Regulation of neurotransmission could explain depression
Why doesn't stress always lead to depression, find researchers?
Washington: Researchers have found that changes in the regulation of neurotransmission could explain depression immunity.
They have tried to establish that anhedonia-prone rats have more serotonin neurons after exposure to chronic stress, a major symptom of depression, but the effect can be turned around by amygdala activation.
According to the research published in the Journal of Neuroscience, some people are resistant or not pleased with depression and anhedonia, even under chronic stress. Measuring anhedonia vulnerability, researchers trained rats to activate an electrode that stimulated reward circuits in their brain, causing feelings of pleasure.
Social anxiety was experienced once a day by the rats and auto stimulation was given fifteen minutes later. In the rats prone to anhedonia, stress raised the severity of stimulus significantly, while it had little effect on the resilient rats.
In the ventral portion of their dorsal raphe nucleus, which is an area of the brain involved in the management of stress and rewards, the susceptible rats had more serotonin neurons than the resilient ones.
This increase is due to the recruitment of non-serotonin signalling neurons. When the researchers activated neurons in the central amygdala to prevent the increase in serotonin signalling, the rats experienced reduced effects from social stress.
The understanding of depression susceptibility molecular thumbprint can lead to treatments that cause chronic stress resilience.