Why does depression increase Rapid Eye Movement (REM) sleep?

Why Depression Increases REM Sleep

Depression increases REM sleep due to a cholinergic-aminergic imbalance, with reduced serotonergic and noradrenergic activity allowing for increased cholinergic dominance that promotes REM sleep. 1, 2

Neurochemical Mechanisms

Depression alters the delicate balance of neurotransmitters that regulate sleep architecture:

1. Reduced Monoamine Activity

   • Depression is associated with decreased serotonergic and noradrenergic neurotransmission 3
   • These monoamines normally inhibit REM sleep when functioning properly 2
   • In depression, the functional decrease of serotonergic tone removes this inhibition 3

2. Cholinergic Dominance

   • Cholinergic neurons from the pedunculopontine and lateral dorsal tegmental nuclei become more active during REM sleep 4
   • Acetylcholine promotes REM sleep by inhibiting the REM-off cells in the brainstem 4
   • In depression, the balance shifts toward cholinergic dominance due to reduced monoamine activity 2

Sleep Architecture Changes in Depression

Depression produces several characteristic changes in REM sleep:

• Shortened REM latency: The interval between sleep onset and first REM period decreases 1
• Increased REM density: Higher frequency of rapid eye movements during REM periods 1
• Increased REM duration: Total time spent in REM sleep increases 1
• Altered dream content: More negative emotional content in dreams 5

Supporting Evidence from Antidepressant Effects

The relationship between depression and REM sleep is further demonstrated by antidepressant effects:

• Most antidepressants suppress REM sleep, particularly those that increase serotonin function 6
• Selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants significantly reduce REM sleep and increase REM latency 6
• These medications correct the REM sleep abnormalities seen in depression by restoring monoaminergic inhibition 6, 3

Neuroanatomical Basis

The American Academy of Sleep Medicine guidelines explain the neuroanatomical circuits involved:

• The sublaterodorsal nucleus and precoeruleus region contain "REM-on" neurons that promote REM sleep 4
• These neurons are normally inhibited by "REM-off" neurons, which are activated by:
  • Norepinephrine from the locus coeruleus
  • Serotonin from the raphe nuclei
  • Hypocretin from the lateral hypothalamus 4
• In depression, reduced activity in these inhibitory pathways allows for REM disinhibition 4, 2

Clinical Implications

Understanding this relationship has important clinical implications:

• REM sleep alterations may serve as biological markers for depression 1
• These changes can predict relapse and recurrence of depressive episodes 1
• REM sleep abnormalities may precede clinical depression and help identify high-risk individuals 1
• The therapeutic effect of sleep deprivation in depression may work through similar mechanisms as antidepressants 3

This neurobiological relationship between depression and REM sleep represents a key aspect of the disorder's pathophysiology and provides insights into both diagnostic markers and treatment approaches.