Welcome by Royal Society
Same or seperate? Functions and mechanisms of memory replay during sleep and wake
Dr Susanne Diekelman, University of Tubingen, Germany
Sleep strengthens and stabilizes newly acquired memories in an active process of system consolidation. This process is assumed to rely on covert reactivations of new memories that occur spontaneously after learning, mainly during slow-wave sleep (SWS), but can also be externally triggered by learning-associated memory cues. In a series of experiments, we show that the application of learning-associated odor cues during sleep resulted in an immediate stabilization of new memories, whereas similar odor reactivations in the wake state induced memory labilization. Functional magnetic resonance imaging revealed different activation patterns following reminder presentation during sleep and wakefulness. Moreover, different types of reminders (complete/incomplete) exerted different effects on memory during sleep and wakefulness. While in the wake state, only incomplete reminders but not complete reminders labilized the memory traces, both the incomplete reminder and the complete reminder stabilized memories during sleep. This evidence collectively suggests that reactivation has different effects on memory during wakefulness and sleep, presumably serving different functions for the dynamic long-term storage of memory.
Sleep structure and replay across species
Professor Daniel Margoliash, University of Chicago, USA
The majority of sleep behavioural research is conducted in humans, results which are complemented by extensive animal experiments in rodents. Here we present neural and behavioural evidence for a role of sleep in sensorimotor vocal learning in juvenile and adult songbirds, and for perceptual learning in adult songbirds (the latter mostly behavioural work). We show deep similarities of the behavioural results in songbirds and humans, highlight similarities and differences between the songbird and rodent results, and discuss the implications of these similarities and differences. We show preliminary evidence that within Aves, the complex pattern of sleep observed in songbirds extends at least to parrots. Knowing the extent to which the behavioural and neurophysiological results apply broadly, beyond mammals and perhaps far across the animal kingdom, can open opportunities for developing new advantageous model systems to gain deeper insights into the neurobiology of sleep. Our results, in complement with recent data from reptiles and other poikilotherms and invertebrates, suggest the possibility of a broad diversity of species that exhibit sleep dependent processing. This places constraints on neuronal network models to explain these behaviours.
Sleep replay and memory consolidation in the hippocampus and amygdala
Dr Gabrielle Girardeau, NYU Langone Medical Center, USA
The hippocampus and the amygdala are two structures required for emotional memory. The hippocampus, through place cells, is believed to encode the spatial or contextual part of the memory. During slow-wave sleep, the activity of place cells is replayed in the same order as during the preceding learning epoch. These reactivations specifically occur during local field potential (LFP) short oscillatory events associated with highly synchronous neuronal activity called “ripples”. The group have shown previously that the specific suppression of ripples during sleep impairs performance on a spatial task, underlying their crucial role in memory consolidation. On the other hand, the amygdala processes the emotional valence of an event. Disrupting activity in the basolateral amygdala (BLA) immediately after training impairs performance on emotional tasks like contextual fear conditioning. However, how the amygdala and the hippocampus interact to consolidate an emotional event is yet unknown. To study that, the group designed a new task where the rats learn the location of an aversive stimulus. Using large scale simultaneous neuronal ensemble recordings in the hippocampus and BLA, we found coordinated reactivations between the two structures during sleep following training. Moreover, these reactivations specifically involve a small subset of BLA neurons that are modulated during hippocampal ripples and this modulation increases during sleep ripples following training. Hippocampal ripples during sleep thus emerge as a crucial time windows for intra-hippocampus and cross-structure reactivations sustaining the consolidation of spatial and emotional memories.
Mismatch, labilization and reinforcement during memory reactivation
Dr Olavo Amaral, Federal University of Rio de Janeiro, Brazil
Due to their opposite behavioural outcomes, memory reconsolidation and extinction have usually been considered as separate entities, despite being induced by similar reactivation protocols. Based on modelling and pharmacological data, the group will argue that the two processes nevertheless seem to involve similar sets of plasticity mechanisms. One of these sets seems to be pharmacologically similar to the one involved in initial consolidation and Hebbian plasticity, while the second appears to be more involved with the labilization of existing memories and synaptic changes. Moreover, memory labilization mechanisms resemble those involved in forms of homeostatic plasticity, such as synaptic scaling. With this in mind, the group will discuss whether memory destabilization during reactivation might be a consequence of homeostatic-like plasticity induction, and why mismatch between learning and re-exposure could lead this to happen. On this basis, the group will argue that the field of memory updating might benefit from a paradigm shift in which reconsolidation and extinction, as well as online and offline reactivation, are viewed not as fully distinct processes but as different instantiations of common plasticity systems.
Professor Loren Frank, HHMI and University of California, USA
Hippocampal neurogenesis and forgetting
Professor Paul Frankland, Program in Neuroscience and Mental Health, Hospital for Sick children, Toronto, Canada
Neurogenesis persists throughout life in the hippocampus, and there is a lot of interest in how the continuous addition of new neurons impacts hippocampal memory function. Behavioural studies have shown that artificially elevating hippocampal neurogenesis often facilitates new memory formation. However, since the integration of new neurons remodels existing hippocampal circuits, it has been hypothesized that hippocampal neurogenesis may also promote the degradation (or forgetting) of memories already stored in those circuits. Consistent with this idea, we have recently discovered that elevating rates of hippocampal neurogenesis after memory formation leads to forgetting. This finding changes the way we think about how hippocampal neurogenesis contributes to memory function, suggesting that it regulates a balance between encoding new memories and clearing out old memories.