Stress responses in the aged rat brain
J. Regino Perez-Polo
University of Texas Medical Branch,
Galveston, Texas, 77555-0652
The aged nervous system displays both impaired cognitive functions and
recovery from challenges to its ability to maintain homeostasis. Our
hypothesis is that aging-associated chronic oxidative stress serves to
alter the dynamic ability for the nervous system to respond to acute
insults and return to energy homeostatic setpoints. Here we examine the
response of aged rat hippocampi to normobaric hyperoxia treatments and
demonstrate an attenuation in the DNA binding activity of the NF-ÛB
transcription factors, which are important components of stress
response signal transduction pathways and can determine shifts in
cellular commitments to necrosis, apoptosis, or functional recovery in
the central nervous system. Hyperoxia is an oxidative stressor that
triggers signaling cascades via changes in promoter activation by
transcription factors. The transcription factor NF-ÛB has been shown to
regulate transcription of many genes that play a role in inflammation
and recovery from acute or chronic trauma. The aged-associated changes
in NF-ÛB action may account for some changes in cognitive function.
Key words:
transcription factor, NF-kB, oxidative stress, cell death,
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