Overnight changes in waking auditory evoked potential amplitude reflect altered sleep homeostasis in major depression

Abstract

Objective Sleep homeostasis is altered in major depressive disorder (MDD). Pre-to post-sleep decline in waking auditory evoked potential (AEP) amplitude has been correlated with sleep slow wave activity (SWA), suggesting that overnight changes in waking AEP amplitude are homeostatically regulated in healthy individuals. This study investigated whether the overnight change in waking AEP amplitude and its relation to SWA is altered in MDD. Method Using 256-channel high-density electroencephalography, all-night sleep polysomnography and single-tone waking AEPs pre-and post-sleep were collected in 15 healthy controls (HC) and 15 non-medicated individuals with MDD. Results N1 and P2 amplitudes of the waking AEP declined after sleep in the HC group, but not in MDD. The reduction in N1 amplitude also correlated with fronto-central SWA in the HC group, but a comparable relationship was not found in MDD, despite equivalent SWA between groups. No pre-to post-sleep differences were found for N1 or P2 latencies in either group. These findings were not confounded by varying levels of alertness or differences in sleep variables between groups. Conclusion MDD involves altered sleep homeostasis as measured by the overnight change in waking AEP amplitude. Future research is required to determine the clinical implications of these findings.

Baseline delta sleep ratio predicts acute ketamine mood response in major depressive disorder

“…In contrast, the waking homeostatic component corresponds to synaptic strengthening, a process controlled in part by plasticity-related genes (e.g., brain derived neurotrophic factor (BDNF), activity-regulated cytoskeleton-associated protein (Arc), nerve growth factor 1-alpha (NGF1a) ), and is expressed by the early discharge of sleep slow waves. The fact that ketamine responders had reduced early discharge of sleep slow waves (as indicated by their low SWA and DSR scores) is consistent with the view that ketamine responders—like other patients with MDD (Goldstein et al, 2011; Landsness et al, 2011)—exhibit decreased synaptic homeostasis at baseline. Furthermore, the ability of ketamine to increase SWA (Feinberg and Campbell, 1993) is consistent with both synaptic strengthening and antidepressant efficacy, a property shared by other interventions with rapid antidepressant effects, such as sleep deprivation (Duncan Jr. et al, 1980; Gillin, 2001; Landsness et al, 2011).…”

Effects of partial sleep deprivation on slow waves during non-rapid eye movement sleep: A high density EEG investigation

“…Semi-automatic artifact rejection was applied to remove channels with interrupted contact with the scalp or high-frequency artifact. Spectral analysis of NREM sleep (all N2 and N3 epochs) from 1 to 30Hz was performed for each channel in 6-second epochs (Welch’s averaged modified periodogram with a Hamming window; frequency resolution 0.17Hz), which maintained temporal congruence between spectral analysis and 30-second staging epochs (Goldstein et al, 2012; Plante et al, 2012). Slow wave energy (SWE; integrated power 1–4.5Hz totaled over cumulative 6-second epochs of N2/N3 sleep) was the primary measure of spectral power utilized in this study, with other bands examined on an exploratory basis.…”

Astrocytic adenosine: from synapses to psychiatric disorders

“…MDD has been shown to change the sleep homeostat as measured by auditory evoked potential changes causing consequential changes in SWA. Finally, selectively sleep depriving subjects by only interrupting slow wave sleep is still an effective antidepressant treatment in patients with major depression [73,74].…”