2000 West Coast Worm Meeting abstract 25
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Dept. of Biology University of Utah 257 S. 1400 E. Salt Lake City UT 84112
A fundamental problem in neurobiology is to understand how neuronal circuits function to control behavior. A simple neuronal circuit that controls movement has been identified in the nematode Caenorhabditis elegans. In this circuit, the command interneurons AVA, AVB, AVD, AVE, and PVC are essential for coordinated movement and escape from tactile stimuli.
Our lab has shown that six putative ionotropic glutamate receptor subunits are expressed in the command interneurons and that perturbation of the subunits nmr-1 and glr-1 lead to altered locomotion (see abstract by Brockie et. al.). To better understand how ionotropic glutamate receptors modulate the activity of the locomotory control circuit, we are undertaking an electrophysiological analysis of the receptors expressed in the command interneuron AVA.
We have modified the slit worm dissection to isolate neurons of the locomotory control circuit. Using patch-clamp techniques, we have recorded glutamate-dependent currents from the neuron AVA. The current can be elicited by glutamate, kainate, and NMDA and can be partially blocked by selective pharmacological antagonists. The current rapidly desensitizes to glutamate and recovery from desensitization is slow. The current evoked by NMDA is voltage dependent and exhibits an outward rectification.
We have also determined the electrophysiological defects underlying the behavioral phenotypes observed in the glr-1 and nmr-1 deletion mutants. Both mutants display a diminshed response to glutamate. The nmr-1 mutant, in addition, has an aberrant response to NMDA.
We will describe the dissection used to isolate the command interneuron circuitry, our findings on how glutamate receptors function in wild type and mutant animals, and our initial insights into how glutamate receptors modulate the activity of the locomotory control circuit.