PMID- 8261087
OWN - NLM
STAT- MEDLINE
DCOM- 19940127
LR  - 20190815
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 5
IP  - 1
DP  - 1993 Jan 1
TI  - Injury-induced regulation of ciliary neurotrophic factor mRNA in the adult rat 
      brain.
PG  - 25-33
AB  - Ciliary neurotrophic factor (CNTF) is a pleiotropic molecule that acts as a 
      neurotrophic factor for a wide range of embryonic neurons as well as a 
      differentiation factor for sympathetic neuroblasts and O2A progenitor cells in 
      culture. CNTF messenger RNA (mRNA) is present at very low levels in the normal 
      adult rat central nervous system (CNS), but is dramatically up-regulated after an 
      aspiration lesion of dorsal hippocampus and overlying cortex, in the area 
      coincident with glial scar. The increased level of CNTF mRNA in lesioned 
      hippocampus is maximal by 3 days and is sustained for up to 20 days, the longest 
      time point examined. In contrast, mRNA levels for brain-derived neurotrophic 
      factor (BDNF) and neurotrophin-3 (NT-3) were slightly decreased during the same 
      period. In situ hybridization experiments revealed that cells expressing CNTF 
      mRNA were concentrated at the margin of the wound, and also present within the 
      gelfoam which filled the lesion cavity. This distribution of CNTF-expressing 
      cells corresponded very closely to that of cells expressing high levels of glial 
      fibrillary acidic protein mRNA at the wound site. Paralleling the observed 
      increase in CNTF mRNA, increased levels of CNTF-like neurotrophic activity were 
      apparent in soluble extracts of the lesioned tissues. This neurotrophic activity 
      for ciliary ganglion neurons was completely blocked by the addition of 
      neutralizing antiserum against CNTF. Basic fibroblast growth factor, which has 
      been shown by others to increase after a similar lesion paradigm (Frautschy et 
      al., Brain Res., 553, 291-299, 1991), does not contribute appreciably to this 
      trophic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Ip, N Y
AU  - Ip NY
AD  - Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591.
FAU - Wiegand, S J
AU  - Wiegand SJ
FAU - Morse, J
AU  - Morse J
FAU - Rudge, J S
AU  - Rudge JS
LA  - eng
PT  - Journal Article
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Ciliary Neurotrophic Factor)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Brain/*metabolism
MH  - Brain Injuries/*metabolism
MH  - Brain-Derived Neurotrophic Factor
MH  - Chick Embryo
MH  - Ciliary Neurotrophic Factor
MH  - Embryo, Mammalian/cytology/metabolism
MH  - Female
MH  - Ganglia, Parasympathetic/embryology
MH  - Ganglia, Spinal/embryology
MH  - In Situ Hybridization
MH  - Nerve Tissue Proteins/*genetics
MH  - Nodose Ganglion/embryology
MH  - RNA, Messenger/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
AID - 10.1111/j.1460-9568.1993.tb00201.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 1993 Jan 1;5(1):25-33. doi: 10.1111/j.1460-9568.1993.tb00201.x.