of retrogradely labeled, as well as unlabeled, cells. Total ganglion cell density in central nasal retina was not different from that of controls at 2 or 4 months, but by 6 months had decreased to 68% of control values. The proportion of cells labeled with HRP did not change at 2 months, but decreased from 84% in controls to less than 1% by 4 months, and none were labeled at 6 months. Surviving ganglion cells in central retina showed atrophy of the cell body, a finding not apparent in data from the retinal periphery. Shrinkage occurred in the few cells labeled with HRP surviving at 4 months, as well as among the unlabeled cells surviving at 4 and 6 months. These results show that the survival of central retinal ganglion cells in the cat continues to depend on intact target neurons beyond the period of development. Mature ganglion cells in central retina respond to loss of appropriate targets first by axon terminal retraction and then by atrophy and cell death. However, when compared to the response of cells located in far peripheral retina following dLGN neuron loss, central ganglion cells take longer to undergo axonal retraction and a greater proportion of the central ganglion cells, although atrophied, survive after 6 months.

Analysis of Variance↗

PubMed1997

Transplantation-induced atrophy of normal and hypertrophic rat hearts: effect on cardiac myocytes and capillaries.

Changes in tissue structure of hearts undergoing atrophy following heterotopic isotransplantation were studied. Both normal and hypertrophic hearts were used, originating from male and female rats. Aortic constriction produced in newborn rats, resulted in an 86 and 155% increase of left ventricular mass in male and female rats, respectively. On day 50, control and experimental animals were killed, half of their hearts were analysed morphometrically, while remaining hearts were transplanted into the abdominal cavity of recipient rats. Transplantation resulted in significantly decreased cardiac mass in control hearts (approximately 50% decrease compared to values at transplantation), and an even more pronounced decrease in hypertrophic hearts. Cardiac hypertrophy was characterized by significant decreases in capillary and myocyte densities. While myocyte density simply reflected changes in cell size, evidence for additional capillary growth was found (the aggregate length of capillaries per left ventricle increased by 57-88%). Cardiac atrophy resulted in increased capillary density, despite evidence of some capillary involution in transplanted hearts (aggregate length of capillaries decreased by 30-35% and 52-64% for transplants of normal and of hypertrophic hearts, respectively). Myocyte density increased due to a proportional decrease in the size of cardiac myocytes. In transplanted hearts, an increasing number of myocytes containing nuclei located close to the nearest capillary, suggests that changes in myocyte size are not symmetrical. The present study demonstrated the remarkable plasticity of the heart in neonatal animals; they were capable of large increases and decreases in cardiac mass within a few weeks, with more pronounced changes in female rats. These changes were accompanied by changes in myocardial structure, indicating some capillary growth in cardiac hypertrophy, and involution of coronary capillaries in cardiac atrophy.

Animals↗

PubMed2000

Administration of opiate receptor antagonist inhibits mucosal atrophy of the gut in fasting rats.

OBJECTIVE: The objective of this study was to determine whether the opiate mu receptor antagonist naloxone would prevent atrophy of the gut in 24-h-fasted rats. METHODS: Male Sprague-Dawley rats (n = 76, body weight 200-225 g) were catheterized in the jugular vein on Day 0. The rats were fed standard rat chow for 4 days. On Day 4, the diet was changed to the standard liquid diet, and the rats were allowed free access to the liquid diet. On Day 7, the rats were randomized into five groups: (1) free fed, (2) free fed plus naloxone, (3) pair fed, (4) fasting, (5) free fed plus morphine, (6) fasting plus naloxone. Either naloxone (0.16 mg/kg/h) or morphine (0. 21 mg/kg/h) was continuously infused via venous catheter for 24 h. On Day 8, 24 h after fasting or free feeding, the animals were sacrificed. RESULTS: Twenty-four hours of fasting caused atrophy of the jejunum and elevated morphine levels in the brain (free fed, 931. 3 +/- 122.3 fmol/g, vs fasting, 1419.0 +/- 150.0, P < 0.05). Morphine infusion reduced villus height, mucosal weight, and protein content in jejunum as compared with the free fed rats receiving saline. Administration of naloxone caused an increase in villus height (fasting, 587.0 +/- 25.8 microm, vs fasting plus naloxone, 670.0 +/- 17.4, P < 0.05), mucosal weight (fasting, 17.4 +/- 1.8 mg/cm, vs fasting plus naloxone, 22.6 +/- 1.9, P < 0.05), and protein content (fasting, 13.5 +/- 0.7 microg/cm, vs fasting plus naloxone, 16.7 +/- 0.6, P < 0.05) in jejunum. CONCLUSION: Mucosal atrophy of the jejunum is caused by endogenous opioid in fasting rats.

