Understanding the molecular footprint of susceptibility to depression could lead to treatments that induce resistance to chronic stress.
Some people are resistant to depression and anhedonia, one of the main symptoms of depression that is characterized by the inability to feel satisfaction, even when exposed to chronic stress. Scientists have now discovered that changes in neurotransmission may explain this intrinsic immunity to depression.
According to new research on experimental models susceptible to anhedonia, published in ‘JNeurosci’, the journal of the American Neuroscience Society, these models have more serotonin neurons after exposure to chronic stress, but the effect can be reversed by activating the amygdala.
To measure susceptibility to anhedonia, these individuals were trained to activate an electrode that stimulated reward circuits in their brain, causing feelings of pleasure. The subjects experienced social stress once a day and were then given access to self-stimulation fifteen minutes later.
In the anhedonia-susceptible model, stress dramatically increased the intensity of stimulation needed to feel pleasure, while it had little effect on the resistant model.
Compared to resistant subjects, susceptible subjects had more serotonin neurons in the ventral part of the dorsal nucleus of the rafe, an area of the brain involved in stress regulation and reward.
This increase is due to recruitment of signaling neurons other than serotonin. When researchers activated neurons in the central amygdala to prevent increased serotonin signaling, individuals experienced reduced effects from social stress.