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  • Recurrent Inhibition  (3)
  • Microglia  (2)
  • β-amyloid  (2)
  • B7 molecules  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Rapid appearance of β-amyloid precursor protein immunoreactivity in glial cells follwing excitotoxic brain injury (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 23-28 
    Details
    ISSN: 1432-0533
    Keywords: Amyloid precursor protein ; β-amyloid ; Quinolinic acid ; Astrocytes ; Microglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Clinical and experimental data have indicated an up-regulation of amyloid precursor protein (APP) after various types of CNS injury. In the present study the cellular source of lesion-induced APP has been investigated an a neurotoxic CNS model. Quinolinic acid injection into the striatum results in neuronal degeneration, while glial cells survive. APP immunoreactivity was detected in glial cells starting at postoperative day 3 and persisted until day 21, the last time point studied. Double immunocytochemistry identified the majority of APP-immunoreactive cells as glial fibrillary acidic protein-immunoreactive astrocytes. There was no evidence of amyloid fibril deposition during this time. It is concluded that following excitotoxic neuronal degneration APP is mainly produced by reactive astrocytes in the lesioned area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294255
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Rapid appearance of β-amyloid precursor protein immunoreactivity in glial cells following excitotoxic brain injury (1994)
    Springer
    Acta neuropathologica 89 (1994), S. 23-28 
    Details
    ISSN: 1432-0533
    Keywords: Key words     Amyloid precursor protein ; β-amyloid ; Quinolinic acid ; Astrocytes ; Microglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract      Clinical and experimental data have indicated an up-regulation of amyloid precursor protein (APP) after various types of CNS injury. In the present study the cellular source of lesion-induced APP has been investigated in a neurotoxic CNS model. Quinolinic acid injection into the striatum results in neuronal degeneration, while glial cells survive. APP immunoreactivity was detected in glial cells starting at postoperative day 3 and persisted until day 21, the last time point studied. Double immunocytochemistry identified the majority of APP-immunoreactive cells as glial fibrillary acidic protein-immunoreactive astrocytes. There was no evidence of amyloid fibril deposition during this time. It is concluded that following excitotoxic neuronal degneration APP is mainly produced by reactive astrocytes in the lesioned area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294255
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Major histocompatibility complex class II expression by activated microglia caudal to lesions of descending tracts in the human spinal cord is not associated with a T cell response (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 528-536 
    Details
    ISSN: 1432-0533
    Keywords: Key words Spinal cord injury ; Stroke ; B7 molecules ; Macrophage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lesion-induced microglial/macrophage responses were investigated in post-mortem human spinal cord tissue of 20 patients who had died at a range of survival times after spinal trauma or brain infarction. Caudal to the spinal cord injury or brain infarction, a strong increase in the number of activated microglial cells was observed within the denervated intermediate grey matter and ventral horn of patients who died shortly after the insult (4–14 days). These cells were positive for the leucocyte common antigen (LCA) and for the major histocompatibility complex class II antigen (MHC II), with only a small proportion staining for the CD68 antigen. After longer survival times (1–4 months), MHC II-immunoreactivity (MHC II-IR) was clearly reduced in the grey matter but abundant in the white matter, specifically within the degenerating corticospinal tract, co-localising with CD68. In this fibre tract, elevated MHC II-IR and CD68-IR were still detectable 1 year after trauma or stroke. It is likely that the subsequent expression of CD68 on MHC II-positive microglia reflects the conversion to a macrophage phenotype, when cells are phagocytosing degenerating presynaptic terminals in grey matter target regions at early survival times and removing axonal and myelin debris in descending tracts at later survival times. No T or B cell invasion or involvement of co-stimulatory B7 molecules (CD80 and CD86) was observed. It is possible that the up-regulation of MHC II on microglia that lack the expression of B7 molecules may be responsible for the prevention of a T cell response, thus protecting the spinal cord from secondary tissue damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010000221
