PMID- 1716667
OWN - NLM
STAT- MEDLINE
DCOM- 19911023
LR  - 20190510
IS  - 0022-3069 (Print)
IS  - 0022-3069 (Linking)
VI  - 50
IP  - 5
DP  - 1991 Sep
TI  - Regulation of aberrant neurofilament phosphorylation in neuronal perikarya. I. 
      Production following colchicine application to the sciatic nerve.
PG  - 615-26
AB  - Neurofilament (NF) triplet proteins are normally poorly phosphorylated in 
      neuronal perikarya, the two high molecular weight polypeptides becoming 
      extensively phosphorylated once the NF enters the axon. Abnormal expression of 
      phosphorylated NF (pNF) epitopes in neuronal perikarya has been revealed using 
      monoclonal antibodies in a variety of human and experimental conditions. In the 
      present study, we asked whether pNF epitopes are expressed in sensory neurons in 
      the L4 and L5 dorsal root ganglia (DRG) following blockade of fast axonal 
      transport in a model producing few (less than 1%) degenerating fibers. Colchicine 
      (5 mM) was briefly (45 minutes) applied to the sciatic nerve at mid-thigh twice 
      (once weekly) and the animals studied two weeks following the first colchicine 
      application; contralateral nerves were either treated with saline or crushed. 
      Modest to intense immunoreactivity was found with antibody 07-05 (directed 
      against pNF epitopes on the two high molecular weight NF polypeptides) in 30.4% 
      and 45.1% of DRG neurons from colchicine-treated and crushed nerves, 
      respectively; only a rare cell body demonstrated immunostaining from the 
      contralateral saline-treated nerves. Immunoreactivity was not observed with 
      antibody 07-05 at two and five days following single colchicine application. In a 
      separate study, colchicine or saline was applied (as above) 1-2 cm proximal to a 
      nerve crush. Colchicine application did not influence the extent of DRG neurons 
      expressing pNF epitopes; immunostaining with antibody 07-05 was present in 44.7% 
      and 43.8% of DRG neurons from saline-treated and colchicine-treated crushed 
      nerves, respectively. The results indicate that structural interruption of 
      nerve-target contact is not necessary to induce aberrant NF phosphorylation in 
      neuronal perikarya. It is suggested that loss of a retrogradely transported 
      "trophic" signal(s) triggers this response.
FAU - Gold, B G
AU  - Gold BG
AD  - Center for Research on Occupational and Environmental Toxicology, Oregon Health 
      Sciences University, Portland 97201.
FAU - Austin, D R
AU  - Austin DR
LA  - eng
GR  - NS26265/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neuropathol Exp Neurol
JT  - Journal of neuropathology and experimental neurology
JID - 2985192R
RN  - 0 (Epitopes)
RN  - 0 (Intermediate Filament Proteins)
RN  - 0 (Neurofilament Proteins)
RN  - SML2Y3J35T (Colchicine)
SB  - IM
MH  - Animals
MH  - Colchicine/*pharmacology
MH  - Epitopes
MH  - Ganglia, Spinal/metabolism
MH  - Intermediate Filament Proteins/immunology/*metabolism
MH  - Male
MH  - Nerve Crush
MH  - Neurofilament Proteins
MH  - Neurons/*metabolism
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Sciatic Nerve/*drug effects/metabolism
EDAT- 1991/09/01 00:00
MHDA- 1991/09/01 00:01
CRDT- 1991/09/01 00:00
PHST- 1991/09/01 00:00 [pubmed]
PHST- 1991/09/01 00:01 [medline]
PHST- 1991/09/01 00:00 [entrez]
AID - 10.1097/00005072-199109000-00007 [doi]
PST - ppublish
SO  - J Neuropathol Exp Neurol. 1991 Sep;50(5):615-26. doi: 
      10.1097/00005072-199109000-00007.