Wildtype adult hermaphrodites modulate their rate of locomotion in response to their environment and their recent experience. We have analyzed this behavior genetically and by laser ablation of neurons. Hermaphrodites respond to the presence of a bacterial lawn by slowing their rate of locomotion. Laser ablation experiments indicate that the three classes of dopaminergic neurons, ADE, PDE, and CEP, are required for this response. The role of dopamine in this response is also indicated by the observation that
cat-2(elll2) animals, which lack dopamine (1), fail to decrease their locomotion rate in response to the presence of the bacterial lawn. This defect in
cat-2 animals can be rescued by exogenous dopamine. We are currently investigating the mechanism of this rescue. Preliminary experiments suggest that the dopaminergic neurons differentiate correctly in
cat2 animals. Exposure of
cat2 animals to exogenous dopamine results in formaldehydeinduced fluorescence indicative of dopamine in eight cell bodies in the positions of ADE, PDE, and CEP, suggesting that these neurons are present and able to recognize and takeup dopamine. Also, the ciliated dendrites of the CEP neurons appear to be normal at the level of electron microscopy. Taken together, these results suggest that the defect in
cat-2 may lie in t.he synthesis or stability of dopamine rather than in the differentiated identities of the dopaminergic neurons. Because these neurons in
cat-2 mutants appear to have several of the features of normal differentiated dopaminergic neurons, it is possible that the rescue of the behavioral defect of
cat-2 animals results from supplying dopamine to these neurons, allowing them to function as dopaminergic neurons. We are testing this hypothesis by determining the ability of exogenous dopamine to rescue the behavioral defect in
cat-2 animals in which ADE, PDE, and CEP have been killed by laser ablation. If adult hermaphrodites have experienced a brief period of food deprivation, their sensitivity to the bacterial lawn is increased, and they decrease their rate of locomotion to approximately one-third the rate of satiated animals moving through a bacterial lawn. Several observations suggest that the biogenic amine serotonin is required for this increased sensitivity to the bacterial lawn. First, the sensitivities of mutant strains to the bacterial lawn correlate with their sensitivities to exogenous serotonin. Second, mutants that lack both serotonin and dopamine, but not mutants that lack only dopamine, are defective in exhibiting this increased sensitivity to the bacterial lawn. Third, a screen for mutants with defects in the response to the bacterial lawn resulted in the isolation of mutants with defects in many aspects of serotonergic neurotransmission, including serotonin expression, serotonin sensitivity, and sensitivity to fluoxetine, a blocker of serotonin reuptake. Fourth, ablation of the serotonergic NSM neurons resulted in a partial decrease in sensitivity to the bacterial lawn in fooddeprived animals. Killing other serotonergic neurons in addition to the NSMs did not appear to result in a stronger defect in sensitivity to the bacterial lawn. We are currently testing the idea that the partial defect seen in animals lacking the NSMs reflects the fact that the NSMs sense only one aspect of the bacterial lawn. Specifically, we are examining the behavior of animals lacking the NSMs on "artificial lawns" that attempt to mimic the mechanical but not the chemical aspects of a lawn of E. coli. 1. Sulston, J., Dew, M. & Brenner, S. Journal of Comparative Neurology 163, 215226 (1975).