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Mechanisms leading to disseminated apoptosis following NMDA receptor blockade in the developing rat brain.

Abstract：

:The developing rodent brain is vulnerable to pharmacological blockade of N-methyl-d-aspartate (NMDA) receptors which can lead to severe and disseminated apoptotic neurodegeneration. Here, we show that systemic administration of the NMDA receptor antagonist MK801 to 7-day-old rats leads to impaired activity of extracellular signal-regulated kinase 1/2 (ERK1/2) and reduces levels of phosphorylated cAMP-responsive element binding protein (CREB) in brain regions which display severe apoptotic neurodegeneration. Impaired ERK1/2 and CREB activity were temporally paralleled by sustained depletion of neurotrophin expression, particularly brain-derived neurotrophic factor (BDNF). BDNF supplementation fully prevented MK801-induced neurotoxicity in immature neuronal cultures and transgenic constitutive activation of Ras was associated with marked protection against MK801-induced apoptotic neuronal death. These data indicate that uncoupling of NMDA receptors from the ERK1/2-CREB signaling pathway in vivo results in massive apoptotic deletion of neurons in the developing rodent brain.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Hansen HH,Briem T,Dzietko M,Sifringer M,Voss A,Rzeski W,Zdzisinska B,Thor F,Heumann R,Stepulak A,Bittigau P,Ikonomidou C

doi

10.1016/j.nbd.2004.03.013

keywords:

subject

Has Abstract

pub_date

2004-07-01 00:00:00

pages

440-53

issue

2

eissn

0969-9961

issn

1095-953X

pii

S0969996104000749

journal_volume

16

pub_type

杂志文章

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