C. elegans attracted to 0.1- 200 mM NaCl and avoids higher concentrations. Chemoattraction to NaCl is primarily mediated by the ASE neurons, and to a lesser extent by ASI, ADF and ASG. Avoidance of high NaCl concentrations is mediated by ASH (Bargmann & Horvitz, 1991). Animals pre-exposed to 100 mM NaCl, in the absence of food, show strong avoidance of NaCl at all concentrations. We call this behavior gustatory plasticity, and we study the molecular and cellular mechanisms that govern this behavioral switch. First, we tested the contribution of the ASE neurons using
cog-1,
lsy-6 and
che-1 mutants, which have cell fate defects of ASER, ASEL and both ASEs, respectively. Behavioral assays showed that both ASE neurons are required for gustatory plasticity. Next, we tested known avoidance mutants,
odr-3 and
osm-10.
odr-3 mutants showed no avoidance, neither with nor without pre-exposure to 100 mM NaCl. In contrast,
osm-10 mutants showed no avoidance of high NaCl concentrations (osmotic stress), but showed normal gustatory plasticity. Based on these results we have devised a mathematical model to describe the naive response to NaCl and gustatory plasticity. The naive biphasic behavior can be described by the sum of attraction, starting at 0.1 mM, and avoidance, which starts between 100 and 200 mM NaCl. After pre-exposure, attraction is shifted and starts at approximately 100 mM. In addition to normal avoidance, pre-exposure introduces a second avoidance component, starting at 0.1 mM. Our results suggest that the ASE and ASH neurons mainly constitute the attraction and avoidance components in the mathematical model. To study the second avoidance pathway, we expressed the Ca2+ reporter Cameleon in the ASH neurons. We found a graded response of these neurons to increasing concentrations of NaCl. However, animals pre-exposed to 100 mM NaCl for at least 10 minutes showed at least doubled responses to low concentrations of NaCl, whereas responses to high concentrations were unchanged. Interestingly, the response to Cu2+ was also strongly increased after pre-exposure, while the response to glycerol was not changed. Together, these results suggest that pre-exposure to 100 mM NaCl sensitizes the ASH neurons and allows avoidance of low NaCl concentrations. We propose that this response uses the same pathway as the response to Cu2+, which is independent of the osmotic avoidance pathway. We are currently investigating the responses of the ASH neurons in various mutants and determining the responses of the ASE neurons.