Forgetting is regulated through Rac activity in Drosophila.
Initially acquired memory dissipates rapidly if not consolidated. Such memory decay is thought to result either from the inherently labile nature of newly acquired memories or from interference by subsequently attained information. Here we report that a small G protein Rac-dependent forgetting mechanism contributes to both passive memory decay and interference-induced forgetting in Drosophila. Inhibition of Rac activity leads to slower decay of early memory, extending it from a few hours to more than one day, and to blockade of interference-induced forgetting. Conversely, elevated Rac activity in mushroom body neurons accelerates memory decay. This forgetting mechanism does not affect memory acquisition and is independent of Rutabaga adenylyl cyclase-mediated memory formation mechanisms. Endogenous Rac activation is evoked on different time scales during gradual memory loss in passive decay and during acute memory removal in reversal learning. We suggest that Rac's role in actin cytoskeleton remodeling may contribute to memory erasure.
Shuai
Yichun
Y
Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing, P.R. China.
Lu
Binyan
B
Hu
Ying
Y
Wang
Lianzhang
L
Sun
Kan
K
Zhong
Yi
Y
D051339:Actin Depolymerizing Factors / Q000235:genetics; D000818:Animals; D004330:Drosophila / Q000502:physiology*; D029721:Drosophila Proteins / Q000502:physiology*; D008568:Memory / Q000502:physiology; D008569:Memory Disorders; D024521:Mushroom Bodies; D020744:rac GTP-Binding Proteins / Q000502:physiology*
D051339:Actin Depolymerizing Factors; D029721:Drosophila Proteins; C090146:Rac1 protein, Drosophila; D020744:rac GTP-Binding Proteins