Forgetting in C. elegans Is Accelerated by Neuronal Communication via the TIR-1/JNK-1 Pathway
2013; Cell Press; Volume: 3; Issue: 3 Linguagem: Inglês
10.1016/j.celrep.2013.02.019
ISSN2639-1856
AutoresAkitoshi Inoue, Etsuko Sawatari, Naoki Hisamoto, Tomohiro Kitazono, Takayuki Teramoto, Manabi Fujiwara, Kunihiro Matsumoto, Takeshi Ishihara,
Tópico(s)Circadian rhythm and melatonin
ResumoThe 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.
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