High impact information on glr-1

• The ASH sensory neurons mediate withdrawal responses both to mechanical stimuli and to repellents, and ASH makes chemical synapses with glr-1-expressing interneurons [1].
• A mutation in the glr-1 (glutamate receptor) gene eliminates the response to nose touch but not to osmotic repellents [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].
• CONCLUSIONS: Xenon acts in C. elegans to alter locomotion through a mechanism requiring the non-NMDA glutamate receptor encoded by glr-1 [3].
• Interestingly, preincubation on dopamine restored the behavior in worms with defective dopaminergic signaling, but not in glr-1, glr-2, or eat-4 mutants [4].

Anatomical context of glr-1

• Green fluorescent protein (GFP) constructs were used to visualize glr-1 expression in the interneurons of the mechanosensory circuit and synaptobrevin in the tap sensory neurons of trained and untrained worms [5].

Associations of glr-1 with chemical compounds

• Thus, long-term memory in C. elegans is dependent on glr-1 and likely involves changes in the expression or localization of glutamate receptors [5].

Other interactions of glr-1

• Nose touch sensitivity (mediated by ASH sensory neurons) is defective in mutants lacking GLR-1 glutamate receptors (GluRs); however, mutations eliminating the egl-3 PC2 restored nose touch sensitivity to glr-1 GluR mutants [6].

References