A new study sheds light--both literally and figuratively--on the intricate brain cell connections responsible for anxiety.
Scientists at Stanford University recently used light to activate mouse neurons and precisely identify neural circuits that increase or decrease anxiety-related behaviors. Pinpointing the origin of anxiety brings psychiatric professionals closer to understanding anxiety disorders, the most common class of psychiatric disease.
A research team led by Karl Deisseroth, associate professor of psychiatry and behavioral sciences and bioengineering, identified two key pathways in the brain: one which promotes anxiety, and one which alleviates anxiety.
The pathways are in a brain region called the amygdala. Prior research suggests the amygdala plays a role in anxiety, but earlier studies used widespread modifications of the amygdala, through drugs or physical disruption of the brain region, to study the way in which it affects anxiety. This new work, published in this week's Nature, uses a tool called optogenetics--developed by Deisseroth and recently named Method of the Year by Nature Methods--to specifically tease out which pathways contribute to anxiety.
Optogenetics combines genetics and optical science to selectively manipulate the way a neuron fires in the brain. Neurons are electrically excitable cells that convey information through electrical and chemical signaling.
Directed genetic manipulations cause specific neurons to assemble a light-activated protein normally found in algae and bacteria. When triggered by certain wavelengths of light, these proteins allow researchers to increase or decrease neuronal activity in the brain and observe the effects on rodent models in an experiment.
Using optogenetic manipulation of various amygdala pathways, Deisseroth and colleagues examined how mouse behavior was affected. Since mice display anxiety-related behaviors in open spaces
|Contact: Bobbie Mixon|
National Science Foundation