Figure 6.

Mechanism for associative learning, extinction learning, and reconsolidation in the MB. (A,B) Plasticity in MB circuits mediates aversive (A) and appetitive (B) learning. Odor sparsely activates KCs within the MB. Aversive cues activate punishment-encoding DANs, which modulate MBONs promoting approach, whereas appetitive cues activate reward-encoding DANs, which modulate MBONs promoting avoidance. Dopamine depresses active KC-MBON synapses. After aversive learning, this depression shifts the balance of MBON activity towards avoidance (A) whereas after appetitive learning the balance shifts towards approach (B). Extinction of aversive or appetitive memories occurs by readjusting the balance of MBON activity. After aversive learning, presenting the CS+ in the absence of anticipated electric shock causes avoidance-promoting MBONs to recurrently activate reward-encoding DANs, which encode a competing appetitive memory that reduces avoidance (A). After appetitive learning, presenting the CS+ in the absence of anticipated sugar reward causes approach-promoting MBONs to recurrently activate punishment-encoding DANs, resulting in the formation of a competing aversive memory that reduces approach (B). (C) Appetitive memories can be re-activated by exposure to the CS- which induces reconsolidation of the original memory. Reconsolidation requires recurrent DAN activation orchestrated by subsets of MBONs (MBON γ2α′1). Activation of punishment-encoding DANs during CS- exposure and subsequent activation of rewarding-encoding DANs after CS- exposure results in reconsolidation of the original memory, although the exact mechanisms are unclear. Purple arrows depict DAN input to the MB; gray arrows depict KC axons innervating MBONs and are shown in black when activated by odor; brown arrows depict MBON output. Note that the middle panels of (C) show skewed MBON output as it would be elicited by the CS+, representing the CS+ memory; output in response to the CS- or in the absence of odor is not skewed.