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Journal of Neuroscience, Vol 15, 4238-4249, Copyright © 1995 by Society for Neuroscience
Kainic acid-induced neuronal death is associated with DNA damage and a unique immediate-early gene response in c-fos-lacZ transgenic rats
GM Kasof, A Mandelzys, SD Maika, RE Hammer, T Curran and JI Morgan
Roche Institute of Molecular Biology, Roche Research Center, Nutley, New Jersey 07710, USA.
Previously, we established that persistent upregulation of c-fos expression
preceded kainic acid (KA)-induced neuronal death in mice. To discriminate
between events that are products of the seizures elicited by KA and those
that are specifically associated with its neurotoxic actions, we have
examined the expression of cellular immediate-early genes (cIEGs) following
KA or pentylenetetrazol (PTZ) treatment in c- fos-lacZ transgenic rats.
While both chemoconvulsants elicit seizures, only KA causes selective
neuronal death. Following treatment of transgenic rats with KA there was a
protracted expression of Fos-lacZ that lasted for 2-3 d. In contrast, PTZ
elicited a transient increase in the transgene product that lasted about 6
hr. Normally, Fos and Fos- lacZ were detected only in neuronal nuclei.
However, 6 hr following kainic acid (but not PTZ) administration,
beta-galactosidase activity appeared in the cytoplasm of neurons within
vulnerable regions (as determined by the terminal transferase
biotinylated-UTP nick end labeling (TUNEL) procedure). Like c-fos,
transcripts for other cIEGs were elevated for longer periods in the
KA-treated rat hippocampus. In addition, fra-1 and fra-2 were only induced
in the KA-treated rat. These changes in mRNA levels were paralleled by a
sustained increase in AP-1 DNA binding activity. Thus, quantitative and
qualitative changes in AP-1 DNA binding complexes accompany neurotoxic cell
death that are not observed following seizures.
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