Lighting Up Anesthesia – Controlling Propofol With Light

Connie K. Ho for — Your Universe Online

A new study by German researchers found that a light-sensitive element that was mixed with the anesthetic propofol was able to be managed by light and the mixture could possibly be used to treat particular eye disorders.

To begin, the scientists believe that inhibitory neurotransmitters can limit the activity of neurons and this reduction effect acts as the foundation for different anesthetics. In particular, propofol can work with receptors on neural cell membranes that usually attach to the inhibitory neurotransmitter gamma-amino butyric acid (GABA). By attaching to GABA, this allows for negatively charged ion cells to move into the cell via open protein channels. As a result, the cell decreases in its response to incoming stimulus due to the increased amount of electrical potential throughout the membrane. The researchers discovered that propofol was able to increase the response effect, serves as an aesthetic, and allow the GABA receptor to be regulated by light.

“By attaching a molecular switch to propofol, we have obtained a light-sensitive molecule that is a more potent anesthetic than propofol itself, in the dark,” commented Dirk Trauner, a professor of Chemical Biology and Genetics at Ludwig-Maximilians-Universitat Munchen (LMU), in a prepared statement.

The team of investigators utilized a group of tadpoles in their experiment to prove that light was an important variable in the compound´s anesthetic effect. For example, when the tadpoles were exposed to a low concentration of propofol, they were anesthetized. On the other hand, when brightened with violet light, the tadpoles were revitalized but the revitalization only lasted when the light was on. In the dark, the tadpoles stayed unmoving. The scientists discovered that the effect of light could be reversed as the tadpoles became as they were before when they were placed in their normal aquarium.

Based on the findings, the new compound could be utilized to help treat particular types of blindness like retinitis pigmentosa, a condition where the photoreceptors are gradually damaged and causes the loss of sight.

“The inner cells also bear GABA receptors on their surfaces, and in principle they could be turned into light-responsive cells with the help of the new compound, which would allow us to bypass the defective photoreceptors,” explained Trauner in the statement.

The scientists at LMU have conducted similar research projects in the past. In February, chemists led by Trauner announced that they were able to stop the activity of pain-sensitive neurons with an agent that functioned as a photosensitive switch. This “pain switch” helps researchers better understand the neurobiology of pain. As well, this past January, Trauner´s team was also able to successfully convert a “blind” receptor molecule into a photoreceptor. The project was completed with the help of a molecular genetics technique that attached a light-controlled chemical “switch” to a macromolecular receptor that is activated by acetylcholine, an endogenous neurotransmitter. With this optical switch that could control a “blind” neuroreceptor, the researchers were able to better understand the role of the natural receptor in the brain. With these various projects underway, the group of researchers will continue to focus on studies that can allow patients who suffer from blindness to regain their sight.

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