Memory: How the brain constructs dreams

Deep inside the temporal lobe of the brain, the hippocampus has a central role in our ability to remember, imagine and dream.
  1. Erin J Wamsley  Is a corresponding author
  1. Department of Psychology and Program in Neuroscience, Furman University, United States

Our most vivid dreams are a remarkable replication of reality, combining disparate objects, actions and perceptions into a richly detailed hallucinatory experience. How does our brain accomplish this? It has long been suspected that the hippocampus contributes to dreaming, in part due to its close association with memory: according to one estimate, about half of all dreams contain at least one element originating from a specific experience while the subject was awake (Fosse et al., 2003). Although these dreams are rarely a faithful replication of any one memory, fragments of various recent experiences intermingle with other memories (usually related remote and semantic memories) to create a novel dream. Given all this, one might guess that dreams are created by those regions of the brain responsible for memory. However, studies dating back to the 1960s have suggested that patients with a damaged hippocampus still dream (Torda, 1969a; Torda, 1969b; Solms, 2014) and, somewhat amazingly, such patients can have dreams involving recent experiences of which they have no conscious memory (Stickgold et al., 2000)!

But are the dreams of patients with damage to hippocampus truly ‘normal’? Or alternatively, might such damage, while not preventing dreams, alter the form in which they are expressed? Indeed, there is reason to think that the hippocampus supports crucial aspects of dream construction beyond the simple insertion of memories. Recent work in the cognitive neurosciences has established that the hippocampus, in addition to being involved in the formation of memories, is also part of a brain system that is involved in using memory to construct novel imagined scenarios and simulate possible future events (Hassabis et al., 2007; Hassabis and Maguire, 2009; Schacter and Addis, 2007). As a result, patients without a hippocampus find it difficult to imagine scenes that are coherent, possibly because the hippocampus is responsible for combining different elements of memory into a spatially coherent whole.

Now, in eLife, Eleanor Maguire of University College London (UCL) and colleagues – including Goffredina Spanò as first author – report that the dreams of four amnesia patients lacking a hippocampal memory system do not have the richness of detail found in most dreams (Spanò et al., 2020). Besides reporting substantially fewer dreams than the patients in a control group, the four patients with amnesia also reported dreams that were markedly less detailed: their dreams contained fewer details of spatial location (e.g., descriptions like ‘behind the bar’ or ‘to my left I can see’) and fewer sensory details. These observations support the emerging view that dreams are generated by networks in the brain similar to the networks that are involved in recalling memories and constructing imagined scenarios during wakefulness (Fox et al., 2013; Graveline and Wamsley, 2015). Like memory and imagination, a vivid dream requires the construction of detailed, memory-based imagined scenes – and this process appears to rely on the hippocampus.

These observations partially echo the reports of Clara Torda from more than a half century ago, who characterized the dreams of amnesia patients as ‘shorter’, ‘simpler’, ‘repetitious’ and ‘stereotyped’ (Torda, 1969a). But Torda’s papers were written before the invention of noninvasive methods for imaging the brain, so it is not completely clear which structures may have been damaged in her patients. In contrast, the patients in the work of Spanò et al. all have well-characterized lesion sites with damage restricted solely to the hippocampus. This allows us to confidently attribute their impoverished dreams to the loss of the hippocampus itself, rather than to other regions of nearby temporal lobe which might also have a role in dreaming.

As with many studies of rare neurological patients, the latest work must be interpreted with caution due to the small sample size. For example, patient dreams were not significantly shorter than control dreams, leading to an apparently selective deficit in specific types of details reported (such as spatial details and sensory details), rather than a general deficit in the length of the dream. On average, however, the control dreams contained more than twice the number of informative words as the patient dreams, and the lack of a statistical difference between the two groups may be a mere artifact of the low sample size.

