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Volume 17, Number 17,
Issue of September 1, 1997
pp. 6678-6684
Copyright ©1997 Society for Neuroscience
Expression of Zinc Transporter Gene, ZnT-1, Is Induced after
Transient Forebrain Ischemia in the Gerbil
Received April 18, 1997; revised June 16, 1997; accepted June 20, 1997.
Manabu Tsuda1, 5,
Kazunori Imaizumi1, 5,
Taiichi Katayama1, 5,
Kazuo Kitagawa2,
Akio Wanaka4,
Masaya Tohyama3, and
Tsutomu Takagi1
1 Department of Molecular Neurobiology (TANABE),
2 First Department of Internal Medicine, and
3 Department of Anatomy and Neuroscience, Osaka University
Medical School, Osaka, Japan, 4 Department of Cell Science,
Fukushima Medical College, Fukushima, Japan, and 5 Tanabe
Seiyaku Company, Limited, Osaka, Japan
To elucidate the molecular mechanisms underlying neuronal death
after transient forebrain ischemia, we cloned genes expressed after
transient forebrain ischemia in the Mongolian gerbil by a differential
display method. A gerbil homolog of rat zinc transporter, ZnT-1, which
transports intracellular Zn2+ out of cells, was
isolated. Its expression became detectable exclusively in pyramidal
neurons of the CA1 region 12 hr after ischemia and reached a maximum
from day 1 to day 2 as shown by in situ hybridization.
By day 7, expression had disappeared entirely from the cells in the CA1
region, because the neurons had died. No other brain regions exhibited
such a significant level of ZnT-1 mRNA expression during this period.
Zn2+ was shown to accumulate in CA1 pyramidal
neurons expressing ZnT-1 mRNA after the ischemia by using zinquin, a
zinc-specific fluorescent dye. When primary hippocampal neurons were
exposed to a high dose of Zn2+, ZnT-1 mRNA
accumulated. These results suggest that the induction of ZnT-1 mRNA
observed in CA1 neurons was caused by an increase in the intracellular
Zn2+ concentration. It was reported recently that
Zn2+ chelator blocked neuronal death after ischemia
and that the influx of Zn2+ might be a key mechanism
underlying neuronal death. The induction of ZnT-1 mRNA in CA1 pyramidal
neurons fated to die after transient ischemia is of interest to the
study of postischemic events and the molecular mechanisms underlying
delayed neuronal death.
Key words:
brain ischemia;
Zn;
Zn transporter;
ZnT-1;
differential
display;
delayed neuronal death
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