PMID- 10383120
OWN - NLM
STAT- MEDLINE
DCOM- 19990729
LR  - 20091119
IS  - 1059-910X (Print)
IS  - 1059-910X (Linking)
VI  - 45
IP  - 4-5
DP  - 1999 May 15-Jun 1
TI  - Neurotrophin-mediated potentiation of neuronal injury.
PG  - 276-84
AB  - The neurotrophins are a diverse family of peptides which activate specific 
      tyrosine kinase-linked receptors. Over the past five decades, since the 
      pioneering work of Levi-Montalcini and colleagues, the critical role that 
      neurotrophins play in shaping the developing nervous system has become 
      increasingly established. These molecules, which include the nerve growth factor 
      (NGF)-related peptides, NGF, brain-derived neurotrophic factor (BDNF), NT-4/5 and 
      NT-3, promote differentiation and survival in the developing nervous system, and 
      to a lesser extent in the adult nervous system. As survival-promoting molecules, 
      neurotrophins have been studied as potential neuroprotective agents, and have 
      shown beneficial effects in many model systems. However, a surprising "dark side" 
      to neurotrophin behavior has emerged from some of these studies implying that, 
      under certain pathological conditions, neurotrophins may exacerbate, rather than 
      alleviate, injury. How neurotrophins cause these deleterious consequences is a 
      question which is only beginning to be answered, but initial work supports 
      altered free radical handling or modification of glutamate receptor expression as 
      possible mechanisms underlying these effects. This review will focus on evidence 
      suggesting that neurotrophins may enhance injury under certain circumstances and 
      on the mechanisms behind these injury-promoting aspects.
FAU - Behrens, M M
AU  - Behrens MM
AD  - Center for the Study of the Nervous System Injury and Department of Neurology, 
      Washington University School of Medicine, St. Louis, Missouri 63110, USA. 
      behrensm@neuro.wustl.edu
FAU - Strasser, U
AU  - Strasser U
FAU - Lobner, D
AU  - Lobner D
FAU - Dugan, L L
AU  - Dugan LL
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Microsc Res Tech
JT  - Microscopy research and technique
JID - 9203012
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Culture Media)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Receptor, Ciliary Neurotrophic Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/physiology
MH  - Brain-Derived Neurotrophic Factor/pharmacology/physiology
MH  - Cell Hypoxia
MH  - Cells, Cultured
MH  - Culture Media/chemistry
MH  - Microscopy, Confocal
MH  - Mitochondria/metabolism
MH  - Necrosis
MH  - Nerve Growth Factors/pharmacology/*physiology
MH  - Neurons/drug effects/pathology/*physiology
MH  - Neutrophils/metabolism
MH  - Oxidative Stress/physiology
MH  - Receptor Protein-Tyrosine Kinases/metabolism
MH  - Receptor, Ciliary Neurotrophic Factor
MH  - Receptors, Nerve Growth Factor/metabolism
MH  - Time Factors
RF  - 162
EDAT- 1999/06/26 10:00
MHDA- 2000/06/22 10:00
CRDT- 1999/06/26 10:00
PHST- 1999/06/26 10:00 [pubmed]
PHST- 2000/06/22 10:00 [medline]
PHST- 1999/06/26 10:00 [entrez]
AID - 10.1002/(SICI)1097-0029(19990515/01)45:4/5<276::AID-JEMT11>3.0.CO;2-4 [pii]
AID - 10.1002/(SICI)1097-0029(19990515/01)45:4/5<276::AID-JEMT11>3.0.CO;2-4 [doi]
PST - ppublish
SO  - Microsc Res Tech. 1999 May 15-Jun 1;45(4-5):276-84. doi: 
      10.1002/(SICI)1097-0029(19990515/01)45:4/5<276::AID-JEMT11>3.0.CO;2-4.