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Role of Bcl‐2 in the Brain‐derived Neurotrophic Factor Survival Response
Author(s) -
Allsopp Timothy E.,
Kiselev Sergei,
Wyatt Sean,
Davies Alun M.
Publication year - 1995
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1995.tb01116.x
Subject(s) - ciliary neurotrophic factor , neurotrophin , neurotrophic factors , neuroscience , brain derived neurotrophic factor , biology , nerve growth factor , rna , antisense rna , microbiology and biotechnology , receptor , genetics , gene
Developing neurons die if they fail to obtain an adequate supply of neurotrophins from their targets but how neurotrophins suppress cell death is not known. Although over‐expression of exogenous Bcl‐2 can prevent the death of cultured neurons deprived of members of the nerve growth factor family of neurotrophins it is not known if this effect is physiologically relevant. To determine if Bcl‐2 participates in the neurotrophin survival response we used antisense bcl‐2 RNA to inhibit endogenous Bcl‐2 expression. Here we show that brain‐derived neurotrophic factor (BDNF)‐dependent neurons are killed by antisense bcl‐2 RNA in the presence of BDNF. However, when these neurons were supported with ciliary neurotrophic factor (CNTF) their survival was not affected by antisense bcl‐2 RNA. Likewise, the survival of CNTF‐dependent ciliary neurons was not affected by antisense bcl‐2 RNA. Our findings suggest that Bcl‐2 is required for the BDNF survival response and that alternative, Bcl‐2‐independent survival mechanisms operate in sensory and parasympathetic neurons exposed to CNTF.