[
International Worm Meeting,
2021]
Animals respond to environmental stimuli whose intensity varies by approximately 1010-fold, although neural responses can only change by 102-fold, which requires proper adjustment of the relationship between the environmental stimuli and the neural response. One example of this adjustment is neural gain control, defined as the change in the slope of a neural response to a stimulus, instead of a general reduction (adaptation) or enhancement (sensitization) of the response. However, these mechanisms are poorly elucidated. Here, we report that the neural gain control in the ASH nociceptive neuron occurs by asymmetric modulation of the first- and second-order time-differentials of sensory stimulus. Previously, we showed that the worm's avoidance behavior to the repulsive odor 2-nonanone is enhanced by pre-exposure to the odor as a type of non-associative learning (Kimura et al., J Neurosci 2010). We now found that the ASH responses, which are activated by increasing the 2-nonanone concentrations (Tanimoto et al., eLife 2017), are modulated by the odor learning. Quantitative odor stimuli analysis revealed that the naive ASH neurons respond similarly to small and large linear increases in odor concentration, whereas the pre-exposed ASH neurons only respond to large increases. Analysis of the stimulus-response relationships suggested that this learning-dependent change is a neural gain control of response. Interestingly, mathematical analysis revealed that the ASH response is approximated by the sum of the first- and second-order time-differentials of odor concentration, and the second-order time-differential is greatly suppressed by learning. We found that the terms of the first- and second-order time differential are expressed by the variable coefficients. To test the validity of this model, we compared it with the first-order time-differential only model and second-order time-differential only model using the Bayesian information criterion (BIC). As predicted, in naive ASH neurons, the model of the sum of the first- and second-order time-differentials of odor concentration was the best fit, and the first-order time-differential only model was the best fit in the pre-exposed condition. These results may suggest that the ASH response is mediated by the long (corresponding to the first-order term) and transiently (the second-order term) activated voltage-gated calcium channels and that the contribution of these channels are modulated by the odor stimulus.