Chemosensation underlies the ability of C. elegans to find the peak of concentration gradients of attactant molecules (chemotaxis). A pair of chemosensory neurons, ASER and ASEL, is critical for normal chemotaxis to water-soluble attractant molecules (1). It is not known how these neurons transmit electrical signals from the cilium, the presumed site of chemotransduction, to output synapses in the nerve ring or whether input synapses in the nerve ring affect chemosensory receptor potentials. To address these questions, we made tight-seal, whole-cell patch clamp recordings of ASER, which we identified by locating its fluorescent cell body in the transgenic strain,
lin-15(
n765ts);
gcy-5::GFP (2). Current injection elicited graded, probably regenerative, depolarizations, but not classical action potentials. Voltage-clamp revealed K+ and Ca2+ currents likely to be activated during regenerative depolarizations. Analysis of ASER!s passive properties showed that regenerative depolarizations are not needed for signal transmission between the cilium and nerve ring. We propose, instead, that regenerative depolarizations increase sensitivity to attractant molecules. We also found that steady-state voltage changes at input synapses affect the voltage at the cilium, a result which suggests that input synapses may alter the driving force for channels gated by attractant molecules binding to the cilium. 1. Bargmann, C. I., & Horvitz, H. R. (1991) Neuron 7, 729-42. 2. Yu, S., Avery, L., Baude, E., & Garbers, D. L. (1997) Proc. Natl. Acad. Sci, USA 94, in press.