Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • 2000-2004  (1)
  • 1965-1969  (1)
  • Primary Muscle Spindle Endings  (1)
  • Stroke  (1)
  • 1
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-2013
    Keywords: Primary Muscle Spindle Endings ; Static and Dynamic Sensitivities ; Decerebrate State ; Spinalization ; Deefferentation ; Primäre Muskelspindelendigungen ; Statische und dynamische Empfindlichkeiten ; Dezerebrierungsstarre ; Spinalisierung ; Deefferentierung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 1. Primäre Spindelafferenzen, die bei anaesthesierten Katzen (Fluothane- oder Äther-Stickoxydul-Sauerstoffgemisch) rampenförmige Muskeldehnungen statisch und dynamisch gut beantworten, verlieren nach intercolliculärer Dezerebrierung sowohl an statischer als auch an dynamischer Aktivität. Sofern diese Afferenzen aus Extensoren stammen, führen Spinalisierung und Deefferentierung eine zusätzliche Aktivitätsminderung herbei. 2. Handelt es sich hingegen um primäre Spindelafferenzen, die bei anaesthesierten Katzen ansteigende Muskeldehnungen statisch schlecht oder gar nicht messen, dann nimmt deren Aktivität nach intercolliculärer Dezerebrierung zu, ist allerdings erst nach Deefferentierung maximal. 3. Aus den Ergebnissen wird geschlossen, daß die intercolliculäre Dezerebrierung fusimotorische Spindelsysteme nicht enthemmt.
    Notes: Summary 1. In cats, anesthetized either with mixtures of Fluothane and nitrous oxide or ether and nitrous oxide, primary spindle afferents lose to some extent their static and dynamic responsiveness after intercollicular decerebration, provided that they responded before decerebration quite well to ramp-like muscle extension. If this type of afferents originate from extensor muscles, an additional reduction of their activity is caused by sectioning the spinal cord at Th XII and by deefferentation. 2. In contrast, the static activity of primary endings increases after intercollicular decerebration and spinalization, if their static responsiveness to muscle extension was insufficient before decerebration. In this case, however, maximum activity is not reached until the ventral roots are cut. 3. It is concluded that the intercollicular decerebration does not enhance the activity of primary spindle afferents by release of fusimotor activity.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...