C1 neurons can cause prolonged anxiety

The researchers focused on C1 neurons located in the rostral ventrolateral part of the medulla oblongata (RVLM). This area of the brain is primarily known for regulating breathing and heart function, so it was believed that it was unlikely to contain cells that control complex behavioral responses such as fear and anxiety. Using a specialized targeted stimulation system, the researchers were able to isolate C1 neurons from other similar cells in the RVLM.

It turned out that under stress, C1 neurons are activated and transmit a signal to the periaqueductal gray matter (PAG), a key area of the brain that controls physiological and behavioral responses to stress. Activation of C1 neurons causes immediate anxiety in mice, and if their activity persists, the anxiety state can last up to a week. According to Lindsay Schwartz from the Department of Developmental Neurobiology, the connection between C1 neurons and the PAG is very strong. Normally, this circuit is turned off when the threat disappears, but strong activation can keep it on for too long.

The effect of suppressing C1 neurons was particularly important. It significantly reduced anxious behavior, with the greatest benefit occurring after severe stress. Blocking these neurons during acute stress made the animals less sensitive to subsequent stressful situations. However, suppressing C1 neurons did not affect immediate behavior or disrupt basic autonomic functions.

The authors concluded that C1 neurons appear to increase anxiety without directly affecting autonomic responses. This makes them a more promising target for treatment than general approaches that target signaling pathways throughout the brain and body.