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.
- 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
-
Dreaming and episodic memory: a functional dissociation?Journal of Cognitive Neuroscience 15:1–9.https://doi.org/10.1162/089892903321107774
-
Dreaming as mind wandering: evidence from functional neuroimaging and first-person content reportsFrontiers in Human Neuroscience 7:412.https://doi.org/10.3389/fnhum.2013.00412
-
Dreaming and waking cognitionTranslational Issues in Psychological Science 1:97–105.https://doi.org/10.1037/tps0000018
-
The construction system of the brainPhilosophical Transactions of the Royal Society B: Biological Sciences 364:1263–1271.https://doi.org/10.1098/rstb.2008.0296
-
The cognitive neuroscience of constructive memory: remembering the past and imagining the futurePhilosophical Transactions of the Royal Society B: Biological Sciences 362:773–786.https://doi.org/10.1098/rstb.2007.2087
-
Dreams of subjects with bilateral hippocampal lesionsActa Psychiatrica Scandinavica 45:277–288.https://doi.org/10.1111/j.1600-0447.1969.tb07128.x
Article and author information
Author details
Publication history
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
-
- 50,120
- views
-
- 836
- downloads
-
- 3
- 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)
Memory: How the brain constructs dreams
eLife 9:e58874.
https://doi.org/10.7554/eLife.58874
Further reading
-
- Neuroscience
The specific role that prolactin plays in lactational infertility, as distinct from other suckling or metabolic cues, remains unresolved. Here, deletion of the prolactin receptor (Prlr) from forebrain neurons or arcuate kisspeptin neurons resulted in failure to maintain normal lactation-induced suppression of estrous cycles. Kisspeptin immunoreactivity and pulsatile LH secretion were increased in these mice, even in the presence of ongoing suckling stimulation and lactation. GCaMP fibre photometry of arcuate kisspeptin neurons revealed that the normal episodic activity of these neurons is rapidly suppressed in pregnancy and this was maintained throughout early lactation. Deletion of Prlr from arcuate kisspeptin neurons resulted in early reactivation of episodic activity of kisspeptin neurons prior to a premature return of reproductive cycles in early lactation. These observations show dynamic variation in arcuate kisspeptin neuronal activity associated with the hormonal changes of pregnancy and lactation, and provide direct evidence that prolactin action on arcuate kisspeptin neurons is necessary for suppressing fertility during lactation in mice.
-
- Neuroscience
Unipolar brush cells (UBCs) are excitatory interneurons in the cerebellar cortex that receive mossy fiber (MF) inputs and excite granule cells. The UBC population responds to brief burst activation of MFs with a continuum of temporal transformations, but it is not known how UBCs transform the diverse range of MF input patterns that occur in vivo. Here, we use cell-attached recordings from UBCs in acute cerebellar slices to examine responses to MF firing patterns that are based on in vivo recordings. We find that MFs evoke a continuum of responses in the UBC population, mediated by three different types of glutamate receptors that each convey a specialized component. AMPARs transmit timing information for single stimuli at up to 5 spikes/s, and for very brief bursts. A combination of mGluR2/3s (inhibitory) and mGluR1s (excitatory) mediates a continuum of delayed, and broadened responses to longer bursts, and to sustained high frequency activation. Variability in the mGluR2/3 component controls the time course of the onset of firing, and variability in the mGluR1 component controls the duration of prolonged firing. We conclude that the combination of glutamate receptor types allows each UBC to simultaneously convey different aspects of MF firing. These findings establish that UBCs are highly flexible circuit elements that provide diverse temporal transformations that are well suited to contribute to specialized processing in different regions of the cerebellar cortex.
