drharvey
It's like arguing that a bug is a problem with the UI, not the code...
Meta-analysis has shown that approximately 80% of all cases of depression are initially caused by a major life stress (1). So "exogenous" factors seem to play a large role in triggering most depression. That said, not everyone develops depression following a major life stress - people have different levels of "endogenous" stress resilience/susceptibility. "Endogenous" stress resilience can be modulated, however, by "exogenous" interventions. For example, resilience can be increased by behavioral stress inoculation or even exercise, and it can be decreased by things like sleep deprivation or illness. It can also be partially inherited (i.e., if someone's parents were "exogenously" stressed, the offspring can inherit lower levels of stress resilience through "endogenous" epigenetic changes) (2).
And though 80% of initial depressive episodes may be triggered by stress, this tight correlation between stress and depression does not persist as strongly after the first depressive episode. Essentially, once someone has been depressed a first time, they are then "endogenously" more susceptible to subsequent episodes of depression.
So, is it exogenous or endogenous? Long story short, in most cases, it's both. Even if it doesn't start as both, it becomes both. And both "exogenous" and "endogenous" contributing factors interact in an on-going dynamic process.
1. http://hammenlab.psych.ucla.edu/pubs/05stressand.pdf 2. http://www.ncbi.nlm.nih.gov/pubmed/26410355
I also completely agree that the sedative-level dose given to soldiers after stress might have worked by blocking traumatic memory formation. It has already been established that blocking or "erasing" stress memories may prevent PTSD (here's just one example: http://www.medscape.com/viewarticle/819452).
In the studies in mice, ketamine was no longer in the animals' systems by the time they were stressed. So they were not sedated. And the researchers tested memory formation to confirm it was not affected. Thus, it seems that ketamine's protective effect in mice isn't just because memory is disrupted. That said, it is always possible they missed something.
From what I can find, it doesn't seem like anyone has even looked yet to see how this ketamine-vaccine strategy effects neuroplasticity. At this stage, it's probably best to consider the post-stress effect of ketamine in soldiers (1), the pre-stress protection in mice (2), and the neuroplastic effects of ketamine (3) as three separate things.
You are correct, this is a new finding. It does not, however, come from the study looking at soldiers. In that study, ketamine was actually given after stress (not as a 'vaccine'). Those researchers also failed to replicate that effect when they looked a larger group of soldiers. The first study was done in 2008 and the second one was done in 2014. Believe me, if they had found a protective effect in humans 7 years ago, you would have heard about it by now.
The research that actually shows the ketamine might be a 'vaccine' has all come out this year (2015). And, so far, it's all only in mice. The scientific publication referred to in the Nautilus article is "Ketamine as a Prophylactic Against Stress-Induced Depressive-Like Behavior": http://www.biologicalpsychiatryjournal.com/article/S0006-322.... At least two other research teams at other universities (FSU & UC-Boulder) have independently also found similar effects, but none of that is published yet (though it was presented this year at the national Society for Neuroscience conference). In other words: yes, it's new.
Additionally, neuroscientists at Mt. Sinai, the NIMH, and UC-Boulder (among others) have found that bacteria and immune cells might also be used to 'vaccinate' against stress. Again, most of that research--though not all of it--is still not published yet, and has only been presented at conferences so far.