Contribution of chemical and electrical transmission to the low delta-like intrinsic retinal oscillation in mice: A role for daylight-activated neuromodulators.

Exposure to natural daylight increases dopamine release in the retina, which directly slows the lengthening of the eye and decreases the worsening of nearsightedness.

In mice, retinal electrical oscillations at low delta frequencies are controlled by GABA and glycine signaling, gap junctions, and daylight-triggered dopamine and nitric oxide, which lower the oscillation rate during daylight.

In mice, a specific pattern of electrical activity in the retina called low delta-like oscillations does not require input from light-sensing cells but stops when communication between nerve cells in the inner retina is blocked, showing that the activity originates in inner retinal circuits.

Blocking GABA and glycine receptors in mouse retinas increases the frequency of a specific low-frequency brainwave pattern, showing that these neurotransmitters normally reduce the rate of this oscillation.

Blocking electrical connections between retinal neurons in mice lowers the rate of a specific rhythmic brain signal in the retina.

In mice, chemicals that mimic dopamine and nitric oxide reduce a specific pattern of retinal activity that is normally lowered by daylight, showing that these chemicals are involved in how light alters retinal signaling.