The Neuroscience of Light Therapy

Source: Jared Rice/Unsplash

As we approach the winter solstice, you are probably aware that decreasing daylight can have a substantial impact on mood and mental health. Since the 1980s, clinical psychologists and psychiatrists have recognized “winter depression,” or what is often termed seasonal affective disorder (SAD), as a widespread condition.

Despite the fact that SAD is related to light levels, from a neuroscientific viewpoint, its effects have little if anything to do with our visual systems. Instead, it seems to be related to pathways that bypass the main machinery of vision that is housed in the cerebral cortex.

Normal vision

To make a visual image capable of being perceived, light is captured by photoreceptors in the retina at the back of the eye and turned into neural signals. After some processing by other classes of neurons, these signals are gathered up by a group of neurons called ganglion cells, whose axons leave the eye and connect to the network backbone of the brain called the thalamus. Signals are then sent on to the cortex, which is a central hub underlying visual consciousness.

Light-level cells

The brain’s pathway for sensing general light levels—which is the pathway implicated in SAD—starts in the eye, but it then takes a detour away from visual channels. This pathway uses an entirely different class of cells to gauge light levels, which was only discovered in the year 2000. In fact, gauging light levels is accomplished by a class of ganglion cells that captures photons directly and gets relatively little input from photoreceptors. Since the scientific name for these neurons is 47 letters long, I’ll call them light-level cells. Their job is essentially to measure overall illumination levels, which is related to the amount of sunlight.

From the eye, signals from light-level cells are sent to several areas below the cortex. These include the hypothalamus, which is involved in setting the circadian rhythms that regulate our waking and sleeping cycles. It makes sense that decreasing daylight would lead to changes in activity in the hypothalamus. For example, the hypothalamus would coordinate shifts in many neurochemical systems to adjust for earlier bedtimes, including those involved in digestion and metabolism. But why should such changes necessarily affect mood?

A brain imaging study of the amygdala

A new brain imaging study provides some insight into this question. Australian researchers focused on activity in the amygdala. They present evidence that light “quiets” this area. Many people are familiar with the amygdala because it is involved in emotional responses, though it is not strictly the “emotion center” of the brain.

What’s interesting is that this area also gets input from the light-level cells of the eye. In mice, light-level cells deliver their signals directly to the amygdala. It is not known whether these direct connections exist in humans; it is likely such connections do exist, but even if they don’t, there are other short paths from light-level cells to the amygdala that could deliver this information.

The researchers measured changes in blood flow to the amygdala as participants’ eyes were bathed in warm-colored white light inside the brain scanner. They found that when the light was on, blood flow to the amygdala went down compared to when the participant was in the dark. They interpret lower amygdala activity as a reduction in fear response, which equates to a greater sense of well-being. Thus the researchers have articulated a potential route for light levels to affect mood, though the study did not investigate whether light exposure reduced feelings of fear or increased feelings of well-being.

SAD and vigilance

I would put these results in slightly different terms. We tend to assume the amygdala’s activity is a barometer of emotion—with more activity equating to more (and worse) feelings, especially fear. In fact, a recent meta-analysis of human brain imaging studies found essentially no relationship between activity in the amygdala and conditioned fear.

Instead, the amygdala is better seen as a vigilance center. The amygdala contributes in crucial ways to where we direct our attention, and its activity increases both for aversive stimuli and for attractive stimuli. Anything that we need to be consciously aware of—good or bad—is what the amygdala is searching for.

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Thus, if the amygdala is less active, we may be in a state of lowered attention rather than a state of lowered fear. As diurnal creatures who are active during daylight and who rely heavily on vision, it makes sense that we should relax our attention during the day when we can see well and that we should be more alert when active at night when our vision is much worse. In darker months, we may spend more time being extra-vigilant, which can be draining and lead to a more depressed mood. Consider how much more draining it is to drive at night compared to daytime.

This interpretation is bolstered by research in mice, which are nocturnal animals. A mouse feels most comfortable in the dark and has exquisite senses of hearing, touch, and smell to help it get around with little or no light. Mice are quite averse to light and are only likely to venture out in daylight if they are starving.

So while mice might appreciate more hours of darkness, humans generally do not. Perhaps by way of light-level cells and the amygdala, the extra vigilance required during long periods of darkness may leave us drained and, ultimately, depressed. More research is needed to confirm the connection to the amygdala and to get a better understanding of SAD more generally. Fortunately, light therapy is already well established as a way to alleviate SAD.

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