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Mitochondrial disruption in the intestine signals to the nervous system to induce the formation of aversive memory to bacterial sensory cues. The neural circuit for this aversive memory include sensory neurons (triangles) that detect bacterial odors, metabolites and carbon dioxide, the RIC neuron that forms the memory, and the AIY neuron that retrieves the memory upon re-encounter of the bacterial cues. Mitochondrial stress alters the neural response of RIC to enables the formation of this aversive memory.
Physiological stress induces aversive memory formation and profoundly impacts animal behavior. In C. elegans, concurrent mitochondrial disruption induces aversion to the bacteria that the animal inherently prefers, offering an experimental paradigm for studying the neural basis of aversive memory. The research team led by Prof. Chun-Liang Pan found that, under mitochondrial stress, octopamine secreted from the RIC modulatory neuron targets the AIY interneuron through the SER-6 receptor to trigger learned bacterial aversion. RIC responds to systemic mitochondrial stress by increasing octopamine synthesis and acts in the formation of aversive memory. AIY integrates sensory information, acts downstream of RIC, and is important for the retrieval of aversive memory. Systemic mitochondrial dysfunction induces RIC responses to bacterial cues that parallel stress induction, suggesting that physiological stress activates latent communication between RIC and the sensory neurons. These findings provide insights into the circuit and neuromodulatory mechanisms underlying stress-induced aversive memory.
This article was published in Current Biology on Nov. 30, 2022: https://www.cell.com/current-biology/fulltext/S0960-9822(22)01768-7?fbclid=IwAR0uN4GsGsFNSKfPXiMs9SstW-YpliPdv1UBXdwkUpTfarSlwdz9cuCuk1w
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