Molecular mechanism of neural functions underlying sensory behaviors in the nematode C.elegans

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Animals modify their behaviors upon reception of various environmental stimuli. It however remains largely unknown how, at the molecular level, the stimuli are processed and integrated in the nervous system, thereby generating the behavioral outputs. To address molecular mechanism on sensory reception and neural plasticity, we utilized thermotaxis behavior, a temperature memory and feeding state-regulated behavior, in the small nematode Caenorhabditis elegans. C.elegans is an ideal system to elucidate molecular basis of behavioral plasticity because of its complete knowledge of neural wiring and powerful accessibility to genetic and molecular analyses. We showed here that 1) temperature is not only sensed but also remembered by AFD and AWC sensory neurons, 2) starvation signal inhibits thermotaxis interneurons that are downstream of AFD and AWC through insulin-like peptide, and 3) association between temperature and feeding state requires functional changes in thermotaxis interneurons. We also found that Lithium, a drug for patients with bipolar disorder, affects synaptic localization in RIA interneuron, which is essential for proper thermotaxis behavior.