Animals↗

PubMed2002

Voxel-based morphometric comparison of hippocampal and extrahippocampal abnormalities in patients with left and right hippocampal atrophy.

We used voxel-based morphometry (VBM), an automatic whole-brain MR image analysis technique, to investigate gray matter abnormalities in patients with temporal lobe epilepsy (TLE), in whom hippocampal atrophy (HA) was demonstrated by application of the Cavalieri method of modern design stereology. VBM results (P < 0.05, corrected) indicated preferential gray matter concentration (GMC) reduction in anterior hippocampus in patients with left HA and posterior hippocampus in patients with right HA. GMC reduction was also found in right dorsal prefrontal cortex in left and right HA patients. Prefrontal atrophy may be due to epileptiform excitotoxic discharges from the reciprocally connected pathological hippocampus, and may be the underlying biological cause for executive dysfunction in patients with TLE. GMC excess in ipsilateral parahippocampal, cerebellar, and pericallosal regions was common to both left and right HA groups relative to controls, and is hypothesized to reflect diminished gray-white matter demarcation, underlying white matter atrophy, or structural displacement due to cerebrospinal fluid expansion. However, bilateral temporal lobe GMC excess was observed in left HA patients, while ipsilateral temporal lobe GMC excess was observed in right HA patients. This work demonstrates methodological consistency between automated VBM and manual stereological analysis of the hippocampus in group comparisons, indicates widespread extrahippocampal gray matter abnormalities in unilateral HA, and suggests that there may be inherent differences in the effect of TLE on temporal lobe structures depending on the side of HA.

Adolescent↗

PubMed1994

Time course of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced thymic atrophy in the Wistar rat.

Exposure to sublethal doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Wistar rats results in thymic atrophy and reduced thymic cellularity. In a first experiment, rats were once orally intubated with 0, 1, 5, 25, 50, and 150 micrograms TCDD/kg body wt and sacrificed at Day 10. The dose that produced one-half of the maximal thymic involution was estimated at about 10-20 micrograms/kg. The time course (Days 0-21) of thymic atrophy induced by a single oral intubation of 25 micrograms TCDD/kg body wt revealed four phases. In phase 1 (initiation phase, Days 0-2) a decrease in proliferative activity was seen in cortical thymocytes, whereas no changes occurred in thymic cellularity. Phase 2 (lymphodepletion phase, Days 2-8) was characterized by an initial strong depletion of immature CD4+CD8+ double-positive (DP) cells (Day 4), followed by a more gradual decrease in the number of mature thymocytes (Day 6). On Day 8 the lymphodepletion was maximal. In phase 3 (stationary phase, Days 8-13) no changes occurred in thymic cellularity. Although the first signs of recovery were already seen on Day 6, indicated by a recovery in proliferative activity in the thymus cortex, an increase in thymic cellularity was observed first after Day 13 (phase 4, recovery phase, Day 13 onward). Reversibility of thymic atrophy is therefore observed within the estimated half-life of TCDD in the rat thymus (> 16 days). We conclude that TCDD exerts a rapidly reversible effect on an intrathymic cortical target cell population.

Administration, Oral↗

PubMed1997

Organotin-induced apoptosis as observed in vitro is not relevant for induction of thymus atrophy at antiproliferative doses.

The organotin compounds di-n-butyltin dichloride (DBTC) and tri-n-butyltin chloride (TBTC) selectively cause thymus atrophy. Previously, DBTC and TBTC were shown to inhibit proliferation of immature thymocytes, but other studies demonstrated that TBTC but not DBTC increased apoptosis in vitro and also in vivo. In this study, we examined whether apoptosis is increased in vitro by DBTC and TBTC at various concentrations and periods of incubation and whether apoptosis is involved in the induction of thymus atrophy at selective antiproliferative doses. In vitro, DBTC or TBTC at a concentration of 3 microM significantly increased DNA fragmentation in freshly isolated rat thymocytes after preincubation for 10 min followed by a 22-hr culture period. After continuous exposure for 22 hr, apoptosis was observed to be optimum at 1 microM TBTC and 0.3 microM DBTC and lower or absent at higher concentrations. Apparently, apoptosis induced by organotins in vitro depends on both duration and concentration of exposure. Selective antiproliferative doses of DBTC nor TBTC increased apoptosis on day 1 or 2 after single oral exposure. In contrast, the corticosteroid dexamethasone caused a depletion of both small and large thymocytes and a marked increase of apoptosis on both days 1 and 2 after dosing. Thus, although apoptosis is involved in the in vitro cytotoxic effects of both organotin compounds, it seems not involved in thymus atrophy at a dose that selectively inhibits immature thymocyte proliferation.

