Abstract：
:Excitotoxic stimulation of NMDA receptors results in the activation of a variety of cellular responses. The inducible transcription factor NF-kappaB is known to be involved in excitotoxic responses by neurons. Here, we show that NF-kappaB activation occurs in a biphasic manner in hippocampal slices following a 20-min N-methyl- d-aspartate (NMDA) exposure. The biphasic activation profile consists of an early, rapid phase at 0.5-1 h post-insult, and a delayed phase evident 10-24 h post-insult. Endogenous inhibitors of NF-kappaB, IkappaBs, were examined for their involvement in the biphasic activation. IkappaBbeta exhibited marked degradation in response to the excitotoxity, while changes in the levels of IkappaBalpha and p105 isoforms were not detected. The initial decline in IkappaBbeta occurred in as little as 30 min post-NMDA exposure, coinciding with early NF-kappaB activity. A second, more gradual phase of IkappaBbeta degradation was also evident, possibly giving rise to the delayed activation of the transcription factor. While both phases of NF-kappaB activation were disrupted by the NMDA receptor antagonist AP5, they were distinct with regard to the composition of activated complexes and their responsiveness to altered culture conditions. The two phases of NF-kappaB activity also were associated with distinct gene regulation events. Up-regulation of bcl-2 message occurred early after the excitotoxic insult and remained up-regulated for an extended period. In contrast, bax message initially remained unchanged after the insult, but then exhibited an increase 24 h later, corresponding with the second phase of the NF-kappaB response. These results indicate that distinct phases of NF-kappaB activation are generated in the excitotoxic hippocampus, and that the phases may be involved in opposing cellular responses.
journal_name
Acta Neuropatholjournal_title
Acta neuropathologicaauthors
Caba E,Bahr BAdoi
10.1007/s00401-004-0876-5subject
Has Abstractpub_date
2004-09-01 00:00:00pages
173-82issue
3eissn
0001-6322issn
1432-0533journal_volume
108pub_type
杂志文章abstract：:In order to further evaluate the parameters whereby intracerebral administration of recombinant α-synuclein (αS) induces pathological phenotypes in mice, we conducted a series of studies where αS fibrils were injected into the brains of M83 (A53T) and M47 (E46K) αS transgenic (Tg) mice, and non-transgenic (nTg) mice. ...
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journal_title：Acta neuropathologica
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journal_title：Acta neuropathologica
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journal_title：Acta neuropathologica
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journal_title：Acta neuropathologica
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journal_title：Acta neuropathologica
pub_type： 杂志文章
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更新日期：1978-12-15 00:00:00
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journal_title：Acta neuropathologica
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journal_title：Acta neuropathologica
pub_type： 杂志文章
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更新日期：1976-05-18 00:00:00
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journal_title：Acta neuropathologica
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更新日期：2003-09-01 00:00:00
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journal_title：Acta neuropathologica
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journal_title：Acta neuropathologica
pub_type： 杂志文章
doi：10.1007/BF00690850
更新日期：1979-05-15 00:00:00
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journal_title：Acta neuropathologica
pub_type： 杂志文章
doi：10.1007/BF00685374
更新日期：1982-01-01 00:00:00
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journal_title：Acta neuropathologica
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doi：10.1007/BF00296179
更新日期：1994-01-01 00:00:00
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journal_title：Acta neuropathologica
pub_type： 杂志文章
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更新日期：1977-11-28 00:00:00
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journal_title：Acta neuropathologica
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更新日期：2000-04-01 00:00:00
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journal_title：Acta neuropathologica
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更新日期：2003-07-01 00:00:00
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journal_title：Acta neuropathologica
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更新日期：2006-07-01 00:00:00
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journal_title：Acta neuropathologica
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更新日期：2015-10-01 00:00:00
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pub_type： 杂志文章
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更新日期：1989-01-01 00:00:00
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journal_title：Acta neuropathologica
pub_type： 杂志文章
doi：10.1007/BF00703319
更新日期：1977-08-16 00:00:00
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doi：10.1007/s00401-013-1122-9
更新日期：2013-07-01 00:00:00
