Emotion found to physically affect action

During high-stress situations such as making a goal in soccer, some athletes experience a rapid decline in performance under pressure, known as ‘choking’. Now, researchers at the Salk Institute for Biological Sciences have uncovered the signals that might explain this phenomenon, with the results published in the journal eLife.

It was previously believed that the brain’s emotion and movement loops worked like parallel closed circuits, operating independently to relay important information. However, researchers suspected that there could be some influence of emotion on movement due to the observation that, in neuropsychiatric conditions such as depression, decreased physical movement is a symptom and could be linked to disrupted emotional processing and reduced motivation. But scientists did not know much about the connections within each circuit or how the circuits might interact.

“We wanted to explore how emotion information reaches the movement circuitry in the brain by using a combination of cutting-edge viral and optogenetic techniques,” said Sho Aoki, co-first author on the study and a postdoctoral fellow in the lab of Associate Professor Xin Jin.

The scientists sought to trace these circuits in rodent models to better understand each step of neuronal communication. They focused on the emotion and movement brain loops, starting from a region involved in emotion (the medial prefrontal cortex) and a region involved in movement (the primary motor cortex). They used multiple genetic and viral tracing tools, including a technique developed by Salk Professor Ed Callaway’s lab, to observe how each loop was organised in the brain.

To the researchers’ surprise, they found a one-way communication pathway from the emotion loop to the movement loop through an area located deep in the brain called the basal ganglia, which includes structures involved in guiding behaviour and thus essentially acts as a crossroads for the emotion circuit to directly influence the movement circuit to control action. To confirm the novel pathway, the authors used optogenetics — a technique that uses light to control cells — to investigate the precise function of the neurons in this region, as well as studying each neural circuit in isolation from the rest of the brain.

“This finding is very exciting as it is the first time that a comprehensive circuit mechanism has been found showing how emotional states can influence movement through connections in … the basal ganglia,” said Assoc Prof Jin, who served as senior author on the paper. “We did not previously know much about this pathway.”

The study could lead to new strategies for treating disorders with disrupted movement, such as obsessive-compulsive disorder, anxiety and depression. Assoc Prof Jin noted, “Psychiatric diseases such as depression and anxiety can alter actions in a dramatic way by either decreasing or increasing movement. This mechanism represents a likely way that emotional states are related to changes in action control in psychiatric diseases.”

Additionally, this unidirectional communication may be relevant for recovery from spinal cord injury. Researchers previously focused on movement centres of the brain because spinal cord injury is a movement issue; however, since these results suggest emotional states can influence brain movement centres, experiencing positive emotions such as motivation may aid patients in the recovery process. Activating emotion centres could likewise stimulate movement centres and facilitate recovery, according to the Salk co-first authors Jared Smith and Hao Li.

Further, these results suggest that emotional states could directly influence sports performance. So the next time you feel anxious during a game, Assoc Prof Jin advises calming down and letting the action take care of itself.

Image caption: A cluster of basal ganglia output neurons (green) that convey emotion information to the movement circuit to control action. Dopaminergic neurons (red) are also present in the image. Image credit: Salk Institute.

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