MECHANOSENSORY SIGNALING IN C-ELEGANS MEDIATED BY THE GLR-1 GLUTAMATE-RECEPTOR

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.