Abstract:
:We investigated the temporal course of blood-nerve barrier (BNB) breakdown during the evolution of tellurium neuropathy, ricin neuropathy, and Wallerian degeneration following nerve transection or nerve crush. Blood-nerve barrier permeability was assessed with a 4,000-molecular weight fluoresceinated dextran from three days to 19 weeks after onset of neuropathy. Blood-nerve barrier breakdown was present during the first two weeks in all four models of neuropathy. Restoration of the BNB to the dextran began within four weeks and was complete by 14 weeks in tellurium neuropathy, a model of demyelinating neuropathy characterized by rapid remyelination, and after nerve crush, a model of Wallerian degeneration characterized by rapid axonal regeneration into distal stump. In contrast, there was persistence of BNB breakdown beyond 14 weeks in ricin neuropathy, a model of neuropathy with no axonal regeneration or remyelination, and after nerve transection, a model of Wallerian degeneration characterized by minimal axonal regeneration into distal stump. We conclude from these data that alterations in the BNB over the course of neuropathy differ among various types of neuropathy, and that these alterations are dependent on the form of nerve fiber injury. The lack of regenerating or remyelinating axons in ricin neuropathy and after nerve transection may be responsible for the persistent BNB breakdown found in these neuropathies.
journal_name
J Neuropathol Exp Neuroljournal_title
Journal of neuropathology and experimental neurologyauthors
Bouldin TW,Earnhardt TS,Goines NDdoi
10.1097/00005072-199111000-00004subject
Has Abstractpub_date
1991-11-01 00:00:00pages
719-28issue
6eissn
0022-3069issn
1554-6578journal_volume
50pub_type
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