Nonetheless, these observations and a handful of similar studies are helping us to understand how the hippocampus contributes to the dreaming process. The work of Spanò et al. – who are based at UCL, the Royal Free Hospital in London, University Hospital Bonn and the universities of Arizona and Oxford – suggests hippocampal damage disrupts dreaming in ways that mirror how it also disrupts imagination. This suggests that, rather than being an entirely distinct phenomenon, dreaming is a part of a continuum of spontaneous, constructive thought and imagery continuously generated across the sleep and waking states.

References

    1. Graveline YM
    2. Wamsley EJ
    (2015) Dreaming and waking cognition
    Translational Issues in Psychological Science 1:97–105.
    https://doi.org/10.1037/tps0000018
    1. Hassabis D
    2. Maguire EA
    (2009) The construction system of the brain
    Philosophical Transactions of the Royal Society B: Biological Sciences 364:1263–1271.
    https://doi.org/10.1098/rstb.2008.0296

Article and author information

Author details

  1. Erin J Wamsley

    Erin J Wamsley is in the Department of Psychology and Program in Neuroscience, Furman University, Greenville, United States

    For correspondence
    erin.wamsley@furman.edu
    Competing interests
    No competing interests declared
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-4465-3890

Publication history

  1. Version of Record published: June 8, 2020 (version 1)

Copyright

© 2020, Wamsley

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 49,386
    views
  • 788
    downloads
  • 2
    citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Erin J Wamsley
(2020)
Memory: How the brain constructs dreams
eLife 9:e58874.
https://doi.org/10.7554/eLife.58874
  1. Further reading

Further reading

    1. Developmental Biology
    2. Neuroscience
    Melody C Iacino, Taylor A Stowe ... Mark J Ferris
    Research Article Updated

    Adolescence is characterized by changes in reward-related behaviors, social behaviors, and decision-making. These behavioral changes are necessary for the transition into adulthood, but they also increase vulnerability to the development of a range of psychiatric disorders. Major reorganization of the dopamine system during adolescence is thought to underlie, in part, the associated behavioral changes and increased vulnerability. Here, we utilized fast scan cyclic voltammetry and microdialysis to examine differences in dopamine release as well as mechanisms that underlie differential dopamine signaling in the nucleus accumbens (NAc) core of adolescent (P28-35) and adult (P70-90) male rats. We show baseline differences between adult and adolescent-stimulated dopamine release in male rats, as well as opposite effects of the α6 nicotinic acetylcholine receptor (nAChR) on modulating dopamine release. The α6-selective blocker, α-conotoxin, increased dopamine release in early adolescent rats, but decreased dopamine release in rats beginning in middle adolescence and extending through adulthood. Strikingly, blockade of GABAA and GABAB receptors revealed that this α6-mediated increase in adolescent dopamine release requires NAc GABA signaling to occur. We confirm the role of α6 nAChRs and GABA in mediating this effect in vivo using microdialysis. Results herein suggest a multisynaptic mechanism potentially unique to the period of development that includes early adolescence, involving acetylcholine acting at α6-containing nAChRs to drive inhibitory GABA tone on dopamine release.

    1. Neuroscience
    Daniel Hoops, Robert Kyne ... Cecilia Flores
    Short Report

    Dopamine axons are the only axons known to grow during adolescence. Here, using rodent models, we examined how two proteins, Netrin-1 and its receptor, UNC5C, guide dopamine axons toward the prefrontal cortex and shape behaviour. We demonstrate in mice (Mus musculus) that dopamine axons reach the cortex through a transient gradient of Netrin-1-expressing cells – disrupting this gradient reroutes axons away from their target. Using a seasonal model (Siberian hamsters; Phodopus sungorus) we find that mesocortical dopamine development can be regulated by a natural environmental cue (daylength) in a sexually dimorphic manner – delayed in males, but advanced in females. The timings of dopamine axon growth and UNC5C expression are always phase-locked. Adolescence is an ill-defined, transitional period; we pinpoint neurodevelopmental markers underlying this period.