Learning and forgetting information acquired from surrounding is a crucial process for the animals to strive for survival in changing environments. However, working mechanisms in learning and forgetting remain unclear. C. elegans shows a weak chemoattraction after prolonged exposure to an attractive odorant in the absence of food. Adapted wild-type animals are able to recover their chemoattraction toward the conditioned odorant after 4 hours of normal cultivation on food. We regard this behavioral recovery as forgetting. Previous study showed that TIR-1/JNK-1 pathway in AWC neurons plays a role to regulate forgetting the adaptation memory retained in AWA neurons. Still, the mechanism and neuronal network between AWC and AWA underlying forgetting are not known. To study how AWC regulate forgetting in AWA, we investigated several interneurons which work downstream of AWC and AWA neurons in the olfactory circuit. We discovered that animals lacking functional AIA interneurons showed normal adaptation but displayed a defect in forgetting of olfactory adaptation to both diacetyl and isoamylalcohol. This suggests that AIA play a role in forgetting of two distinct types of olfactory adaptation. Furthermore, acute silencing of AIA during recovery using Drosophila histamine-gated chloride channel (HisCl1) was sufficient to cause a forgetting defect in olfactory adaptation, suggests that the activity of AIA during recovery is required to actively regulate forgetting. To elucidate the forgetting mechanisms in which AIA are associated, we inspected the interaction of AIA interneurons with TIR-1 pathway by examining the effect of AIA interneurons in tir-1(gf) animal. The strain not only suppressed a weak adaptation phenotype in tir-1(gf), but also showed prolonged retention of adaptation, suggesting that AIA work downstream of TIR-1 pathway in regulate forgetting. We also found that mutation in egl-21 gene, a gene which encoded carboxypeptidase E (CPE) protein required for neuropeptides processing, caused abnormality in forgetting in olfactory memory, indicates that neuropeptide might play a certain role in regulation of forgetting. However, our results suggested that AIA did not regulate forgetting via neuropeptide release. To examine how AIA engage in active forgetting, we are currently studying the effect of AIA on AWA calcium responses to diacetyl.

Affiliations:
- Graduate School of System Life Sciences, Kyushu University, Fukuoka, Fukuoka, JP
- Department of Biology, Faculty of Sciences, Kyushu University, Fukuoka, JP