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Faculty of Medicine
Document Details
Document Type
:
Article In Journal
Document Title
:
"GAP-43 and p75NGFR immunoreactivity in presynaptic cells following neurotransmission blockade by botulinum toxin in rat"
"GAP-43 and p75NGFR immunoreactivity in presynaptic cells following neurotransmission blockade by botulinum toxin in rat"
Document Language
:
English
Abstract
:
Peripheral nerve lesion results in changes in protein expression by neurons and denervated Schwann cells. In the present study we have addressed the question whether similar changes take place following functional denervation. Using immunohistochemistry and immunoelectron microscopy we examined changes in growth-associated protein (GAP-43) and low-affinity nerve growth factor receptor (p75NGFR) in rat gastrocnemius muscle following botulinum toxin-induced paralysis. GAP-43 and p75NGFR were selected because they are not expressed by mature intact motor neurons or Schwann cells, but are expressed following nerve lesion in both motor neurons and denervated Schwann cells. In control muscle, GAP-43 and p75NGFR immunoreactivity was seen only in nerve fibres near blood vessels. Two weeks after toxin injection, GAP-43 immunoreactivity could be seen at the motor endplates and in axons. Intensity of staining increased with longer survival and reached a peak between 4 and 8 weeks post-injection. Ultrastructurally, GAP-43 immunoreactivity was confined to nerve terminals and axons, whereas Schwann cells remained negative. Immunostaining for p75NGFR also increased following toxin injection and was detected in some terminal Schwann cells and in perineurial cells of small nerve fascicles near the paralyzed target cells, but not in axons. These results show that changes in expression of GAP-43 in motor neurons following functional denervation closely resemble the changes following anatomical interruption of nerve-muscle contact. GAP-43 was not expressed in Schwann cells, indicating that its upregulation in these cells is induced by loss of axonal contact or nerve degeneration products. There is no support for a role of p75NGFR in incorporation of neurotrophins in axons. The restriction of p75NGFR expression to terminal Schwann cells and perineurial cells in close proximity to the paralyzed target suggests a role for a target-derived signal or, alternatively, macrophages in eliciting this expression.
ISSN
:
1319-1004
Journal Name
:
Journal of Neurocytology
Volume
:
23
Issue Number
:
3
Publishing Year
:
1994 AH
1994 AD
Article Type
:
Article
Added Date
:
Sunday, March 28, 2010
Researchers
Researcher Name (Arabic)
Researcher Name (English)
Researcher Type
Dr Grade
Email
شريف حسن
Hassan, Sherif
Researcher
Doctorate
Files
File Name
Type
Description
26215.1
1
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