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  • 4
    Electronic Resource
    Electronic Resource
    Recurrente Hemmung der Extensor-Fusimotoneurone? (1971)
    Springer
    Pflügers Archiv 329 (1971), S. 23-33 
    Details
    ISSN: 1432-2013
    Keywords: Extensor γ-Motoneurones ; Recurrent Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The antidromic effect of ventral root or muscle nerve stimulation has been studied on functionally isolated γ-efferents to the medial gastrocnemius muscle in the intercollicular decerebrate cat. Tetanic stimulation of the ventral root at levels below the threshold for the investigated γ-efferents decreases the activity of 10 out of 19 γ-motoneurones. This effect is greater in cats with intact contralateral dorsal roots. Tetanic stimulation of synergic muscular nerves inhibits some of the investigated γ-motoneurones, whereas tetanic stimulation of antagonistic muscular nerves fails to have any inhibitory effect. It is suggested that the recurrent inhibition of γ-motoneurones is mediated via at least one additional interneuron between the Renshaw cell and the γ-motoneuron.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00586898
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  • 5
    Electronic Resource
    Electronic Resource
    Length-dependent autogenetic inhibition of extensor γ-motoneurones in the decerebrate cat (1974)
    Springer
    Pflügers Archiv 346 (1974), S. 251-262 
    Details
    ISSN: 1432-2013
    Keywords: Extensor γ-Motoneurones ; Autogenetic Inhibition ; Recurrent Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of stretching the triceps surae muscle on the resting discharge of functionally isolated and identified γ-efferents in the medial gastrocnemius nerve were studied in intercollicular decerebrate cats. Extension of the muscle decreases the activity of 9 out of 25 γ-motoneurones. This inhibition becomes apparent at about 8 mm muscle length and increases with increasing extension. Only those γ-efferents exhibiting this length-dependent inhibition are found to be inhibited by repetitive antidromic stimulation of the ventral root or the homonymous muscle nerve. We suggest that inhibition of fusimotor neurones by muscle stretch is at least partly mediated by the recurrent collaterals of the α-motoneurones activated by the stretch. 11 γ-motoneurones were predominantly excited by muscle stretch applied to the detached Achilles tendon as well as by squeezing the tendon. Nociceptors within the tendon or surrounding fascia are probably responsible.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00595711
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Disinhibition der Extensor-Motoneurone nach intercolliculärer Dezerebrierung (1969)
    Springer
    Pflügers Archiv 311 (1969), S. 148-158 
    Details
    ISSN: 1432-2013
    Keywords: Decerebrate State ; Extensor Motoneurones ; Recurrent Inhibition ; Disinhibition ; Schlüsselwörter ; Dezerebrierungsstarre ; Extensor-Motoneurone ; Recurrente Inhibition ; Disinhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Trotz kontinuierlicher Anaesthesie und Unterbrechung der Gamma-Spindelschleife löst die natürliche oder elektrische Reizung homonymer Ia-Afferenzen mit konstanter Stärke nach intercolliculärer Dezerebrierung an Extensor-Motoneuronen regelmäßigere Antworten, Verkürzung der Reflexzeit, Zunahme der Entladungsfrequenz, Verstärkung der post-tetanischen Potenzierung und Rekrutierung aus. Da der Grad der recurrenten Hemmung abnimmt, schließen wir, daß die gesteigerte Erregbarkeit der Extensor-Motoneurone im Zustand der Dezerebrierung mit Disinhibition verbunden ist. Die mit einem konstanten Quantum reflexwirksamer Afferenzen erhaltenen Resultate sprechen für unsere Annahme, daß Spastizität nicht hauptsächlich auf fusimotorischer Enthemmung beruht.
    Notes: Summary Even with continued anesthesia and interrupted gamma-loop intercollicular decerebration leads in extensor motoneurones (excited by electrical or natural stimulation of homonymous Ia-afferents with constant strength) to the following phenomona: more regular responses, shortening of reflex time, increase of discharge frequency, enhancement of post-tetanic potentiation, and recruitment. Because the degree of recurrent inhibition is diminished we conclude that the higher excitability of extensor motoneurones in the decerebrate state is correlated with disinhibition. Furthermore the results obtained with the afferent input for motoneurones kept constant favour our assumption that spasticity is not based merely on the release of fusimotor activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00587037
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    Paper (German National Licenses)
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