PMID- 16633891
OWN - NLM
STAT- MEDLINE
DCOM- 20070424
LR  - 20211020
IS  - 0272-4340 (Print)
IS  - 0272-4340 (Linking)
VI  - 26
IP  - 4-6
DP  - 2006 Jul-Aug
TI  - CREB and NF-kappaB transcription factors regulate sensitivity to excitotoxic and 
      oxidative stress induced neuronal cell death.
PG  - 385-405
AB  - 1. Glutamate-NMDA receptor excitotoxicity and oxidative stress are two common 
      mechanisms associated with most neurodegenerative diseases. We hypothesize that 
      the vital state of neurons is regulated in part by two key transcription factors, 
      CREB and NF-kappaB. To test this hypothesis we used hippocampal-entorhinal cortex 
      slice cultures. 2. Glutamate neurotoxicity and oxidative stress neurotoxicity, 
      using hydrogen peroxide (H(2)O(2)) are both associated with a decrease in CREB 
      DNA binding and an increase in NF-kappaB DNA binding. 3. Agents that modulate 
      CREB and NF-kappaB DNA-binding activity alter neurotoxicity. Rolipram, a 
      phosphodiesterase IV inhibitor, increased CREB DNA binding activity and decreased 
      toxicity, whereas TNFalpha, increased NF-kappaB DNA-binding activity and 
      increased neurotoxicity to both glutamate and H(2)O(2). Ethanol decreased CREB 
      and increased NF-kappaB DNA-binding activity and increased neurotoxicity to both 
      glutamate and H(2)O(2). 4. Brain-derived neurotrophic factor (BDNF) is a 
      transcriptionally regulated trophic factor whose expression follows sensitivity 
      to toxicity suggesting it is one of the transcriptionally regulated factors that 
      contributes to neuronal vitality secondary to the balance of 
      CREB-NF-kappaB-activated transcription. Together these studies suggest that 
      neurotoxicity through glutamate-NMDA receptors or oxidative stress is dependent 
      upon CREB and NF-kappaB DNA transcription that regulates vitality of neurons.
FAU - Zou, Jian
AU  - Zou J
AD  - The Bowles Center For Alcohol Studies, Department of Pharmacology, School of 
      Medicine, CB#7178, University of North Carolina at Chapel Hill, Chapel Hill, 
      North Carolina 27599-7178, USA.
FAU - Crews, Fulton
AU  - Crews F
LA  - eng
PT  - Journal Article
DEP - 20060422
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotoxins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3K9958V90M (Ethanol)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - BBX060AN9V (Hydrogen Peroxide)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cell Death/drug effects
MH  - Cells, Cultured
MH  - Cyclic AMP Response Element-Binding Protein/metabolism/*physiology
MH  - DNA-Binding Proteins/metabolism
MH  - Ethanol/pharmacology
MH  - Gene Expression Regulation
MH  - Glutamic Acid/pharmacology
MH  - Hydrogen Peroxide/pharmacology
MH  - NF-kappa B/metabolism/*physiology
MH  - Neurons/*drug effects/metabolism/physiology
MH  - Neuroprotective Agents/metabolism
MH  - Neurotoxins/*pharmacology
MH  - Oxidative Stress/*physiology
MH  - Rats
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2006/04/25 09:00
MHDA- 2007/04/25 09:00
CRDT- 2006/04/25 09:00
PHST- 2006/01/17 00:00 [received]
PHST- 2006/02/28 00:00 [accepted]
PHST- 2006/04/25 09:00 [pubmed]
PHST- 2007/04/25 09:00 [medline]
PHST- 2006/04/25 09:00 [entrez]
AID - 10.1007/s10571-006-9045-9 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2006 Jul-Aug;26(4-6):385-405. doi: 10.1007/s10571-006-9045-9. 
      Epub 2006 Apr 22.