Figure 12. A model for the neural mechanics of the MB circuit in controlling food-seeking behavior.

During food seeking, odors activate the KCs and in turn activate MBON-α3, MBON-β2β′2a, MBON-α′2, MBON-γ2α′1 and MBON-γ1pedc>αβ. GABAergic MBON-γ1pedc>αβ inhibits the downstream neurons that suppress food-seeking behavior, including β′2-innervating MBONs and MBON-α1. KC-to-MBON connectivity is regulated by the corresponding DANs. The DANs are regulated by combinations of hunger and satiety signals. When flies are food-satiated, satiety signals like insulin and AstA suppress PPL1-γ2α′1, PPL1-α′2α2, PAM-β′2a, and PAM-β2β′2a DANs. When flies are starved, hunger signals including serotonin (5HT), NPF, and sNPF activate PPL1-α3, PAM-β2β′2a, PAM-β′2a, and PPL1-γ2α′1 DANs, whereas they suppress PPL1-γ1pedc DANs. Dopamine signals pre- and post-synaptically mediated by the DAMB receptor fine-tune the KC-to-MBON connectivity and modulate the collective output of the MBONs driven by food odor. Therefore, hunger state tunes the odor-driven output of the MBONs to regulate food-seeking behavior.

Figure 12—figure supplement 1. A hypothetical model for the MBONs that show reduced responses to yeast odor in hungry flies.

The MBONs have strong connections with neuron A and weak connections with neuron B. When flies are starved, weak activities of the MBONs evoked by yeast odor are sufficient to activate neuron A but not neuron B. The activation of neuron A drives food-seeking behavior. When flies are fed, strong yeast odor-evoked activity in the MBONs activates neuron B, which in turns inhibits neuron A. The outputs from neuron B might be important for other computational functions, but the flies do not exhibit food-seeking behavior. Importantly, in this model the output from MBONs is still required for food-seeking behavior in hungry flies, so silencing these MBONs with UAS-shi^ts1 leads to impaired food-seeking behavior.