(Guardian) 25 years ago, pharmacologist M. E. West of the University of the West Indies in Kingston, Jamaica, noted that local fisherman who smoke cannabis or drink rum made with the leaves and stems of the plant had “an uncanny ability to see in the dark,” which enabled them to navigate their boats through coral reefs. In 2002, another research team travelled to the Rif mountains in Morocco to investigate further. They gave a synthetic cannabinoid to one volunteer, and hashish to three more, then used a newly developed piece of kit to measure the sensitivity of their night vision before and after. Confirming West’s earlier report, they found that cannabis improved night vision in all three of their test subjects.
Now, another study provides hard evidence for the claim, revealing a cellular mechanism by which cannabis might improve night vision. The findings, published recently in the open access journal eLife, could eventually be applied to the treatment patients with degenerative eye diseases such as retinitis pigmentosa.
West had suggested that cannabis might improve vision by acting on the eye muscles to dilate the pupils, so that more light falls on the retina, but other experiments ruled this out by showing that marijuana constricts the pupils. It’s also possible that the drug can influence activity in the visual cortex at the back of the brain, but the CB1 receptor protein, which binds the psychoactive ingredient of cannabis, is found at far higher levels in the eye than in the visual cortex, suggesting that any effects the drug has on vision are likely due to its actions on retinal cells.
Lois Miraucourt of the Montreal Neurological Institute and his colleagues looked not to stoned fishermen, but to tadpoles of the African clawed toad, Xenopus laevis. In one set of experiments, they applied a synthetic cannabinoid to eye tissue preparations from the tadpoles, and used microelectrodes to measure how retinal ganglion cells, whose fibres form the optic nerve, respond to light. The researchers found that this made the cells more sensitive, increasing the rate at which they fired to both bright and dim light stimuli. Closer investigation revealed that this occurred due to inhibition of a protein called NKCC1, via its actions on the CB1 receptor.