Animals↗

PubMed1980

Testicular atrophy produced by phthalate esters.

In a 90-day toxicity study in rats, di-(2-ethylhexyl)phthalate (DEHP) produced testicular atrophy. To characterise further the testicular toxicity of phthalate esters the effect of age on the induction of testicular atrophy has been examined as well as the reversibility of the lesions and the effects of certain other phthalate esters. Seminiferous tubular atrophy, comprising a loss of spermatids and spermatocytes, resulted when 4-week-old rats were given 10 daily doses of DEHP. In similarly treated 10-week old rats up to 50% of tubules were atrophic while the remainder were unaffected. No testicular damage was produced in 15 week-old rats. The lesion produced in 4-week-old rats was reversible whether treatment was stopped prior to, or continued until after the control rats had reached sexual maturity. Normal testicular weight and histology were restored within 12 and 20 weeks respectively. Of a series of di-n-alkyl phthalates from dimethyl to di-n-octyl, the butyl, pentyl and hexyl esters produced testicular lesions similar to DEHP. The testicular effects of DEHP were not influenced by simultaneous administration of testosterone or follicle stimulating hormone (FSH). The mechanism by which phthalate esters exert their effects is discussed in the context of a possible action on Sertoli cell function.

Aging↗

PubMed1998

Differential diagnosis of NPH and brain atrophy assessed by measurement of intracranial and ventricular CSF volume with 3D FASE MRI.

Differential diagnosis of NPH and brain atrophy is sometimes difficult. Recently, a new method using MRI was introduced as a noninvasive, direct technique for the measurement of intracranial CSF volume. Using this new technique, we measured the intracranial and ventricle CSF volume in patients with enlarged ventricles in order to differentiate between NPH and brain atrophy. Ten healthy volunteers (control group) and 21 patients with enlarged ventricles were enrolled in this study. Eleven out of 21 patients were clinically diagnosed as having NPH (shunted group) and the remaining 10 patients were considered to have cerebral atrophy (non-shunted group). Intracranial and ventricular CSF volume in each case were measured by 3D FASE (Fast Asymmetric Spine-Echo) MR imaging sequence with region growing method. Ventricular/intracranial CSF volume ratio was also calculated. Ten out of 11 patients showed improvement in clinical symptoms and/or dementia scale after shunting. Our results clearly indicate that the ventricular volume in the shunted group was enlarged and that the ventricular/intracranial CSF ratio was significantly high. Thus we concluded that enlarged ventricle with high ventricular/intracranial CSF volume ratio strongly suggests NPH.

Adult↗

PubMed1991

Does the absence of clinical expression of choreoathetosis, despite severe striatal atrophy, correlate with plasticity of neuropeptide synthesis?

Neuropeptide and neurotransmitter plasticity has been demonstrated in the central nervous system. Modifications of their synthesis occur following receptor blockade or deafferentiation by surgical lesions. This concept should provid answers to some remaining open questions in human pathology especially in degenerative diseases of the basal ganglia. In a severely atrophied striatum we observed a selective increase in the number of detectable striatal substance P and met-enkephalin neurones which exhibited a striking increase in the intensity of labelling. This increase, instead of the well established reduction of substance P and enkephalins in the atrophied striatum of Huntington's disease, could explain the absence of choreoathetosis which was replaced by rigidity and bradykinesia in the patient. The absence of choreoathetosis, despite severe striatal atrophy, is described in several basal ganglia diseases and could also be related to neurotransmitter or neuropeptide plasticity rather than due to the primary lesion.

Athetosis↗

PubMed1993

The topographic distribution of brain atrophy in Huntington's disease and progressive supranuclear palsy.

