It is the cones and rods inside our eyes that are responsible for sight, so what is their relation to depression?

The monkeys inside your retina

So as not to suffocate ourselves with too much science, leave rods and cones aside and just imagine a cute little monkey. As long as there is light in the room, she keeps playing and everything is fine. However, once it gets dark and no one can see her, our monkey begins constantly feeding herself with bananas. Naturally, as she keeps eating, she is also constantly pooping. This behaviour is then sending a smelly signal further to you, the owner. You are therefore constantly disgusted by the mess around and would rather stay in bed. Since inactivity and disgust are common signs of depression, we may assume that it is the darkness causing the depression rather than the hidden behaviour of the monkey.

Rods work quite like our monkey. When it gets dark, they open their mouths (channels in their membranes) and positive ions start flowing inside them. Just as bananas increased pressure in the monkey’s digestive system, the ions increase the voltage between the inside and outside of the cell; this is called membrane potential. And just as the monkey would poop after eating, the increase in membrane potential results in the rod firing signals to the subsequent cell. The next neuron is normally active, but from receiving these disgusting signals from the rod, it ceases its activity. In the end, your brain is not receiving necessary signals and is “depressed”.

Then, something lights up. A monkey would stop overeating knowing that you are watching her. Inside the rod, chemical substances reactive to light close those channels once they perceive a light source. In turn, the subsequent cell is no more inhibited so it resumes its communication with the brain. Rods send their signals along the optic nerve to the visual areas in the back of the brain and suddenly, you can see. Besides the visual areas, the signals also reach your “inner clock” thereby informing it that it is a bright day and it is time to be motivated, active, and happy.

By this mechanism, light promotes activity. Lack of light, on the other hand, promotes depression.

Dopamine in the eye

Cones are similar but more sophisticated: there are different types specialised to different colours. Their specialization is not without a cost, however, and they need more intensive light to react. On the other hand, they are not overly sensitive like the rods which can easily be blinded by too bright a light. Therefore, we use cones in bright conditions and rods in dim light. Having two different types of cells to see means that we need a system to tell us which one to use at a given moment.

The system of mutual communication between cones and rods is complex (for details, see this study). Importantly for insomnia, depression, and light therapy, it is the neurotransmitter called dopamine that plays a major role in this mechanism. When the light is strong in the middle of the day, dopamine is produced in the retina which stimulates cone vision and suppresses the rods. In the dark, its production is ceased, thus switching the cones off for the rods to do the job instead.

Within the brain, dopamine facilitates many functions, especially those related to motivation. No matter whether we are talking about some heroic endeavours requiring years of austerity or quick, low-level motivation to execute a simple movement, we need dopamine. Naturally, this dopaminergic system is involved in depressions: bad mood and lack of interest seem to be accompanied by a global decrease in dopamine which also affects the retina.

The complex disruption of a depressed person’s life, including his social connections, thoughts, and bodily processes, also involves cones and rods. A study scanning depressed people’s eyes revealed that depression indeed impairs the very first step of vision – and that vision improves after successful treatment of depression. The patients received various antidepressant pills which did not directly affect dopamine levels. Nevertheless, once the patients healed (we do not know how far it was due to the medication), the eyes were functioning normally once more.

Further, this interaction between dopamine and light is deepened by melanopsin, a small light-sensitive molecule in the eye that doesn’t make us see but instead has a profound impact on the inner clock. In the eye, dopamine influences melanopsin gene expression, namely the mRNA. Therefore, increased dopamine produces more melanopsin which in turn delivers stronger activating signals to the inner clock system.

Therefore we know that not only does light affect our mood, our mood may in turn affect our perception of light.

Downward spiral of darkness and depression

Our production of neurotransmitters increases when light is shining on our retinas. This production lessens when we are depressed because our eyes are less reactive to sunshine. In turn, lower production of dopamine does not support production of melanopsin. Consequently, due to lower melanopsin levels, our eyes react to light even less, thus creating a downward spiral. In the end, our inner clockwork is ticking less intensely which disrupts our sleep-wake rhythm. Moreover, insufficient input from melanopsin decreases levels of other stimulating neuromodulators besides dopamine including serotonin and noradrenaline.

While weak, this dopaminergic loop might be a contributing factor to the vicious cycle of depression. This is especially relevant to SAD which is related to a lack of light in the environment as well as a lack of melanopsin in our retinas. Of course, this does not place the centre of depression to the eye. It does, however, aptly illustrate the interaction between light and affective disorders, thereby placing the clinical findings of effectiveness of light therapy of depression and sleep on solid ground.

Equipped with understanding of the light effects on our sleep-wake cycle, mood and cognition, you can finally check the last piece of the Science Behind Light Therapy series, describing novel findings connecting light exposure, digestion and cardiovascular risks, and still somewhat speculative application of light therapy in obesity treatment: