C. elegans will orient and travel in a straight uninterrupted path directly towards the negative pole of a DC electric field (Sukul and Croll, 1978: J Nematol 10:314-317). We have developed a population assay to measure electrotaxis behavior in a static electric field. Behavioral sensitivity to an electric field is determined by measuring average speeds and approach angles at different field strengths. During the course of these studies, we also uncovered two novel electric field responses in C. elegans: an initial increase in velocity to field stimulus, and an immediate reversal upon a decrease of field strength (off stimulus response). In examining the neural basis for this behavior we have identified a mutant, eat-4, that is severely disrupted in three aspects of electrotaxis behavior: velocity, directional behavior, and reversals. Testing the response of transgenic strains with neuron-specific rescue of the wild-type eat-4 gene to an electric field stimulus has revealed a role for the amphid sensory neuron (AWC) in regulating aspects of velocity and directional sensing, but no role in the reversal behavior. In the neuron-specific rescue of the wild-type eat-4 gene in ASK neurons, we observed an increase in directional sensing, but no recovery of increased velocity or reversal behavior. With neuron-specific rescue of wild-type eat-4 in both sensory neurons, AWC and ASK in the same animal no recovery of velocity speeds or directional sensing was observed, suggesting that ASK may function to inhibit the AWC-dependent circuit responsible for electrotaxis behavior. We are currently generating neuron-specific rescue of wild-type eat-4 in ASH and ASJ amphid neurons to explore the remaining aspects of electrotaxis behavior. To identify the neural circuits operating in electrotaxis, we also examined the role of two interneurons, AIY and AIB, which make synaptic connections to AWC. To test the role of AIY and AIB interneurons we examined two mutants, glr-1 and glc-3, which have defects in an AMPA-type glutamate receptor and a glutamate-gated chloride channel, respectively. We observed that glc-3 mutant animals display defects in initiating velocity increases in response to an electric field, while glr-1 mutant animals exhibited directional defects during migration in an electric field. Neuron-specific rescue of wild-type glc-3 in AIY recovered the increase in velocity whereas rescue of glr-1 in AIB recovered directional behavior to electric field stimulus. Our data suggests that EAT-4-expressing amphid neurons including AWC are coupled to regulate direction and velocity responses to a static electric field largely through the interneurons AIB and AIY.

Affiliation:
- Biological Sciences, Central Washington University, Ellensburg, WA.