The hippocampus retains the traces of negative stressful experiences that can lead to depression-related behaviours
In individuals facing depression, daily interactions and activities become challenging. Depression can be associated with social avoidance (e.g. refusing to enter situations in which they may be forced to interact with other people out of fear of judgement or criticism). Physicians and other mental health workers have documented a decrease in memory function among their patients dealing with depressive disorders. A research team based at the Douglas Research Centre and at McGill University has shown that neuronal memories of stressful experiences can be explained by biological traces in a specific brain region, the hippocampus, and that these are linked to depression-related symptoms.
An article by Dr. Tak Pan Wong of the Douglas Research Centre, a professor in the McGill’s Department of Psychiatry, was published today in the Journal of Neuroscience. This study used a mouse model of depression using social stress to show that a biological marker in the hippocampus could explain some of the cognitive difficulties that are frequently associated with depression.
Experience-related memory is thought to be recorded through networks of neurons that activate in a concerted manner to encode memories – these networks are termed “engrams”. In susceptible mice, repeated experiences of social stress lead to the overactivation of certain engrams in the hippocampus and to the appearance of depression-related symptoms.
Further, Wong and his team were able to modify these memory traces to influence social avoidance behaviour. When engrams were activated, susceptible mice exhibited more social avoidance behaviours, and inversely, when they were disactivated, social avoidance behaviours were decreased.
This discovery, highlighted by the prestigious Society for Neuroscience for its innovative aspects and potential impact, offers a new pathway to understand the cellular mechanisms of cognitive decline linked to depression. Even if individual responses to social stress are very variable, the identification of this mechanism in mice suggests new potential targets for the treatment of depression in humans.
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