Defensive Activation Theory Can Answer Why We Dream (Neuroscience)

Eagleman and colleagues hypothesized that the circuitry underlying dreaming serves to amplify the visual system’s activity periodically throughout the night, allowing it to defend its territory against takeover from other senses.

One of neuroscience’s unsolved mysteries is why brains dream. Do our bizarre nighttime hallucinations carry meaning, or are they simply random neural activity in search of a coherent narrative? And why are dreams so richly visual, activating the occipital cortex so strongly? Eagleman and colleagues in their recent paper, leverage recent findings on neural plasticity to propose a novel hypothesis.

Just as sharp teeth and fast legs are useful for survival, so is neural plasticity: the brain’s ability to adjust its parameters (e.g., the strength of synaptic connections) enables learning, memory, and behavioral flexibility.

On the scale of brain regions, neuroplasticity allows areas associated with different sensory modalities to gain or lose neural territory when inputs slow, stop, or shift. For example, in the congenitally blind, the occipital cortex is taken over by other senses such as audition and somatosensation. Similarly, when human adults who recently lost their sight listen to sounds while undergoing functional magnetic resonance imaging (fMRI), the auditory stimulation causes activity not only in the auditory cortex, but also in the occipital cortex. Such findings illustrate that the brain undergoes changes rapidly when visual input stops.

Rapid neural reorganization happens not only in the newly blind, but also among sighted participants with temporary blindness. In one study, sighted participants were blindfolded for five days and put through an intensive Braille-training paradigm. At the end of five days, the participants could distinguish subtle differences between Braille characters much better than a control group of sighted participants who received the same training without a blindfold. The difference in neural activity was especially striking: in response to touch and sound, blindfolded participants showed activation in the occipital cortex as well as in the somatosensory cortex and auditory cortex, respectively. When the new occipital lobe activity was intentionally disrupted by magnetic pulses, the Braille-reading advantage of the blindfolded subjects went away. This finding indicates that the recruitment of this brain area was not an accidental side effect—it was critical for the improved performance. After the blindfold was removed, the response of the occipital cortex to touch and sound disappeared within a day.

Of particular interest here is the unprecedented speed of the changes. When sighted participants were asked to perform a touching task that required fine discrimination, investigators detected touch-related activity emerging in the primary visual cortex after only 40 to 60 minutes of blindfolding. The rapidity of the change may be explained not by the growth of new axons, but by the unmasking of pre-existing non-visual connections in the occipital cortex.

It is advantageous to redistribute neural territory when a sense is permanently lost, but the rapid conquest of territory may be disadvantageous when input to a sense is diminished only temporarily, as in the blindfold experiment. This consideration leads Eagleman and colleagues to propose a new hypothesis for the brain’s activity at night. In the ceaseless competition for brain territory, the visual system in particular has a unique problem: due to the planet’s rotation, we are cast into darkness for an average of 12 hours every cycle. (This of course refers to the vast majority of evolutionary time, not to our present electrified world). Given that sensory deprivation triggers takeover by neighboring territories, how does the visual system compensate for its cyclical loss of input?

Eagleman and colleagues suggested that the brain combats neuroplastic incursions into the visual system by keeping the occipital cortex active at night. They term this the Defensive Activation theory. In this view, dream sleep exists to keep the visual cortex from being taken over by neighboring cortical areas. After all, the rotation of the planet does not diminish touch, hearing, taste, or smell. Only visual input is occluded by darkness.

“We suggest that the brain preserves the territory of the visual cortex by keeping it active at night. In our “defensive activation theory,” dream sleep exists to keep neurons in the visual cortex active, thereby combating a takeover by the neighboring senses. In this view, dreams are primarily visual precisely because this is the only sense that is disadvantaged by darkness. Thus, only the visual cortex is vulnerable in a way that warrants internally-generated activity to preserve its territory.”, said Eagleman.

In humans, sleep is punctuated by REM (rapid eye movement) sleep about every 90 minutes. This is when most dreaming occurs. Although some forms of dreaming can occur during non-REM sleep, such dreams are quite different from REM dreams; non-REM dreams usually are related to plans or thoughts, and they lack the visual vividness and hallucinatory and delusory components of REM dreams.

REM sleep is triggered by a specialized set of neurons in the pons, Increased activity in this neuronal population has two consequences. First, elaborate neural circuitry keeps the body immobile during REM sleep by paralyzing major muscle groups. The muscle shut-down allows the brain to simulate a visual experience without moving the body at the same time. Second, they experience vision when waves of activity travel from the pons to the lateral geniculate nucleus and then to the occipital cortex (these are known as ponto-geniculo-occipital waves or PGO waves). When the spikes of activity arrive at the occipital pole, they felt as though they were seeing even though our eyes are closed. They found that the visual cortical activity is presumably why dreams are pictorial and filmic instead of conceptual or abstract.

Fig. 1. PGO waves. As a prelude to REM sleep, waves of activity move from the brainstem into the occipital cortex. We suggest that this infusion of activity is necessitated by the rotation of the planet into darkness: the visual system needs extra cyclic activation to keep its territory intact.

These nighttime volleys of activity are anatomically precise. The pontine circuitry connects specifically to the lateral geniculate nucleus, which passes the activity on to the occipital cortex, only. The high specificity of this circuitry supports the biological importance of dream sleep: putatively, this circuitry would be unlikely to evolve without an important function behind it.

“As predicted, we found that species with more flexible brains spend more time in REM sleep each night. Although these two measures—brain flexibility and REM sleep—would seem at first to be unrelated, they are in fact linked.”, said Eagleman.

Fig. 2. Representation of the Defensive Activation theory. With the onset of sleep, visual synaptic connections are weakened by encroachment from other sensory areas. When a threshold is reached (dotted line), PGO waves are initiated and drive activity into the occipital lobe. This process repeats cyclically throughout the sleep cycle.

Their Defensive Activation theory makes a strong prediction: the higher an organism’s neural plasticity, the higher its ratio of REM to non-REM sleep. This relationship should be observable across species as well as within a given species across the lifespan. They thus set out to test their hypothesis by comparing 25 species of primates on behavioral measures of plasticity and the fraction of sleep time they spend in REM and found that measures of plasticity across 25 species of primates correlate positively with the proportion of rapid eye movement (REM) sleep.

They further found that plasticity and REM sleep increase in lockstep with evolutionary recency to humans. Finally, they concluded that their hypothesis is consistent with the decrease in REM sleep and parallel decrease in neuroplasticity with aging.

Reference: David M. Eagleman, Don A. Vaughn, “The Defensive Activation theory: dreaming as a mechanism to prevent takeover of the visual cortex”, bioRxiv, 2020. doi:

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