Abstract
The N-methyl-D-aspartate (NMDA) subtype of glutamate receptor is important for synaptic plasticity and nervous system development and function. We have used genetic and electrophysiological methods to demonstrate that NMR-1, a Caenorhabditis elegans NMDA-type ionotropic glutamate receptor subunit, plays a role in the control of movement and foraging behavior. nmr-1 mutants show a lower probability of switching from forward to backward movement and a reduced ability to navigate a complex environment. Electrical recordings from the interneuron AVA show that NMDA-dependent currents are selectively disrupted in nmr-1 mutants. We also show that a slowly desensitizing variant of a non-NMDA receptor can rescue the nmr-1 mutant phenotype. We propose that NMDA receptors in C. elegans provide long-lived currents that modulate the frequency of movement reversals during foraging behavior.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Genetically Modified
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Caenorhabditis elegans / genetics*
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Caenorhabditis elegans Proteins*
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Electrophysiology
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Gene Deletion
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Gene Expression / physiology
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Interneurons / chemistry
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Interneurons / physiology
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Locomotion / physiology*
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Maze Learning / physiology
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Membrane Potentials / physiology
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Molecular Sequence Data
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Mutagenesis / physiology
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Phenotype
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Receptors, AMPA
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Receptors, Glutamate / analysis
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Receptors, Glutamate / genetics
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Receptors, Glutamate / metabolism
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Receptors, N-Methyl-D-Aspartate / analysis
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Receptors, N-Methyl-D-Aspartate / genetics*
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Receptors, N-Methyl-D-Aspartate / metabolism
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Sequence Homology, Amino Acid
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Synaptic Transmission / physiology*
Substances
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Caenorhabditis elegans Proteins
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NMR-1 protein, C elegans
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Receptors, AMPA
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Receptors, Glutamate
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Receptors, N-Methyl-D-Aspartate
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glr-1 protein, C elegans