Depression involves prolonged sadness and hopelessness, impaired thinking, distorted Self-appraisals, biased memory processing, and unpleasant dreams/nightmares. It has been known for some time that there is a strong relation between sleep and depression. When we get depressed we sleep too much or too little and we wake up too early in the morning. We never feel totally refreshed by sleep and sleep, when it comes, is fitful and punctuated by too many awakenings. I know of no cases of depression without profound disruption of sleep. It may even be that disruption of sleep can trigger depressive episodes. Why is depression so intimately related to sleep? Can an understanding of this relationship help us to treat depressive episodes? One indication that the answer to this question is yes is that one or two nights of deliberate sleep deprivation can result in lifting of mood symptoms for some depressed patients.
So then, why might sleep and depression be related? REM (rapid eye movement) sleep abnormalities are prime candidate sources of depression symptomology because it exactly reproduces the known pathophysiology of major depressive disorder (MDD). Both lesion and neuroimaging studies suggest that the pathogenesis of MDD involves abnormally high levels of activity in paralimbic structures and ventromedial prefrontal cortex (vmPFC) and abnormally low levels of activity in dorsolateral prefrontal cortex (dPFC). The person with depression therefore cannot effectively recruit dPFC to regulate paralimbic and vmPFC-related negative emotional activity via reappraisal/suppression strategies. Attention in the field has therefore turned to the question of why paralimbic/vmPFC structures are chronically overactivated and dPFC structures underactivated in major depressive disorder (MDD) so that more effective strategies can be developed to modulate these systems appropriately.
While a host of genetic, neurochemical and psychological factors have been implicated in production of depressive symptomology none of these factors link up directly with the known pathophysiology of MDD. One proximate mechanism that does directly yield the pathophysiologic pattern of hyperactive paralimbic/vmPFC systems and hypoactive dPFC systems is REM dis-inhibition. Paralimbic/vmPFC hyperactivation and dPFC hypoactivation exactly characterizes ‘normal' REM-related brain activation/deactivation patterns throughout the sleep cycle. Several times each night REM selectively and intensively activates key structures in paralimbic/vmPFC systems (e.g., amygdala, vmPFC itself etc) and down regulates dPFC systems. To the best of our knowledge this pattern of vmPFC overactivation and dPFC hypoactivation occurs naturally only in REM. REM, furthermore, is also associated with production of negative affect and selective consolidation of negative emotional memories. Is it any surprise then that REM and depression are so intimately related?
The above facts would seem to suggest that you could get rid of depression by getting rid of REM and that seems to be what happens with many anti-depressants. These drugs tend to suppress REM and some studies have shown that the greater the REM suppression the greater the anti-depressant effect. The problem with this REM suppressant strategy of course is that we do not know what REM normally does. It surely was not created by Mother Nature to induce depressive symptoms so prematurely suppressing it may be associated with long term health consequences. On the other hand it may be that suppressing one facet of REM physiology would be enough to reduce depressive symptoms. We simply do not know enough about REM and mood functions to say for sure. Unfortunately funding for sleep research is being cut-a short sighted policy if ever there was one.