CATALOGO DEI PRODOTTI DELLA RICERCA

Axonal transport of neurofilament is accelerated in peripheral nerve during 2,5-hexanedione intoxication.

MONACO, Salvatore;
1989-01-01
1989
Inglese
STAMPA
Sì, ma tipo non specificato
BRAIN RESEARCH
491
2
328
334
7
2475210
WOS:A1989AF22400011
2-s2.0-0024373687
https://dx.doi.org/10.1016/0006-8993(89)90067-X
Axonal transport; 2; 5-Hexanedione; Neurofilament; Giant axonal neuropathy; Acceleration of transport
The neurotoxic compound 2,5-hexanedione (2,5-HD) causes an axonopathy characterized by the presence of neurofilament (NF)-containing enlargements in the preterminal segments of central and peripheral axons. The 2,5-HD axonopathy is a good model for human acquired and inherited giant axonal neuropathies. Recently, we reported that following 2,5-HD administration, axonal transport of NF is markedly and selectively accelerated in the primary visual system. We have now studied slow axonal transport in the sciatic system of rats intoxicated with 0.5% 2,5-HD in drinking water. Following radiolabeling, transported proteins were examined after polyacrylamide gel electrophoresis and fluorography. The bulk of radiolabeled NF subunits was located 30–50 mm from the spinal cord in 2,5-HD treated animals and 10–25 mm in controls. The rate of transport of the three NF subunits was 0.7 mm/day in controls and 1.2 mm/day in 2,5-HD treated animals. The rate of transport of tubulin was not significantly changed. Electrophysiological studies of soleus nerve and muscle showed no evidence of denervation after 6 weeks of intoxication. It is concluded that, following 2,5-HD administration, transport of NF is preferentially accelerated in both central and peripheral axons. A pathogenetic mechanism based on the acceleration of NF transport is proposed, which may explain the formation and the distal or proximal location of NF-containing axonal enlargements in giant axonopathies.
http://dx.doi.org/10.1016/0006-8993(89)90067-X
none
info:eu-repo/semantics/article
Monaco, Salvatore; Jacob, J.; Jenich, H.; Patton, A.; Autilio Gambetti, L.; Gambetti, P.
6
01 Contributo in rivista::01.01 Articolo in Rivista
262
01.01 Articolo in Rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/231595
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