A new study suggests that a single molecular deficiency in the brain’s energy signaling system may be a common cause for both depression and anxiety.
A groundbreaking study conducted by Tian-Ming Gao and colleagues at Southern Medical University demonstrated how adenosine triphosphate (ATP) signaling triggers factors like depression and anxiety in male mice.
Adenosine Triphosphate (ATP) is known as the cell’s main source of energy, but it also acts as a neurotransmitter that helps neurons to communicate effectively.
The healthy communication between brain cells is crucial for controlling emotions, as the researchers focused their work on the hippocampus, a region specifically involved in memory, stress responses, and the beginning of despondency.
Pivotal role of Connexin 43 to retain brain’s energy health
The researchers analyzed that male mice prone to develop depressive and anxiety-like behaviors after long-term stress and energy depletion.
These mice also produced less of a key protein required for ATP release.
It has been observed that connexin 43 forms channels that allow ATP to navigate between certain cells, making it a significant part of how the brain retains healthy energy and signaling levels.
In order to scrutinize whether reduced ATP release provoked mood-related symptoms, the team genetically reduced connexin 43 in cells that normally release ATP.
To test whether reduced ATP release resulted in mood-related symptoms, the team removed connexin 43 in cells that commonly release ATP.
The same experiment was performed in another group of mice that had not been exposed to longer periods of stress.
The results showed that even without a high-stakes situation, lowering levels of connexin 43 activated depressive behaviors and reduced ATP levels.
Research findings further suggested that interference in ATP release alone could influence emotional behavior.
This recovery underscores the idea that ATP plays a pivotal role in modulating mood.
Regulatory pathway for Depression and Anxiety
This marks the first evidence that ATP depletion in the hippocampus drives both depressive and anxiety behaviors, thereby exposing a shared molecular pathway for such conditions.
This revelation is crucial because depression and anxiety that coexist together can be intractable to treat simultaneously with previous therapies.
The research team was able to develop interventions to address conditions simultaneously.
It also plans to incorporate both male and female mice to analyze whether these mechanisms operated similarly, as the future of understanding disorders lies not just in the neural circuits, but also central to the cellular energy health of the brain.