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Mechanosensory signalling in C. elegans mediated by the GLR-1 glutamate receptor. Export

Nature, Vol. 378 (1995), pp. 78-81.

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C. elegans / WormBase's tags for this article

amino_acid_sequence animals_transgenic article base_sequence c06e14 caenorhabditis_elegans caenorhabditis_elegans_genetics caenorhabditis_elegans_metabolism celegans c_elegans dna_primers elegans glr-1 interneurons_metabolism mec-4 membrane_proteins_genetics membrane_proteins_metabolism molecular_sequence_data motor_neurons_metabolism mutagenesis_insertional nematode nerve_tissue_proteins_genetics nerve_tissue_proteins_metabolism neurons_metabolism polymerase_chain_reaction receptors_glutamate_genetics receptors_glutamate_metabolism sequence_deletion signal_transduction synapses_physiology t01c87 wormbase

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Neuronal signalling across synapses involves activation of many neurotransmitter receptors on postsynaptic cells. glr-1 encodes a potential glutamate receptor in the nematode Caenorhabditis elegans which is most similar to vertebrate AMPA-type ionotropic glutamate receptors(1). glr-1 is expressed in motor neurons and interneurons, including interneurons implicated in the control of locomotion(2). Here we investigate the contribution of glr-1 to the normal signalling of these neurons, by generating a deletion mutation in glr-1. We find that mutant worms are deficient in their ability to withdraw backwards when mechanically stimulated, but they withdraw normally in response to chemical repellents. The ASH sensory neurons mediate withdrawal responses both to mechanical stimuli and to chemical repellents(3,4), and ASH makes chemical synapses with glr-1-expressing interneurons. Our results suggest that postsynaptic interneurons use different neurotransmitter receptors to process two sensory stimuli detected by one sensory neuron.


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