Role of astrocytes in the formation of anxiety has been identified

This mechanism is based on a response to norepinephrine, a stress hormone that is released into the amygdala from a region of the brain called the locus coeruleus. When the level of norepinephrine in the brain increases in response to a stressor, the adrenergic receptors on the surface of astrocytes activate the release of calcium. This process is directly correlated with the intensity of anxiety: the faster and more intense the calcium signal, the faster the organism stops exploring its environment and enters a state of defensive freezing or avoidance.

This connection was experimentally confirmed using tests of behavior in aversive (disgusting or fear-inducing) conditions. It was found that individuals with high innate anxiety have a significantly lower threshold for astrocyte activation. Interestingly, data on the activity of these cells provides a more accurate prediction of a subject’s behavior and location in a dangerous area compared to neuronal activity. This suggests that astrocytes act as alarm dispatchers, processing incoming signals from other parts of the brain and shaping the final emotional response.

The identified causal relationship between astrocyte adrenoreceptor activity and anxious behavior opens up new possibilities for pharmacology. While traditional medications primarily target neural transmission, new therapeutic approaches can focus on regulating the functions of glial cells. This is crucial for treating generalized anxiety disorder, where threat assessment mechanisms malfunction even in the absence of actual danger.