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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

nmr-1  -  Protein NMR-1

Caenorhabditis elegans

 
 
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High impact information on nmr-1

  • We also show that a slowly desensitizing variant of a non-NMDA receptor can rescue the nmr-1 mutant phenotype [1].
  • Electrical recordings from the interneuron AVA show that NMDA-dependent currents are selectively disrupted in nmr-1 mutants [1].
  • A null mutant of nmr-1, which encodes a C. elegans NMDA receptor, was completely resistant to the behavioral effects of N(2)O, whereas a non-NMDA receptor-null mutant was normally sensitive [2].
  • Mutation of glr-1, encoding a non-NMDA glutamate receptor subunit, abolished the behavioral effects of xenon; however, mutation of nmr-1, which encodes the pore-forming subunit of an NMDA glutamate receptor previously shown to be required for nitrous oxide action, did not significantly alter xenon response [3].

References

  1. The C. elegans glutamate receptor subunit NMR-1 is required for slow NMDA-activated currents that regulate reversal frequency during locomotion. Brockie, P.J., Mellem, J.E., Hills, T., Madsen, D.M., Maricq, A.V. Neuron (2001) [Pubmed]
  2. Nitrous oxide (N(2)O) requires the N-methyl-D-aspartate receptor for its action in Caenorhabditis elegans. Nagele, P., Metz, L.B., Crowder, C.M. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  3. Xenon acts by inhibition of non-N-methyl-D-aspartate receptor-mediated glutamatergic neurotransmission in Caenorhabditis elegans. Nagele, P., Metz, L.B., Crowder, C.M. Anesthesiology (2005) [Pubmed]
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