The topographic distribution of brain atrophy was quantified by image analysis of fixed coronal brain slices from 12 patients dying with Huntington's disease (HD) and from 4 other patients dying with progressive supranuclear palsy (PSP). In HD, atrophy was maximal within the caudate nucleus, putamen and globus pallidus. However, the cerebral cortex was also atrophied with reductions in cross-sectional area within frontal, temporal and parietal lobes. In general, more white matter than grey matter was lost leading to an elevation in the grey/white matter ratio. The amygdala and thalamus were reduced in area. In PSP, lesser reductions in cortical area than those of HD were seen, these again being mostly due to a loss of white matter, resulting in an elevation of the grey/white ratio. The globus pallidus and thalamus were decreased in area, but no changes in the caudate nucleus and putamen were measured.

Adult↗

PubMed1989

Testicular atrophy and loss of nerve growth factor-immunoreactive germ cell line in rats exposed to n-hexane and a protective effect of simultaneous exposure to toluene or xylene.

Testicular and germ cell line morphology in rats were studied 2 weeks, 10 months and 14 months after cessation of a 61-day inhalation exposure to 1000 ppm n-hexane. Androgen biosynthetic capacity of testis, testosterone blood concentration, vas deferens morphology and noradrenaline (NA) concentration, epididymal sperm morphology, and fertility were also studied. Severe testicular atrophy involving the seminiferous tubules with loss of the nerve growth factor (NGF) immunoreactive germ cell line was found. Total loss of the germ cell line was found in a fraction of animals up to 14 months post-exposure, indicating permanent testicular damage. No impairment of androgen synthesis or androgen dependent accessory organs was observed. Simultaneous administration of 1000 ppm n-hexane and 1000 ppm toluene, or 1000 ppm n-hexane and 1000 ppm xylene, did not cause germ cell line alterations or testicular atrophy. Toluene and xylene were thus found to protect from n-hexane induced testicular atrophy.

Animals↗

PubMed1989

Preliminary exclusion of an X-linked gene in Leber optic atrophy by linkage analysis.

The maternal inheritance in Leber optic atrophy suggests that it may be caused by a cytoplasmic or mitochondrial defect. However, the strong male bias and the strict tissue specificity can not be readily explained by a single mitochondrial gene defect alone. Wallace suggested a hypothesis that the disease could be the result of an interaction between an X-linked gene and a mitochondrial DNA defect. Linkage relationships between Leber optic atrophy and 15 X-chromosome markers were analyzed in three large Tasmanian families. The results of two-point linkage analysis showed no close linkage between Leber optic atrophy and any of the 15 markers. The results of multipoint linkage analysis suggested the exclusion of the assumed X-linked gene from almost the whole X chromosome in these families.

Female↗

PubMed1995

The topographic distribution of brain atrophy in cortical Lewy body disease: comparison with Alzheimer's disease.

The topographic distribution of brain atrophy was quantified by image analysis of fixed coronal brain slices from four patients dying with cortical Lewy body disease (CLBD) all with Alzheimer-type pathology and compared to that in four other patients of similar age and gender dying with Alzheimer's disease (AD) alone. The pattern of atrophy in CLBD (+AD) was broadly similar to that in AD alone, suggesting that tissue loss was due mostly to parallel Alzheimer-type pathological changes and that the presence of Lewy bodies in cortical and subcortical neurons contributed little, if anything, to the overall degree of atrophy.

Aged↗

PubMed1991

Striatonigral degeneration, olivopontocerebellar atrophy and "atypical" Pick disease.

A 75-year-old woman with parkinsonism plus was found at autopsy to have striatonigral degeneration (SND), olivopontocerebellar atrophy (OPCA) and intracytoplasmic neuronal inclusions, mostly confined to the hippocampus and pontine nuclei. These inclusions were intensely argyrophilic, ubiquitinated and expressed variable immunoreactivity for neurofilament but not for tau-1 and Alz 50 proteins. Ultrastructurally, they were formed of skeins of intermediate filaments averaging 11 nm in diameter. They were considered to represent Pick bodies. There was no cortical atrophy, gliosis or sponginess. To our knowledge, SND and OPCA in association with Pick's disease has not been previously reported. In addition, intracytoplasmic oligodendroglial inclusions were present in the deeper layers of the cortex, especially the pericentral gyri, the striatum and the white matter of certain regions of the cerebral hemispheres, as well as in the cerebellum. These inclusions which have been previously reported in multisystem atrophy, had to be distinguished from cortical Lewy bodies, Pick bodies, and the nonspecific ubiquitinated bodies in the white matter of the aged brain, mainly by their topographical distribution and immunostaining properties.

Aged↗