Abstract
Active memory forgetting is a well-regulated biological process thought to be adaptive and to allow proper cognitive functions. Recent efforts have elucidated several molecular players involved in the regulation of olfactory forgetting in Drosophila, including the small G protein Rac1, the dopamine receptor DAMB, and the scaffold protein Scribble. Similarly, we recently reported that dopaminergic neurons mediate both learning- and forgetting-induced plasticity in the mushroom body output neuron MBON-γ2α′1. Two open questions remain: how does forgetting affect plasticity in other, highly plastic, mushroom body compartments and how do genes that regulate forgetting affect this cellular plasticity? Here, we show that forgetting reverses short-term synaptic depression induced by aversive conditioning in the highly plastic mushroom body output neuron MBON-γ1pedc>α/β. In addition, our results indicate that genetic tampering with normal forgetting by inhibition of small G protein Rac1 impairs restoration of depressed odor responses to learned odor by intrinsic forgetting through time passing and forgetting induced acutely by shock stimulation after conditioning or reversal learning. These data further indicate that some forms of forgetting truly erase physiological changes generated by memory encoding.
Highlights
Animals live in an exceptionally dynamic and noisy environment
Expression of RacN17 in Kenyon cells (KC) secondary paired odor (Figure 4B). These results indicated that during adulthood impaired memory trace restoration of genetically interfering with memory forgetting by expression of initial contingency and induced a strong depression to the dominant negative (DN) RacN17 in KC impairs restoration of olfactory responses in mushroom body output neuron (MBON)-γ1pedc>α/β induced by intrinsic memory loss (Figure 2), acute forgetting induced by a non-associative stimuli (Figure 3), and acute forgetting by new associations or memory updating (Figure 4)
Our study indicates that forgetting reverses synaptic depression induced by aversive conditioning in MBON-γ1pedc>α/β
Summary
Animals live in an exceptionally dynamic and noisy environment. Organisms experience a plethora of sensory inputs but just a small fraction of these will remain as memories, and forgetting is the fate of the vast majority. If memories were high-fidelity records of this information, we might soon saturate the capacities of the brain. There seems to be copious space to store new information. This space may be provided continuously by active forgetting. A system that consistently eliminates obsolete information would be more efficient in recalling useful memories. The lack of forgetting may make our memories as noisy as the environment itself. Inflexible memory maintenance is incompatible with behavioral flexibility; a network strong at maintaining memories will be inferior at acquiring updating information.
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