PMID- 14651807
OWN - NLM
STAT- MEDLINE
DCOM- 20040116
LR  - 20161025
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 20
IP  - 11
DP  - 2003 Nov
TI  - Apoptosis of spinal cord neurons by preventing depletion nicotine attenuates 
      arachidonic acid-induced of neurotrophic factors.
PG  - 1201-13
AB  - Increased levels of free fatty acids and, in particular, arachidonic acid can 
      lead to induction of apoptosis of spinal cord neurons. Because of the importance 
      of neurotrophic factors in cell survival and death, mRNA and protein levels of 
      brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor 
      (FGF-2) were studied in cultured spinal cord neurons treated with arachidonic 
      acid. In addition, the present study focused on the effects of nicotine and 
      neuronal nicotinic acetylcholine receptors (nAChRs) on these processes. A 2-h 
      exposure to arachidonic acid markedly diminished expression of BDNF and FGF-2. 
      These effects were fully prevented by pretreatment with 10 microM nicotine. 
      Mecamylamine (a non-specific antagonist of nAChRs) and alpha-bungarotoxin (a 
      specific antagonist of the nAChRalpha7) completely inhibited nicotine-mediated 
      protection against arachidonic acid-induced alterations of BDNF and FGF-2. In 
      addition, nicotine, BDNF and FGF-2 fully protected against arachidonic 
      acid-induced apoptosis of spinal cord neurons. BDNF and FGF-2 were effective in 
      prevention of apoptotic cell death even when applied 2 h after the beginning of 
      arachidonic acid treatment. These results suggest that arachidonic acid can 
      induce apoptosis of spinal cord neurons by depletion of neurotrophic factors and 
      that nicotine can protect against these effects through the nAChRalpha7-mediated 
      pathway.
FAU - Garrido, Rosario
AU  - Garrido R
AD  - Department of Surgery, University of Kentucky Medical Center, Lexington, Kentucky 
      40536, USA.
FAU - Springer, Joe E
AU  - Springer JE
FAU - Hennig, Bernhard
AU  - Hennig B
FAU - Toborek, Michal
AU  - Toborek M
LA  - eng
GR  - P42 ES007380/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Nicotinic Antagonists)
RN  - 0 (Receptors, Nicotinic)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 27YG812J1I (Arachidonic Acid)
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Arachidonic Acid/toxicity
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/drug effects
MH  - Cells, Cultured
MH  - Embryo, Mammalian
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fibroblast Growth Factor 2/biosynthesis/drug effects
MH  - Mice
MH  - Nerve Growth Factors/biosynthesis/*drug effects
MH  - Neurons/*drug effects/pathology
MH  - Neuroprotective Agents/*pharmacology
MH  - Nicotine/*pharmacology
MH  - Nicotinic Antagonists/pharmacology
MH  - Receptors, Nicotinic/drug effects/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Spinal Cord/drug effects
EDAT- 2003/12/04 05:00
MHDA- 2004/01/17 05:00
CRDT- 2003/12/04 05:00
PHST- 2003/12/04 05:00 [pubmed]
PHST- 2004/01/17 05:00 [medline]
PHST- 2003/12/04 05:00 [entrez]
AID - 10.1089/089771503322584628 [doi]
PST - ppublish
SO  - J Neurotrauma. 2003 Nov;20(11):1201-13. doi: 10.1089/089771503322584628.