Abstract：
:Cerebellar granule neurons produce homogenous cultures that provide a unique opportunity for quantifying the apoptosis by propidium iodide- and deoxynucleotidyl transferase-flow cytometry combined analysis and for studying its regulation by neurotrophins. Nerve growth factor (NGF) was found to promote postmitotic survival by preventing apoptosis of newly formed and early differentiated granule neurons. This regulation could be through protein bcl-2, which was underexpressed in apoptotic granule neurons and up-regulated by NGF in a dose-dependent manner. Antibodies against low affinity NGF receptors (p75NTR) mimicked the effects of NGF, suggesting that this receptor, which is transiently expressed at high levels in postmitotic granule neurons, is involved in apoptosis signaling. Since these neurons constitutively produce NGF, this is the first demonstration of an autocrine regulation of apoptosis in the CNS. Preliminary results strongly suggest that neurotrophin-3 (NT-3) and brain derived neurotrophic factor (BDNF) are also involved in the regulation of cell death, by first promoting necrosis and then protecting the remaining cells from apoptosis. In contrast, NGF may protect against two forms of cell death and act preferentially at early stages of granule neuron development. The possibility that these neurotrophins may act in parallel and/or in sequence to regulate survival of developing granule neurons through different mechanisms is discussed in the light of findings on neurotrophin and p75NTR patterns, and p75NTR/high affinity Trk receptor coexpression.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Muller Y,Tangre K,Clos Jdoi
10.1016/s0197-0186(96)00147-7subject
Has Abstractpub_date
1997-08-01 00:00:00pages
177-91issue
2eissn
0197-0186issn
1872-9754pii
S0197-0186(96)00147-7journal_volume
31pub_type
杂志文章abstract：:Homozygous deletion or mutation in the survival motor neuron (SMN)1 gene causes proximal spinal muscular atrophy (SMA), whereas SMN2 acts as a modifying gene that can influence the severity of SMA. It has been suggested that restoration of the SMN protein level in neuronal cells may prevent cell loss and may be helpfu...
journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
pub_type： 杂志文章,评审
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journal_title：Neurochemistry international
pub_type： 杂志文章
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pub_type： 杂志文章
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journal_title：Neurochemistry international
pub_type： 杂志文章
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更新日期：1992-01-01 00:00:00
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
pub_type： 杂志文章
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journal_title：Neurochemistry international
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pub_type： 杂志文章,评审
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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