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  • 1
    Electronic Resource
    Electronic Resource
    Effects of cholinergic depletion on glutamic acid decarboxylase immunoreactivity in the somatosensory cortex of rats (1997)
    Springer
    Anatomy and embryology 196 (1997), S. 27-38 
    Details
    ISSN: 1432-0568
    Keywords: Key words Cortex ; GABA ; Immunotoxin ; Nucleus basalis of Meynert ; Somatosensory cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The purpose of these experiments was to determine the effects of cholinergic depletion on the morphology and staining density of barrels formed by glutamic acid decarboxylase-positive neuropil in the posteromedial barrel subfield of the somatosensory cortex. The density and distribution of glutamic acid decarboxylase immunoreactive neuropil were examined after highly selective lesions of cholinergic neurons in the nucleus basalis of Meynert with an immunotoxin, IgG 192-saporin. Glutamic acid decarboxylase immunoreactivity was also examined in animals subjected to a whisker-pairing experience and lesion of acetylcholine inputs from the nucleus basalis of Meynert. Seven to 9 weeks after intraventricular injection of the immunotoxin, animals were perfused with a zinc aldehyde fixative and glutamic acid decarboxylase immunoreactivity was examined in 30-μm tangential sections. Cholinergic depletion caused reduced glutamic acid decarboxylase immunoreactivity in selective regions of the posteromedial barrel subfield. The density of neuropil and cell bodies immunoreactivie for glutamic acid decarboxylase was significantly reduced in septa and perimeters of barrel walls. The length, width, and area of barrels were reduced 10–20% in cholinergic-depleted animals compared with controls. The density of glutamic acid decarboxylase immunoreactivity in the hollow of barrels was not affected by this treatment. Whisker pairing did not significantly change the density of glutamic acid decarboxylase immunoreactivity in barrels. These observations are discussed in regard to how long-term cholinergic depletion affects the function of different fiber systems in the posteromedial barrel subfield cortex and how some sensory functions may be compromised.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004290050077
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  • 2
    Electronic Resource
    Electronic Resource
    Ubiquitin marks the reactive swellings of diffuse axonal injury (1993)
    Springer
    Acta neuropathologica 85 (1993), S. 503-507 
    Details
    ISSN: 1432-0533
    Keywords: Ubiquitin ; Neurofilament ; Diffuse axonal injury ; Immunohistochemistry ; Head Trauma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ubiquitin is a protein that targets proteins for non-lysosomal degradation. It has been found to be present in a number of inclusions characteristic of neurodegenerative diseases. Using the fluid percussion model of diffuse axonal injury (DAI), we now report that the reactive axonal swellings and the retraction balls produced in this model stain positively with antiubiquitin immunohistochemistry. Furthermore, the affected axons become ubiquitin positive quickly (with-in the first 6 h after injury). Anti-ubiquitin immunohistochemistry compares well with the recently reported ability of antibodies to low molecular weight neurofilament proteins to demonstrate reactive axonal change in DAI, and it could provide additional clues to the pathogenesis of axonal transection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00230489
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Diffuse axonal injury: Windows for therapeutic intervention allowed by its pathobiology (1993)
    Springer
    Virchows Archiv 423 (1993), S. 153-156 
    Details
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01614764
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  • 4
    Electronic Resource
    Electronic Resource
    Synaptophysin immunoreactivity in temporal lobe epilepsy-associated hippocampal sclerosis (1999)
    Springer
    Acta neuropathologica 98 (1999), S. 179-185 
    Details
    ISSN: 1432-0533
    Keywords: Key words Image analysis ; Hippocampal sclerosis ; Synaptophysin ; Temporal lobe epilepsy ; Partial ; complex seizures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously devised a semiquantitative grading system for hippocampal sclerosis (HS) in specimens resected for intractable temporal lobe epilepsy. The grades range from zero to four based on the amount and distribution of neuronal loss and gliosis. In the present study hippocampal sections from 25 patients who had temporal lobe epilepsy and had previously been assigned a grade were examined with synaptophysin immunohistochemistry, and the synaptic content in specific hippocampal fields was correlated with the results of the HS grading system. There was evidence of both significant synaptic loss and increased synaptic density in different fields of the hippocampus with increasing HS. A marked decrement of synaptic immunostaining was present in fields CA1 and CA4 that were highly correlated with HS grade. Sector CA4 seemed to respond in a more