Mice deficient in Golf are anosmic
Mice deficient in Golf are anosmic
复制标题
DOI：
10.1016/s0896-6273(00)80435-3
复制
发表时间：
1998-01-01
期刊：
影响因子：
16.2
通讯作者：
Axel, R
中科院分区：
文献类型：
--
作者：
Belluscio, L;Gold, GH;Axel, R
我们已经使用基因靶向研究G α亚基，G（olf）在嗅觉信号转导中的作用。G（olf）无效突变的纯合子小鼠显示出初级嗅觉感觉神经元对各种气味的电生理反应显著降低。尽管这种深刻的减少，在响应气味，地形图的初级感觉投射到嗅球保持不变的G（olf）突变体。超过75%的G（olf）突变小鼠不能哺乳并在出生后2天内死亡。罕见的幸存纯合子交配和生育，但突变的女性表现出不足的母性行为。存活的纯合子突变小鼠也表现出多动行为。这些行为表型与G（olf）表达的模式一起表明G（olf）是嗅觉信号转导所需的，并且也可能在大脑中更集中地作为必需的信号分子起作用。
We have used gene targeting to examine the role of the G alpha subunit, G(olf) in olfactory signal transduction. Mice homozygous for a null mutation in G(olf) show a striking reduction in the electrophysiological response of primary olfactory sensory neurons to a wide variety of odors. Despite this profound diminution in response to odors, the topographic map of primary sensory projections to the olfactory bulb remains unaltered in G(olf) mutants. Greater than 75% of the G(olf) mutant mice are unable to nurse and die within 2 days after birth. Rare surviving homozygotes mate and are fertile, but mutant females exhibit inadequate maternal behaviors. Surviving homozygous mutant mice also exhibit hyperactive behaviors. These behavioral phenotypes, taken together with the patterns of G(olf) expression, suggest that G(olf) is required for olfactory signal transduction and may also function as an essential signaling molecule more centrally in the brain.