EAT-4, a Homolog of a Mammalian Sodium-Dependent Inorganic Phosphate Cotransporter, Is Necessary for Glutamatergic Neurotransmission inCaenorhabditis elegans

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Abstract
TheCaenorhabditis elegansgeneeat-4affects multiple glutamatergic neurotransmission pathways. We find thateat-4encodes a protein similar in sequence to a mammalian brain-specific sodium-dependent inorganic phosphate cotransporter I (BNPI). Like BNPI in the rat CNS,eat-4is expressed predominantly in a specific subset of neurons, including several proposed to be glutamatergic. Loss-of-function mutations ineat-4cause 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.