Probing new mechanisms of depression and anxiety
Male mice that were more likely to acquire depressive- and anxiety-like symptoms following long-term stress had less ATP levels and reduced expression of a protein involved in ATP release (connexin 43). When the research team genetically dampened or deleted connexin 43 in cells that release ATP in another group of mice, this alone led to depressive- and anxiety-like behaviors and lowered ATP levels. Bridging the findings together, in distressed mice, restoring connexin 43 in the hippocampus brought ATP levels up to normal and improved behavioral outcomes.
Says Gao, “This is the first direct evidence that deficient ATP release in [a region of the] hippocampus drives both depressive- and anxiety-like behaviors, revealing a shared molecular pathway [for these conditions].” Gao also emphasizes that the findings linking connexin 43 to this mechanism point to a potential treatment target for treating depression and anxiety when they occur at the same time. Of note, the researchers plan to assess both sexes in future studies.
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About JNeurosci
JNeurosci was launched in 1981 as a means to communicate the findings of the highest quality neuroscience research to the growing field. Today, the journal remains committed to publishing cutting-edge neuroscience that will have an immediate and lasting scientific impact, while responding to authors' changing publishing needs, representing breadth of the field and diversity in authorship.
About The Society for Neuroscience
The Society for Neuroscience is the world's largest organization of scientists and physicians devoted to understanding the brain and nervous system. The nonprofit organization, founded in 1969, now has nearly 35,000 members in more than 95 countries.
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