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. 2013 Nov 26;110(48):19597-602.
doi: 10.1073/pnas.1317010110. Epub 2013 Nov 11.

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Oliver G Bosch  1 , Julia S Rihm, Milan Scheidegger, Hans-Peter Landolt, Philipp Stämpfli, Janis Brakowski, Fabrizio Esposito, Björn Rasch, Erich Seifritz
Affiliations

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Oliver G Bosch et al. Proc Natl Acad Sci U S A. .

Abstract

In many patients with major depressive disorder, sleep deprivation, or wake therapy, induces an immediate but often transient antidepressant response. It is known from brain imaging studies that changes in anterior cingulate and dorsolateral prefrontal cortex activity correlate with a relief of depression symptoms. Recently, resting-state functional magnetic resonance imaging revealed that brain network connectivity via the dorsal nexus (DN), a cortical area in the dorsomedial prefrontal cortex, is dramatically increased in depressed patients. To investigate whether an alteration in DN connectivity could provide a biomarker of therapy response and to determine brain mechanisms of action underlying sleep deprivations antidepressant effects, we examined its influence on resting state default mode network and DN connectivity in healthy humans. Our findings show that sleep deprivation reduced functional connectivity between posterior cingulate cortex and bilateral anterior cingulate cortex (Brodmann area 32), and enhanced connectivity between DN and distinct areas in right dorsolateral prefrontal cortex (Brodmann area 10). These findings are consistent with resolution of dysfunctional brain network connectivity changes observed in depression and suggest changes in prefrontal connectivity with the DN as a brain mechanism of antidepressant therapy action.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Functional connectivity maps (n = 12) of the brain using the PCC as seed region and comparing two conditions, normal wakefulness (A) and sleep deprived (B) (main effects, P < 0.05 cluster corrected).
Fig. 2.
Fig. 2.
The contrast of the two conditions shows a reduced connectivity between the PCC seed and the bilateral ACC (BA 32; coordinates: +5, +43, +3; z score = 3.7173, significance = 0.000201; cluster size = 359 mm) after sleep deprivation (SD) compared with normal wakefulness (NW).
Fig. 3.
Fig. 3.
Functional connectivity maps (n = 12) of the brain using the DN as seed region and comparing the two conditions, normal wakefulness (A) and sleep deprived (B) (main effects, P < 0.05 cluster corrected).
Fig. 4.
Fig. 4.
The contrast of the two conditions shows an increased connectivity between the DN seed and two areas (A) on the right middle (BA 10, DLPFC, spot 1: coordinates: +38, +46, +18; z score = 3.5413, significance = 0.000498; cluster size = 324 mm) and (B) on the right superior frontal gyrus (BA 10, DLPFC; spot 2: coordinates: +23, +46, +18; z score = 4.202, significance = 0.000026; cluster size = 1,092 mm) after SD compared with NW.
Fig. 5.
Fig. 5.
Comparison of the locations of the DMN-CCN spots of Fig. 1 after (A) normal wakefulness and (C) SD with the DN spots of Fig. 4 after (B) normal wakefulness and (D) SD. An axial cut was generated at the location of the DN spots, keeping the positive and negative correlations of the PCC seed overlaid on the same average anatomy to show in detail the location of these spots with respect to the CCN spots.
See this image and copyright information in PMC

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