Sex‐Specific Effects of Stress on Respiratory Control: Plasticity, Adaptation, and Dysfunction

2021 ◽  
pp. 1-38
Author(s):  
Luana Tenorio‐Lopes ◽  
Richard Kinkead

2019 ◽  
Vol 5 (3) ◽  
pp. 162-176 ◽  
Author(s):  
Kelly Barko ◽  
William Paden ◽  
Kelly M. Cahill ◽  
Marianne L. Seney ◽  
Ryan W. Logan


Hippocampus ◽  
2013 ◽  
Vol 23 (9) ◽  
pp. 797-811 ◽  
Author(s):  
Arnaud Tanti ◽  
Willy-Paul Westphal ◽  
Virginie Girault ◽  
Bruno Brizard ◽  
Severine Devers ◽  
...  


2016 ◽  
Vol 121 (3) ◽  
pp. 781-791 ◽  
Author(s):  
Ryma Boukari ◽  
Orlane Rossignol ◽  
Cécile Baldy ◽  
François Marcouiller ◽  
Aida Bairam ◽  
...  

We tested the hypothesis that membrane progesterone receptors (mPR) contribute to respiratory control in adult male and female mice. Mice were implanted with osmotic minipumps for continuous infusion of small interfering RNA (siRNA) directed against mPRα, mPRβ, or a control solution in the fourth ventricle (to target brain stem respiratory areas) for 14 days. We then performed respiratory and metabolic recordings by whole body plethysmography at rest and in response to hypoxia (12% O2) or hypercapnia (5% CO2, 5 min each). For each treatment, we have verified with immunohistochemistry that the staining intensity of mPRα or mPRβ in the brain stem is decreased. At rest, the siRNA against mPRα and mPRβ increased respiratory frequency in males only. The siRNA against mPRβ almost tripled the frequency of apneas in male and in female mice, while the siRNA against mPRα had no effect. Regarding respiratory chemoreflex, the siRNA against mPRβ suppressed the response to hypoxia in male and female mice and reduced by ∼50% the response to hypercapnia, while the siRNA against mPRα had more limited effects. Interestingly, control females had higher ventilatory response to hypoxia and hypercapnia than males, and these sex-specific effects were suppressed by the siRNA against mPRβ, whereas they were still present after treatment with the siRNA against mPRα. We conclude that mPRβ reduces apnea frequency in male and female mice and establishes sex-specific ventilatory chemoreflex.



2019 ◽  
Author(s):  
Alexandra B. Moussa-Tooks ◽  
Eric Larson ◽  
Alex F. Gimeno ◽  
Emma Leishman ◽  
Lisa A. Bartolomeo ◽  
...  

AbstractStudies of early-life stress traditionally focus on glucocorticoid signaling as a modulator of neurodevelopmental risk, but emerging evidence points to the role of the endocannabinoid system in long-term stress-induced neural remodeling. Existing studies on stress-induced endocannabinoid dysregulation have focused on changes to cerebrum that are temporally proximal to stressors, but little is known about temporally distal effects, especially in cerebellum, which is vulnerable to early developmental stress and is dense with cannabinoid receptors. Further, sex-specific effects of stress on cerebellar endocannabinoid tone are understudied. Following a naturalistic rodent model of early-life stress, limited bedding at postnatal days 2-9, adult (postnatal day 70) cerebellar and hippocampal endocannabinoids and related lipids and mRNA were assessed, and behavioral performance was evaluated. Regional and sex-specific effects were present at baseline and following early-life stress. Limited bedding impaired peripherally-measured basal corticosterone in adult males only. In the CNS, early-life stress (1) decreased 2-arachidonoyl glycerol and arachidonic acid in the cerebellar deep nuclei in males only; (2) decreased 2-arachidonoyl glycerol in females only in cerebellar Crus I; and (3) increased dorsal hippocampus prostaglandins in males only. Transcriptomics for cerebellar interpositus nucleus revealed substantial sex effects, with minimal effects of stress. Stress did impair novel object recognition in both sexes and social preference in females. Taken together, the cerebellar endocannabinoids system exhibits robust sex-specific differences, malleable through early-life stress and perhaps also contributing to sexual differentiation of the brain. The current study may foster future research into stress as a risk factor for cerebellar-related dysfunctions.



Animal Stress ◽  
1985 ◽  
pp. 161-175 ◽  
Author(s):  
James P. Henry ◽  
Patricia Stephens-Larson


2016 ◽  
Vol 80 (5) ◽  
pp. 406-414 ◽  
Author(s):  
Michael Q. Steinman ◽  
Natalia Duque-Wilckens ◽  
Gian D. Greenberg ◽  
Rebecca Hao ◽  
Katharine L. Campi ◽  
...  


2011 ◽  
Vol 28 (2) ◽  
pp. 347-363 ◽  
Author(s):  
Richard B. Felson ◽  
D. Wayne Osgood ◽  
Julie Horney ◽  
Craig Wiernik


Metabolites ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 187
Author(s):  
Elie Farhat ◽  
Hang Cheng ◽  
Caroline Romestaing ◽  
Matthew Pamenter ◽  
Jean-Michel Weber

Hypometabolism is a hallmark strategy of hypoxia tolerance. To identify potential mechanisms of metabolic suppression, we have used the goldfish to quantify the effects of chronically low oxygen (4 weeks; 10% air saturation) on mitochondrial respiration capacity and fuel preference. The responses of key enzymes from glycolysis, β-oxidation and the tricarboxylic acid (TCA) cycle, and Na+/K+-ATPase were also monitored in various tissues of this champion of hypoxia tolerance. Results show that mitochondrial respiration of individual tissues depends on oxygen availability as well as metabolic fuel oxidized. All the respiration parameters measured in this study (LEAK, OXPHOS, Respiratory Control Ratio, CCCP-uncoupled, and COX) are affected by hypoxia, at least for one of the metabolic fuels. However, no common pattern of changes in respiration states is observed across tissues, except for the general downregulation of COX that may help metabolic suppression. Hypoxia causes the brain to switch from carbohydrates to lipids, with no clear fuel preference in other tissues. It also downregulates brain Na+/K+-ATPase (40%) and causes widespread tissue-specific effects on glycolysis and beta-oxidation. This study shows that hypoxia-acclimated goldfish mainly promote metabolic suppression by adjusting the glycolytic supply of pyruvate, reducing brain Na+/K+-ATPase, and downregulating COX, most likely decreasing mitochondrial density.



2013 ◽  
Vol 32 ◽  
pp. e24
Author(s):  
L. Sorski ◽  
R. Melamed ◽  
L. Shaashua ◽  
P. Matzner ◽  
N. Gotlieb ◽  
...  


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