graded or continuous way to the pathological insults occurring in temporal lobe epilepsy than did CA1, which appeared to exhibit an all or nothing response. Also, while the width of the outer part of the molecular layer of the dentate (mld) gyrus decreased with increasing HS grade, the inner part of the mld became wider and showed an increased synaptic density so that the overall width of the mld was increased in the high-grade group. We conclude that quantitative measurement of synaptic loss in CA1 and CA4 using synaptophysin immunohistochemistry is a sensitive method for detecting HS and correlates well with the empirically derived HS grading scale, with CA4 exhibiting a more graded response than CA1. In addition, a plasticity response in the inner part of the mld in patients with high-grade HS has been confirmed and quantitated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051067
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  • 5
    Electronic Resource
    Electronic Resource
    192 IgG-saporin (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 519-526 
    Details
    ISSN: 1432-0533
    Keywords: Astrocyte ; Cholinergic ; Immunotoxin ; Microglia ; Nerve growth factor receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that an immunotoxin (IT) directed against the p75 component of the nerve growth factor receptor (NGFr) selectively abolished cholinergic neurons in the basal forebrain of the rat following intraventricular administration. We now report the neuropathological responses in the rat brain to the IT, with particular emphasis on the cholinergic basal forebrain (CBF) and other known p75NGFr-positive brain regions. Animals received intraventricular injections of IT and were allowed to survive for various times. Sections through the entire brain were evaluated using (1) hematoxylin and eosin; (2) glial fibrillary acidic protein immunohistochemistry; and (3)Griffonia simplicifolia lectin histochemistry. The only clearly degenerating cells following IT treatment were located in the CBF or in the Purkinje cell layer of the cerebellum. A marked microglial response was demonstrated that was tightly linked both topographically and temporally to the loss of neurons in these areas. The astroglial response was mild in the same regions in which the microglial response was obvious. The other areas of rat brain including the terminal fields of CBF projections showed no consistent reactive cellular responses in IT-treated animals. This study extends and corroborates previous work indicating speciticity of IT, demonstrates active neuronal degeneration by conventional pathological methods for the first time, and illustrates the unexpected and novel finding that the predominant pathological response to the IT-induced loss of neurons is microglial. Both the high degree of specificity and the distinctive glial response distinguish the IT model from other experimental models of CBF neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571506
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    192 IgG-saporin (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 519-526 
    Details
    ISSN: 1432-0533
    Keywords: Key words Astrocyte ; Cholinergic ; Immunotoxin ; Microglia ; Nerve growth factor receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that an immunotoxin (IT) directed against the p75 component of the nerve growth factor receptor (NGFr) selectively abolished cholinergic neurons in the basal forebrain of the rat following intraventricular administration. We now report the neuropathological responses in the rat brain to the IT, with particular emphasis on the cholinergic basal forebrain (CBF) and other known p75NGFr-positive brain regions. Animals received intraventricular injections of IT and were allowed to survive for various times. Sections through the entire brain were evaluated using (1) hematoxylin and eosin; (2) glial fibrillary acidic protein immunohistochemistry; and (3) Griffonia simplicifolia lectin histochemistry. The only clearly degenerating cells following IT treatment were located in the CBF or in the Purkinje cell layer of the cerebellum. A marked microglial response was demonstrated that was tightly linked both topographically and temporally to the loss of neurons in these areas. The astroglial response was mild in the same regions in which the microglial response was obvious. The other areas of rat brain including the terminal fields of CBF projections showed no consistent reactive cellular responses in IT-treated animals. This study extends and corroborates previous work indicating specificity of IT, demonstrates active neuronal degeneration by conventional pathological methods for the first time, and illustrates the unexpected and novel finding that the predominant pathological response to the IT-induced loss of neurons is microglial. Both the high degree of specificity and the distinctive glial response distinguish the IT model from other experimental models of CBF neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571506
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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