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Nonapoptotic function of BAD and BAX in long-term depression of synaptic transmission.

Abstract：

:It has recently been found that caspases not only function in apoptosis, but are also crucial for nonapoptotic processes such as NMDA receptor-dependent long-term depression (LTD) of synaptic transmission. It remains unknown, however, how caspases are activated and how neurons escape death in LTD. Here we show that caspase-3 is activated by the BAD-BAX cascade for LTD induction. This cascade is required specifically for NMDA receptor-dependent LTD but not for mGluR-LTD, and its activation is sufficient to induce synaptic depression. In contrast to apoptosis, however, BAD is activated only moderately and transiently and BAX is not translocated to mitochondria, resulting in only modest caspase-3 activation. We further demonstrate that the intensity and duration of caspase-3 activation determine whether it leads to cell death or LTD, thus fine-tuning of caspase-3 activation is critical in distinguishing between these two pathways.

journal_name

Neuron

journal_title

Neuron

authors

Jiao S,Li Z

doi

10.1016/j.neuron.2011.04.004

subject

Has Abstract

pub_date

2011-05-26 00:00:00

pages

758-72

issue

4

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(11)00306-0

journal_volume

70

pub_type

杂志文章

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