Optogenetic control of neurons
Physically, optogenetic controllers are light-sensitive ion channels. These channels can either close or open in response to light, and whether they're closed or open has a huge effect on the neuron's function. Neurons communicate through electrical signals. They receive on or off signals from the other neurons around them, make some of their own internal computations, and then, if the situation is right, send their own on or off signal to the next group of neurons. All of these signals are processed by the neuron through changes in its electrical state, and those changes are created by charged particles (ions) moving through specialized channels in its membrane. Some signals cause a certain ion channel to open, which allows a specific ion to leave the cell, changing the whole neuron's electrical state. By keeping track of this electrical state, the neuron knows when to send its own signal. Optogenetic controllers are ion channels that can overwhelm any other signals the neuron is receiving and therefore dictate its behavior. The power of optogenetic controllers is in their efficiency. If they tell the neuron that it should fire a signal to the next neurons, it will, and vice versa. This means that researchers can completely control the behavior of whatever neurons they can shine light on, which is extremely useful in neuroscience. By turning neurons on or off when you want, you can see what role they play and how they effect the neurons further downstream. In this way, you can figure out the role of specific areas in the animal's brain-- how they are involved in its sight or food-searching behavior, for example.
Most optigenetic controllers are channels that occur naturally in algae, plants, or archaea (a form of bacteria). When scientists find a light-sensitive ion channel, they sequence the responsible gene and insert it into the genome of the animal they want to investigate (at this point, usually mice or rats). An animal with the inserted optogenetic gene produces the light-sensitive ion channel in their neurons. Since the brain isn't normally exposed to light, it has no effect on their function unless the researchers deliberately shine light onto the tissue.
The possibilities for applications of optogenetic control are nearly endless. It's been used in studies of everything from taste memory to spatial navigation to sleep to strokes. These experiments are significantly expanding our knowledge of how the brain functions, and many of them are working towards human medical applications. Just last week a study was published where researchers were able to halt the progress of a type of seizure in rats that can come with traumatic brain injuries. In humans, this kind of epilepsy can only be stopped by using drugs or surgically removing the area that originates the seizure. These treatments stop the seizure but also stop any normal function of that brain area. With optogenetic control, the scientists were able to selectively disrupt the affected area only when there was a seizure, meaning they could stop the seizure but keep the area intact and functioning normally the rest of the time. If their technique is translated to humans, it would be a huge step up in our ability to treat epilepsy.
One of the major hopes for optogenetic control is that it will be successfully developed for use in primates. Primate brains are obviously much more similar to ours than those of mice. Optogenetic control allows scientists to conduct small-scale and causal research, which are almost never conducted in humans because of ethical concerns. Since primates are the closest we can get, it would be extremely informative to be able to use optogenetic control in primate research. Last month a group of researched published an article detailing a successful test-run of optogenetic control in monkeys. This technique is progressing by leaps and bounds, and scientists are quickly taking it up for its novel abilities.
(External sources: Toward the second generation of optogenetic tools, Closed-loop optogenetic control of thalamus as a tool for interrupting seizures after cortical injury, Saccadic eye movements evoked by optogenetic activation of primate V1)