RT Journal Article
SR Electronic
T1 Expression of Zinc Transporter Gene, ZnT-1, Is Induced after Transient Forebrain Ischemia in the Gerbil
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 6678
OP 6684
DO 10.1523/JNEUROSCI.17-17-06678.1997
VO 17
IS 17
A1 Manabu Tsuda
A1 Kazunori Imaizumi
A1 Taiichi Katayama
A1 Kazuo Kitagawa
A1 Akio Wanaka
A1 Masaya Tohyama
A1 Tsutomu Takagi
YR 1997
UL http://www.jneurosci.org/content/17/17/6678.abstract
AB 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.