TheCaenorhabditis elegansGeneunc-25Encodes Glutamic Acid Decarboxylase and Is Required for Synaptic Transmission But Not Synaptic Development

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Abstract
The neurotransmitter GABA has been proposed to play a role during nervous system development. We show that theCaenorhabditis elegansgeneunc-25encodes glutamic acid decarboxylase (GAD), the GABA biosynthetic enzyme.unc-25is expressed specifically in GABAergic neurons. Null mutations inunc-25eliminate the UNC-25 protein or alter amino acids conserved in all known GADs, result in a complete lack of GABA, and cause defects in all GABA-mediated behaviors. Inunc-25mutants the GABAergic neurons have normal axonal trajectories and synaptic connectivity, and the size and shape of synaptic vesicles are normal. The number of synaptic vesicles at GABAergic neuromuscular junctions is slightly increased. Cholinergic ventral nerve cord neurons, which innervate the same muscles as GABAergic ventral cord neurons, have normal morphology, connectivity, and synaptic vesicles. We conclude that GAD activity and GABA are not necessary for the development or maintenance of neuromuscular junctions inC. elegans.