PMID- 8594213
OWN - NLM
STAT- MEDLINE
DCOM- 19960409
LR  - 20071114
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 12
IP  - 5
DP  - 1995 Oct
TI  - Neurotrophic factors in central nervous system trauma.
PG  - 853-70
AB  - Although regeneration of injured neurons does not occur after trauma in the 
      central nervous system (CNS), there is often significant recovery of functional 
      capacity with time. Little is currently known about the molecular basis for such 
      recovery, but the increased trophic activity in injured CNS tissue and the known 
      properties of neurotrophic factors in neuronal growth and maintenance suggest 
      that these polypeptides are probably involved in recovery of function. Members of 
      the neurotrophin family, including nerve growth factor (NGF), brain-derived 
      neurotrophic factors (BDNF), and neurotrophin 3 (NT-3), are capable of supporting 
      survival of injured CNS neurons both in vitro and in vivo. They also stimulate 
      neurite outgrowth, needed for reorganization of the injured CNS, and the 
      expression of key enzymes for neurotransmitter synthesis that may need to be 
      upregulated to compensate for reduced innervation. The effects of the 
      neurotrophins are mediated through specific high affinity trk receptors (trk A, 
      B, C) as well as a common low affinity receptor designated p75NGFR. Another class 
      of neurotrophic polypeptides also provides candidate recovery-promoting 
      molecules, the heparin-binding growth factors' acidic and basic fibroblast growth 
      factor (aFGF, bFGF). FGFs not only sustain survival of injured neurons but also 
      stimulate revascularization and certain glial responses to injury. Both the 
      neurotrophins and the FGFs, as well as their respective receptors, have been 
      shown to be upregulated after experimental CNS injury. Further, administration of 
      neurotrophins or FGF has been shown to reduce the effects of experimental injury 
      induced by axotomy, excitotoxins, and certain other neurotoxins. The cellular 
      basis for the potential therapeutic use of neurotrophic molecules is discussed as 
      well as new strategies to increase neurotrophic activity after CNS trauma based 
      on the recently obtained information on pharmacological and molecular control of 
      the expression of these genes.
FAU - Mocchetti, I
AU  - Mocchetti I
AD  - Department of Cell Biology, Georgetown University School of Medicine, Washington 
      D.C. 20007, USA.
FAU - Wrathall, J R
AU  - Wrathall JR
LA  - eng
GR  - NS 01675/NS/NINDS NIH HHS/United States
GR  - NS28130/NS/NINDS NIH HHS/United States
GR  - NS32671/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Nerve Growth Factors)
SB  - IM
MH  - Animals
MH  - Brain/*metabolism
MH  - Brain Injuries/drug therapy/*metabolism
MH  - Central Nervous System Diseases/drug therapy/*metabolism
MH  - Humans
MH  - Nerve Growth Factors/biosynthesis/*metabolism/therapeutic use
MH  - Spinal Cord/*metabolism
MH  - Spinal Cord Injuries/drug therapy/*metabolism
RF  - 186
EDAT- 1995/10/01 00:00
MHDA- 1995/10/01 00:01
CRDT- 1995/10/01 00:00
PHST- 1995/10/01 00:00 [pubmed]
PHST- 1995/10/01 00:01 [medline]
PHST- 1995/10/01 00:00 [entrez]
AID - 10.1089/neu.1995.12.853 [doi]
PST - ppublish
SO  - J Neurotrauma. 1995 Oct;12(5):853-70. doi: 10.1089/neu.1995.12.853.