Lee R Y, Sawin E R, Chalfie M, Horvitz H R, Avery L
Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9148, USA.
J Neurosci. 1999 Jan 1;19(1):159-67. doi: 10.1523/JNEUROSCI.19-01-00159.1999.
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.
秀丽隐杆线虫基因eat-4影响多种谷氨酸能神经传递途径。我们发现eat-4编码一种蛋白质,其序列与哺乳动物脑特异性钠依赖性无机磷酸盐共转运体I(BNPI)相似。与大鼠中枢神经系统中的BNPI一样,eat-4主要在特定的神经元亚群中表达,包括几个被认为是谷氨酸能的神经元。eat-4功能丧失突变导致谷氨酸能化学传递缺陷,但似乎对神经元的其他功能影响很小。我们的数据表明,通过EAT-4和BNPI等转运体导入谷氨酸能神经元的磷酸根离子是谷氨酸能神经传递所特需的。