EAT-4, a homolog of a mammalian sodium-dependent inorganic phosphate cotransporter, is necessary for glutamatergic neurotransmission in Caenorhabditis elegans

被引:262
作者
Lee, RYN
Sawin, ER
Chalfie, M
Horvitz, HR
Avery, L
机构
[1] Univ Texas, SW Med Ctr, Dept Mol Biol & Oncol, Dallas, TX 75235 USA
[2] MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA
[3] Columbia Univ, Dept Biol Sci, New York, NY 10027 USA
关键词
C-; elegans; behavior; genetics; glutamate; synaptic neurotransmission; sodium-dependent inorganic phosphate cotransporter;
D O I
10.1523/JNEUROSCI.19-01-00159.1999
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The Caenorhabditis elegans gene eat-4 affects multiple glutamatergic neurotransmission pathways. We find that eat-4 encodes a protein similar in sequence to a mammalian brain-specific sodium-dependent inorganic phosphate cotransporter I (BNPI). Like BNPI in the rat CNS, eat-4 is expressed predominantly in a specific subset of neurons, including several proposed to be glutamatergic. Loss-of-function mutations in eat-4 cause defective glutamatergic chemical transmission but appear to have little effect on other functions of neurons. Our data suggest that phosphate ions imported into glutamatergic neurons through transporters such as EAT-4 and BNPI are required specifically for glutamatergic neurotransmission.
引用
收藏
页码:159 / 167
页数:9
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