Sleep deprivation potentiates HPA axis stress reactivity in healthy adults.

2014 ◽  
Vol 33 (11) ◽  
pp. 1430-1434 ◽  
Author(s):  
Jared Minkel ◽  
Marisa Moreta ◽  
Julianne Muto ◽  
Oo Htaik ◽  
Christopher Jones ◽  
...  
2021 ◽  
Vol 53 (8S) ◽  
pp. 371-371
Author(s):  
Maria Dourida Mitarachi ◽  
Marinela Tzanela ◽  
Athina Asimakopoulou ◽  
Efi Botoula ◽  
Michael Koutsilieris ◽  
...  

2020 ◽  
Author(s):  
Chen Xing ◽  
Yanzhao Zhou ◽  
Huan Xu ◽  
Mengnan Ding ◽  
Yifan Zhang ◽  
...  

Abstract Background: Sleep loss leads to a spectrum of mood disorders such as anxiety, cognitive dysfunction and motor coordination impairment in many individuals. However, the underlying mechanisms are largely unknown. Methods: In this study, we examined the effects of sleep deprivation (SD) on depression and the mechanism by subjecting rats to a slowly rotating platform for 3 days to mimic the process of sleep loss. Sleep-deprived animals were tested behaviorally for anxiety- and depressive-like behaviors. We further studied the effects of SD on hypothalamic-pituitary-adrenal (HPA) axis activity, and at the end of the experiment, brains were collected to measure the circadian clock genes expression in the hypothalamus, glial cell activation and inflammatory cytokine alterations. Results: Our results indicated that SD for 3 days resulted in anxiety- and depressive-like behaviors. SD exaggerated cortisol response to HPA axis, significantly altered the mRNA profile of circadian clock genes, and induced neuroinflammation by increasing the expression of glial cell markers, including the microglial marker ionized calcium-binding adapter molecule 1 (Iba1) and the astroglial marker glial fibrillary acidic protein (GFAP). The expression of M1 and M2 microglial markers (Arg-1 and CD206, respectively) and pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) were increased in the brain. Conclusion: These results indicated that SD for 3 days induced anxiety- and depression-like behaviors in rats by impairing the regulation of circadian clock genes and inducing neuroinflammation, ultimately resulting in brain injury.


2006 ◽  
Vol 31 (2) ◽  
pp. 197-208 ◽  
Author(s):  
A SGOIFO ◽  
B BUWALDA ◽  
M ROOS ◽  
T COSTOLI ◽  
G MERATI ◽  
...  

2011 ◽  
Vol 12 ◽  
pp. S14
Author(s):  
Nanette S. Danielsson ◽  
Shane MacDonald ◽  
Markus Jansson-Fröjmark ◽  
Steven J. Linton ◽  
Allison G. Harvey

2012 ◽  
Vol 17 (3) ◽  
pp. 975-983 ◽  
Author(s):  
Göksel Açar ◽  
Mustafa Akçakoyun ◽  
Ibrahim Sari ◽  
Mustafa Bulut ◽  
Elnur Alizade ◽  
...  

2017 ◽  
Vol 19 (4) ◽  
pp. 246-258 ◽  
Author(s):  
Samira S. Valvassori ◽  
Wilson R. Resende ◽  
Gustavo Dal-Pont ◽  
Heron Sangaletti-Pereira ◽  
Fernanda F. Gava ◽  
...  

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P4993-P4993
Author(s):  
M. Sunbul ◽  
B. Kanar ◽  
T. Kivrak ◽  
E. Durmus ◽  
I. Sari ◽  
...  

2018 ◽  
Author(s):  
Jesse T Kaye ◽  
Gaylen Fronk ◽  
Aleksandra Zgierska ◽  
Maireni R. Cruz ◽  
David Rabago ◽  
...  

Rationale: Norepinephrine plays a critical role in the stress response. Clarifying the psychopharmacological effects of norepinephrine manipulation on stress reactivity in humans has important implications for basic neuroscience and treatment of stress-related psychiatric disorders, such as posttraumatic stress disorder and alcohol use disorders. Preclinical research implicates the norepinephrine alpha-1 receptor in responses to stressors. The No Shock, Predictable Shock, Unpredictable Shock (NPU) task is a human laboratory paradigm that is well positioned to test cross- species neurobiological stress mechanisms and advance experimental therapeutic approaches to clinical trials testing novel treatments for psychiatric disorders.Objectives: We hypothesized that acute administration of prazosin, a noradrenergic alpha-1 antagonist, would have a larger effect on reducing stress reactivity during unpredictable, compared to predictable, stressors in the NPU task.Methods: We conducted a double-blind, placebo-controlled, crossover randomized controlled trial in which sixty-four healthy adults (32 female) completed the NPU task at two visits (2mg prazosin vs. placebo).Results: A single acute dose of 2mg prazosin did not reduce stress reactivity in a healthy adult sample. Neither NPU startle potentiation nor self-reported anxiety was reduced by prazosin (vs. placebo) during unpredictable (vs. predictable) stressors.Conclusions: Further research is needed to determine whether this failure to translate preclinical neuroscience to human laboratory models is due to methodological factors (e.g., acute vs. chronic drug administration, brain penetration, study population) and/or suggests limited clinical utility of noradrenergic alpha-1 antagonists for treating stress-related psychiatric disorders.


Sign in / Sign up

Export Citation Format

Share Document