Much maligned as it tends to be in the media, stress is not all bad, and in smaller doses can be tremendously useful when faced with physical danger, a task which requires intense focus and many other situations. As it becomes more extreme or prolonged, however, things change quite dramatically.
One of the ways in which excessive stress can be harmful is in promoting the onset of clinical depression. Even though evidence for a link between stress and depression has been growing for decades – and no matter how common sense it may seem – the biological underpinnings of its relation to mental health remain elusive to this day.
A recent study on rodents, published in The Journal of Neuroscience, has finally shed some light on what might be going on by demonstrating that rats made to develop anhedonia – the inability to enjoy normally pleasurable daily activities – had more serotonin-producing neurons in their brains than healthy controls.
Considering that depression is still thought by some to be a function of decreased levels of cerebral serotonin, as well as the fact that adult brains don’t make new neurons on command, the findings were quite surprising.
Further research suggested that it likely happens by way of “retrofitting” existing neurons to produce serotonin, which they otherwise would not, thereby providing some interesting new data on how this neurotransmitter and stress both play a role in the development of depression.
“Why does stress not lead to symptoms of depression in every stressed individual? We now know that the serotonergic system demonstrates a form of plasticity, hitherto unknown, that is strongly correlated to the behavioural susceptibility of a rodent to stress-induced depression (anhedonia),” said first author on the study Nandkishore Prakash from the University of California, San Diego.
In the future this could lead to the development of a biomarker to indicate who is likely to become anhedonic in the face of mounting stress.
A second key finding was that activating a different group of neurons that form a major input to the dorsal raphe nucleus (the brain region which started producing serotonin in response to stress) reduced the amount of serotonin signalling in the area, thereby also reducing the anhedonic reactions in rat subjects.
While the same still needs to be demonstrated in future studies, the authors maintain that in the future, similar, yet more streamlined and less invasive, procedures could also be used to treat anhedonia in humans.