Long-term memories are stored as stable configurations of neuronal ensembles, termed engrams. While investigation of engram cell properties and functionality in memory recall has been extensive, less is known about how engram cells are affected by forgetting. We describe a form of interference-based forgetting using an object memory behavioral paradigm. By using activity-dependent cell labelling, we show that although retroactive interference results in decreased engram cell reactivation during recall trials, optogenetic stimulation of the labelled engram cells is sufficient to induce memory retrieval. Forgotten engrams may also be reinstated via the presentation of similar or related environmental information. Furthermore, we demonstrate that engram activity is necessary for interference to occur. Taken together, these findings indicate that retroactive interference modulates engram expression in a manner that is both reversible and updatable. Retroactive inference may constitute a form of adaptive forgetting, where in everyday life new perceptual and environmental inputs modulate the natural forgetting process.
Memories are stored as ensembles of engram neurons and their successful recall involves the reactivation of these cellular networks. While progress has been made in understanding the biology of engrams, significant gaps remain in connecting these cell ensembles with the process of forgetting. Here, we examine whether forgetting is governed by changes in engram plasticity and suggest that it helps animals prioritize relevant memory representations for adaptive behavior. We utilized a mouse model of object memory and investigated the conditions in which a memory could be preserved, retrieved, or forgotten. The results indicate that engram activity correlated with the rate of forgetting. Direct modulation of engram activity via optogenetic stimulation or inhibition either facilitated or prevented the recall of an object memory. In addition, the modulation of engram activity was able to prevent forgetting itself. Moreover, through pharmacological and behavioral interventions, we successfully prevented or accelerated forgetting of an object memory. Finally, we show that these results can be explained by a computational model in which engrams that are subjectively less relevant for adaptive behavior are more likely to be forgotten. Together, these findings suggest that forgetting is an adaptive form of engram plasticity that involves circuit remodeling, which allows engrams to switch from an accessible state to an inaccessible state.
Arabidopsis has a single phytaspase (At4g10540) [15], but this family has 12 members in tomato, each having distinct expression patterns and with PCD roles described for some of them [14]. Reichardt et al. now show that phytaspases can also regulate processes other than PCD. Likewise, PSKs are conserved among plant lineages and have universal functions [12] but a role in abscission had not been described until now. Tomato has two PSK receptors, and PSKR1 is required for immune responses involving an intracellular calcium-based signalling cascade [13]. Given their role in immunity and defence, the roles of phytaspases and PSKs in droughtinduced abscission are therefore rather unexpected, raising questions on how these pathways evolved and are regulated to provide specificity.Finally, since the two abscission signalling cascades both contain a subtilase releasing a peptide hormone: how can the identities of both the protease and the peptide hormone be so distinctly different? Has this resulted from recent convergent evolution co-opting different peptide hormones and their receptors, or is prohormone processing by subtilases ancient, and diverged during plant evolution? Together, these studies show the fascinating versality of peptide signalling in plants, controlling different abscission types and other biological phenomena.
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