PMID- 9220451
OWN - NLM
STAT- MEDLINE
DCOM- 19970902
LR  - 20190831
IS  - 0197-0186 (Print)
IS  - 0197-0186 (Linking)
VI  - 31
IP  - 2
DP  - 1997 Aug
TI  - Prevention of apoptotic motoneuron death in vitro by neurotrophins and muscle 
      extract.
PG  - 193-201
AB  - In this study, it is shown that rat motoneurons in culture are highly dependent 
      on trophic support and die in the absence of such support via active cell death, 
      or apoptosis. This apoptotic death occurs in their 'in vitro' life (within 24 h) 
      and can be partially prevented by treating the cultures with neurotrophic 
      substances. The most effective support comes from an extract prepared from 
      embryonic chick muscle: without muscle extract, no healthy, neurite-bearing 
      motoneurons are present, but with 0.3 and 1.2% muscle extract, their numbers 
      increase dose-dependently. Neurotrophins, such as brain-derived neurotrophic 
      factor (BDNF) and neurotrophin-4 (NT-4), cannot replace muscle extract and keep 
      motoneurons alive on their own, but in the presence of muscle extract (0.3%) they 
      have a significant effect on survival (increase up to four times, compared to 
      0.3% muscle extract). At the same time, they prevent apoptotic cell death. 
      Selective motoneuron death has been implicated in the neurodegenerative disease 
      amyotrophic lateral sclerosis (ALS). Despite strong evidence that motoneurons in 
      ALS die via apoptosis, this has not been shown unequivocally in post mortem 
      material. This study shows that motoneurons are very sensitive to conditions that 
      initiate apoptosis, and that cell death can be prevented to a large degree with 
      relatively low concentrations of neurotrophic factors. In view of the fact that 
      several patient trials with neurotrophic factors already are underway, studies 
      with motoneurons in culture may prove important in understanding the mechanism of 
      cell death and the efficacy of drugs such as neurotrophic factors, but also other 
      types of drug.
FAU - Kaal, E C
AU  - Kaal EC
AD  - Utrecht University, Department of Neurology, The Netherlands.
FAU - Joosten, E A
AU  - Joosten EA
FAU - Bar, P R
AU  - Bar PR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Neurochem Int
JT  - Neurochemistry international
JID - 8006959
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Tissue Extracts)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Cells, Cultured
MH  - Motor Neurons/*drug effects/*physiology
MH  - Muscles/*chemistry
MH  - Nerve Growth Factors/*pharmacology
MH  - Neuroprotective Agents/pharmacology
MH  - Rats/embryology
MH  - Rats, Wistar
MH  - Tissue Extracts/*pharmacology
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
AID - S0197-0186(96)00148-9 [pii]
AID - 10.1016/s0197-0186(96)00148-9 [doi]
PST - ppublish
SO  - Neurochem Int. 1997 Aug;31(2):193-201. doi: 10.1016/s0197-0186(96)00148-9.