Have you ever been sad in the winter? If so, you’re not alone. Medaka fish feel it too.
Seasonal affective disorder, or SAD, refers to how season changes in the environment, like the shortening of days and less direct sunlight, can trigger depression and anxiety. In regions of the world at high latitudes, it is estimated that about 10% of the population experiences winter depression, which can include symptoms such as low mood, sleep problems, disrupted circadian rhythms, social withdrawal, decreased libido, and changes in appetite and body weight, and related suicide and social withdrawal. Needless to say, these symptoms are serious, which is why current research into the disorder is so critical.
Researchers from the Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University have used medaka fish as a case study to investigate the molecular mechanism of SAD. From their work, they have identified a drug that is effective at reducing winter depression-like behavior in the fish. Their research was published recently in PNAS.
Medaka fish are known to be a key animal model for winter depression-like behavior, as it is possible to observe their decreased sociability and increased anxiety-like behavior when put in winter conditions.
The authors explain in their study that they used chemical genomics to test the effects of a traditional Chinese medicine, known as celastrol, on the fisk. The authors write: “Using metabolomic and transcriptomic analyses, we found changes in multiple signaling pathways involved in depression, including the NRF2 antioxidant pathway.” NRF2 is a celastrol target that has an important role in the pathophysiology of depression. “Chemical genomics and targeted mutation of the NRF2 gene revealed that seasonal changes in the NRF2 pathway regulate winter depression-like behavior. This study provides insights into the understanding and treatment of seasonally regulated affective disorders,” continue the authors.
The authors hope that their findings will provide insight on the pathology of SAD as well as propose potential new therapeutic targets for future treatments.