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  • 1
    Electronic Resource
    Electronic Resource
    Comparison of the Number of Vasopressin-Producing Hypothalamic Neurons in Rats and Humans (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 7 (1995), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The aim of this study was to assess the number and proportion of vasopressin-producing neurons in the hypothalamic magnocellular nuclei in rats and humans. Accurate and unbiased neuronal counts were estimated using the optical disector method. Arginine vasopressin-containing neurons were immunohistochemically visualized in formalin-fixed tissue sections. The magnocellular neurons were similar in size and morphology in both species. While the human hypothalamus contained significantly more vasopressin-containing neurons compared with the rat (36-fold increase), the proportion of vasopressin-containing neurons between species was similar. In both species, the majority of supraoptic neurons contained vasopressin, however the proportion of vasopressin-containing neurons in the human paraventricular nucleus was double that of the rat (nearly a 100-fold increase in number). These results suggest that the paraventricular nucleus contributes significantly to the release of vasopressin from the posterior pituitary in humans, whereas in rats vasopressin is mainly released by supraoptic neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.1995.tb00801.x
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  • 2
    Electronic Resource
    Electronic Resource
    Ubiquitin-positive achromatic neurons in corticobasal degeneration (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 68-75 
    Details
    ISSN: 1432-0533
    Keywords: Key words Neuropathology ; Ballooned neurons ; Ubiquitin ; Quantitation ; Alien limb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 66-year-old woman presented with an alien limb syndrome without dementia. The course of her illness was unremitting and at autopsy 6 years later her diagnosis was confirmed as corticobasal degeneration without Alzheimer-type pathology. Although the presence of ballooned achromatic cortical neurons and cell loss from the substantia nigra distinguishes such patients, the site and density of achromatic neurons has not previously been quantified. We show that immunohistochemistry for the cell stress protein ubiquitin selectively stains these achromatic neurons, whereas they do not stain for abnormally phosphorylated tau protein. Phosphorylated neurofilament antibodies recognise both ballooned and non-ballooned neurons. In this case, high densities of ubiquitin-positive ballooned neurons were found in frontal cortical regions with the highest densities in layers V and VI of the anterior cingulate cortex. In addition, high densities of ubiquitin-positive ballooned neurons were found in the insular cortex, claustrum and amygdala. These results confirm past reports of frontal pathology, but show that there is also considerable pathology in insular and parahippocampal cortical regions and some subcortical regions. Our findings suggest that the distribution and staining characteristics of ballooned neurons in corticobasal degeneration may help to differentiate these cases pathologically, while the absence of dementia appears to be an important clinical criterion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294461
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Ubiquitin-positive achromatic neurons in corticobasal degeneration (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 68-75 
    Details
    ISSN: 1432-0533
    Keywords: Neuropathology ; Ballooned neurons ; Ubiquitin ; Quantitation ; Alien limb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 66-year-old woman presented with an alien limb syndrome without dementia. The course of her illness was unremitting and at autopsy 6 years later her diagnosis was confirmed as corticobasal degeneration without Alzheimer-type pathology. Although the presence of ballooned achromatic cortical neurons and cell loss from the substantia nigra distinguishes such patients, the site and density of achromatic neurons has not previously been quantified. We show that immunohistochemistry for the cell stress protein ubiquitin selectively stains these achromatic neurons, whereas they do not stain for abnormally phosphorylated tau protein. Phosphorylated neurofilament antibodies recognise both ballooned and non-ballooned neurons. In this case, high densities of ubiquitin-positive ballooned neurons were found in frontal cortical regions with the highest densities in layers V and VI of the anterior cingulate cortex. In addition, high densities of ubiquitin-positive ballooned neurons were found in the insular cortex, claustrum and amygdala. These results confirm past reports of frontal pathology, but show that there is also considerable pathology in insular and parahippocampal cortical regions and some subcortical regions. Our findings suggest that the distribution and staining characteristics of ballooned neurons in corticobasal degeneration may help to differentiate these cases pathologically, while the absence of dementia appears to be an important clinical criterion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294461
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Chronic alcoholism in the absence of Wernicke-Korsakoff syndrome and cirrhosis does not result in the loss of serotonergic neurons from the median raphe nucleus (1996)
    Springer
    Metabolic brain disease 11 (1996), S. 217-227 
    Details
    ISSN: 1573-7365
    Keywords: Alcohol ; serotonin ; neuropathology ; median raphe nucleus ; Wernicke-Korsakoff ; cirrhosis ; thiamine deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have identified alcohol, thiamine deficiency and liver disease as contributing to the neuropathology of alcohol-related brain damage. In order to examine the effects of alcohol toxicity and thiamine deficiency on serotonergic neurons in the median raphe nucleus (MnR), alcoholic and previously published Wernicke-Korsakoff syndrome (WKS) cases without liver disease, were compared with age-matched non-alcoholic controls. While there was no difference between the estimated number of serotonergic neurons in either controls or alcoholics without WKS (means of 63,010±8,900 and 59,560±8,010 respectively), a substantial loss of serotonergic neurons was previously found in WKS cases (mean of 19,050±13,140). Further analysis revealed a significant difference in the maximum daily alcohol consumption between these groups. However, analysis of covariance showed that the number or serotonergic neurons in the MnR did not correlate with the amount of alcohol consumed. Therefore, our results suggest that cell loss in the MnR can be attributed to thiamine deficiency rather than alcoholper se.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02237959
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  • 5
    Electronic Resource
    Electronic Resource
    Mechanisms of cell death in cholinergic basal forebrain neurons in chronic alcoholics (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 81-91 
    Details
    ISSN: 1573-7365
    Keywords: Neurofibrillary tangles ; peroxidase activity ; nucleus basalis ; thiamine deficiency ; alcohol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tau immunoreactivity was examined in post mortem tissue from patients in three groups: neurologically-asymptomatic and neuropathologically normal alcoholics, alcoholics with Wernicke's Encephalopathy (WE) and age matched non-alcoholic controls. Tau-positive granular and fibrillary inclusions were frequently observed within the magnocellular neurons of the cholinergic nucleus basalis, within occasional nucleus basalis neurons in non-WE alcoholics, but not in controls. Tau immunoreactivity was not however observed in cortical, brainstem, diencephalic or non-cholinergic forebrain structures. Peroxidase activity was also examined within the nucleus basalis using diaminobenzidine as an indicator. The majority of neurons in the basal forebrain showed increased peroxidase activity in all WE alcoholics and in some nucleus basalis neurons of non-WE alcoholics, but was rarely seen in controls. Neighboring astrocytes also showed increased peroxidase activity. These results suggest a link between peroxidase activity and the abnormal accumulation of phosphorylated tau. The presence of tau in the nucleus basalis of alcoholics with WE suggests a thiamine-dependent mechanism in tau accumulation and cell death in the cholinergic basal forebrain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991785
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    Paper (German National Licenses)
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