bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/436048

Sleep restriction caused impaired emotional regulation without detectable brain activation changes - a functional magnetic resonance imaging study

Tamm, S.·Nilsonne, G.·Schwarz, J.·Golkar, A.·Kecklund, G.·Petrovic, P.·Fischer, H.·Akerstedt, T.·Lekander, M.
View original source ↗Export metadata ↓

Abstract

Sleep restriction has been proposed to cause impaired emotional processing and emotional regulation by inhibiting top-down control from prefrontal cortex to amygdala. Intentional emotional regulation after sleep restriction has however never been studied using brain imaging. We here aimed to investigate the effect of sleep restriction on emotional regulation through cognitive reappraisal. Forty-seven young (age 20-30) and 33 older (age 65-75) participants (38/23 with complete data and successful sleep intervention) performed a cognitive reappraisal task during fMRI after a night of normal sleep and after restricted sleep (3h). Emotional downregulation was associated with significantly increased activity in dorsolateral prefrontal cortex (pFWE < 0.05) and lateral orbital cortex (pFWE < 0.05) in young, but not in older subjects. Sleep restriction was associated with a decrease in self-reported regulation success to negative stimuli (p < 0.01) and a trend towards perceiving all stimuli as less negative (p = 0.07), in young participants. No effects of sleep restriction on brain activity nor connectivity were found in either age group. In conclusion, our data do not support the idea of a prefrontal-amygdala disconnect after sleep restriction, and neural mechanisms underlying behavioural effects on emotional regulation after insufficient sleep require further investigation.

Source connections

Explore related subjects

neurosciencePreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Tamm, S., Nilsonne, G., Schwarz, J., Golkar, A., Kecklund, G., Petrovic, P., Fischer, H., Akerstedt, T., Lekander, M.. 2018-10-05. Sleep restriction caused impaired emotional regulation without detectable brain activation changes - a functional magnetic resonance imaging study. https://doi.org/10.1101/436048

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Sex differences in fear extinction are conditional, not categorical

Threat memories are dynamic, and their behavioral expression can change with subsequent experience and the passage of time. Extinction training can reduce conditioned fear responses, yet these responses may re-emerge over time through spontaneous recovery. Although biological sex has been implicated as modulatory factor in fear and extinction memory processes, studies have reported inconsistent findings. Here, we investigated how differences in extinction training and the timing of memory assessment influence extinction memory in male and female mice. Using contextual fear conditioning, we assessed fear acquisition and threat retention, characterized within-session and across-session extinction during repeated training, and compared shorter (3-minute) and longer (6-minute) daily extinction sessions. We subsequently evaluated extinction memory retention and spontaneous recovery at a later time point. Estrous-cycle stage in females was monitored daily throughout the experimental protocol to examine its potential association with fear and extinction behavior. We found that males and females demonstrated comparable fear acquisition and threat memory, as well as similar extinction progression across days. During longer extinction sessions, but not shorter, males showed greater within-session reductions in freezing, whereas females exhibited modestly higher overall freezing. We found no significant sex difference in the magnitude of spontaneous recovery. There was no significant association between estrous-cycle stage and freezing behavior. Together, our findings suggest that sex-dependent differences in contextual fear extinction are not uniformly expressed, but rather depend on the experimental conditions under which extinction is assessed

neuroscience↗
bioRxiv2026

LAMA2-related muscular dystrophy alters Schwann cell calcium homeostasis and increases peripheral nerve inflammation

LAMA2-related muscular dystrophy (LAMA2-RD) affects skeletal muscle and peripheral nerves, yet the consequences of LAMA2 deficiency on peripheral nerve integrity beyond early postnatal development remain incompletely understood. We investigated sciatic nerve architecture and molecular alterations across postnatal life in hypomorphic Lama2dy2J/dy2J mice. LAMA2 localizes around the abaxonal surface of myelinating Schwann cells in control nerves. LAMA2-deficient nerves exhibited patchy regions lacking myelinated axons from early postnatal stages into adulthood, including expanded Remak bundles along with axons completely lacking normal Schwann cell ensheathment. In adult nerves, myelin infolding and reduced myelin circularity revealed abnormalities in the architecture of myelin that had formed. Bulk sciatic nerve RNA sequencing identified altered calcium-signaling and immune-related transcriptional signatures. Complementary Fura Red measurements in primary nerve-derived Schwann cell cultures demonstrated decreased intracellular calcium in LAMA2-deficient samples, while ATP-evoked responses were preserved. Older LAMA2-deficient nerves also exhibited increased CD45+CD11b+ myeloid-cell infiltration. Together, these observations extend the characterization of LAMA2-associated neuropathy into adulthood and identify calcium homeostasis and neuroimmune responses as candidate processes relevant to persistent peripheral nerve pathology.

neuroscience↗
bioRxiv2026

Endothelin-1 from Tongue Glands Gates 1 Sodium Taste and Intake

Sodium is an essential nutrient. To survive sodium deficiency, animals dramatically increase their appetite for salt. However, whether and how sodium depletion impacts the taste of salt to drive sodium intake is unknown. Here we show that tongue gland-derived endothelin-1 (EDN1) regulates the amiloride-sensitive, sodium-selective salt taste. Edn1 is specifically expressed in the glands embedded within the tongue. Under normal conditions, EDN1 suppresses salt taste by acting on its receptor EDNRB on the projections of salt-sensing taste neurons innervating taste buds. When internal sodium levels drop, EDN1 expression decreases, lifting this inhibition and enhancing responses to salt. Applying EDN1 directly to the tongue, using a nonionic eutectic-based organogel (Neogel) delivery technology that we establish here, dampens the activity of the salt-sensing taste neurons and reduces salt intake and preference. Conversely, genetic deletion of Ednrb in taste neurons mimics the effects of sodium deficiency, enhancing salt-sensing neuron activity and increasing salt consumption. These findings reveal a peripheral mechanism that regulates salt taste and intake in response to internal sodium levels, highlighting a direct role of the taste pathway in maintaining nutrient homeostasis.

neuroscience↗