Cell Reports
Volume 3, Issue 3, 28 March 2013, Pages 808-819
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Article
Forgetting in C. elegans Is Accelerated by Neuronal Communication via the TIR-1/JNK-1 Pathway

https://doi.org/10.1016/j.celrep.2013.02.019Get rights and content
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Summary

The control of memory retention is important for proper responses to constantly changing environments, but the regulatory mechanisms underlying forgetting have not been fully elucidated. Our genetic analyses in C. elegans revealed that mutants of the TIR-1/JNK-1 pathway exhibited prolonged retention of olfactory adaptation and salt chemotaxis learning. In olfactory adaptation, conditioning induces attenuation of odor-evoked Ca2+ responses in olfactory neurons, and this attenuation is prolonged in the TIR-1/JNK-1-pathway mutant animals. We also found that a pair of neurons in which the pathway functions is required for the acceleration of forgetting, but not for sensation or adaptation, in wild-type animals. In addition, the neurosecretion from these cells is important for the acceleration of forgetting. Therefore, we propose that these neurons accelerate forgetting through the TIR-1/JNK-1 pathway by sending signals that directly or indirectly stimulate forgetting.

Highlights

► Food signals actively regulate forgetting of olfactory adaptation ► TIR-1/JNK-1 pathway accelerates forgetting of adaptation and of associative learning ► Response to diacetyl in AWA neurons is diminished after exposure to diacetyl ► Neurosecretion from AWC neurons is important for the acceleration of forgetting

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