Timing is everything: Does the robust upregulation of noradrenergically regulated plasticity genes underlie the rapid antidepressant effects of sleep deprivation?

Jennifer L. Payne, Jorge A. Quiroz, Carlos A. Zarate, Husseini K. Manji

Research output: Contribution to journalReview article

Abstract

The mechanisms by which sleep deprivation brings about rapid antidepressant effects remain to be elucidated. Biological rhythms have the capacity to temporally dissociate biochemical processes, and imposing a temporal coincidence on normally dissociated events can have striking and unexpected effects. In this context, it is noteworthy that the locus coeruleus (LC) noradrenergic projection is quiescent only during rapid-eye-movement (REM) sleep, when the target tissues display their greatest sensitivity; indeed, the temporal dissociation between the firing of the LC noradrenergic neurons and the sensitivity of its postsynaptic targets in the cortex may have considerable relevance for the antidepressant effects of sleep deprivation. Sleep deprivation rapidly upregulates several plasticity-related genes, effects that are noradrenergically mediated; these are the very same genes that are upregulated by chronic antidepressants. Thus, activating the norepinephrine system during REM sleep (by infusing an α2 antagonist) may allow an interaction with a primed, sensitized postsynaptic milieu, thereby rapidly increasing the expression of plasticity genes and consequently a rapid antidepressant response.

Original languageEnglish (US)
Pages (from-to)921-926
Number of pages6
JournalBiological psychiatry
Volume52
Issue number10
DOIs
StatePublished - Nov 15 2002
Externally publishedYes

Keywords

  • Antidepressant
  • BDNF
  • CREB
  • Circadian rhythm
  • Locus coeruleus
  • Rapid-eye-movement sleep

ASJC Scopus subject areas

  • Biological Psychiatry

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