Acute stress effect on hypothalamus BDNF expression, monoamines levels and adrenal catecholamines in mouse lines differed by 5-HT1A receptor function

Author(s):  
Elena Kondaurova ◽  
Arina Pershina ◽  
Daria Bazovkina
2019 ◽  
Vol 29 ◽  
pp. S249-S250
Author(s):  
E. Kondaurova ◽  
Y. Antonov ◽  
A. Pershina ◽  
E. Bazhenova ◽  
D. Bazovkina ◽  
...  

1995 ◽  
Vol 9 (3) ◽  
pp. 190-195 ◽  
Author(s):  
P.J. Mills ◽  
M.G. Ziegler ◽  
J.E. Dimsdale ◽  
B.L. Parry

2011 ◽  
Vol 15 (02) ◽  
pp. 235-246 ◽  
Author(s):  
Fabio Fumagalli ◽  
Francesca Calabrese ◽  
Alessia Luoni ◽  
Francesca Bolis ◽  
Giorgio Racagni ◽  
...  

2020 ◽  
Vol 24 (4) ◽  
pp. 249-255
Author(s):  
Vladimir G. Bagaev ◽  
V. A. Mitish ◽  
T. C. Sabinina ◽  
O. C. Melnichuk ◽  
P. V. Medinsky ◽  
...  

Introduction. In the present trial, the authors studied anti-stress properties of subnarcotic concentrations of gas Xenon (Xe) which is used for treating children with severe traumas. Purpose. To study anti-stress properties of subnarcotic concentrations of gas Xenon (Xe) which is used for treating children with severe injuries. Material and methods. 10 children, aged 13 ± 3 years, with severe trauma were taken into the study: 6 girls with mine-explosive injuries ( a terrorist attack in Kerch in 2018), 3 boys with multiple dog bites and one patient after a traffic accident. To treat them, 20-30% Xe with O2 was used. A session lasted for 20 minutes; the course included from 5 to 12 sessions. Device KTK-01 (LLC “KseMed”, Russia) was used. Pain intensity was assessed with the numerical rating scale (NRS) , sedative effect - with BIS index and Ramsey sedation scale. Patients’ blood was also examined for the level of somatotropic hormone (STH), cortisol (Co) and insulin. Results. Indications for Xe therapy in children were: persistent pain syndrome (PS) and acute stress disorder (ASD). Patients fell asleep (drug-induced sleep) under 20-30% Xe concentration in the respiratory mixture. The average values of BIS index decreased from 95.5 ± 2.5 U to 86.5 ± 5.0 U (p <0.05), and of Ramsay scale - from 5.5 ± 0.5 to 2.7 ± 1.2 points (p <0.05). Pain intensity by NRS decreased from 4.1 ± 1.8 to 1.1 ± 0.4 points (p <0.05). The level of stress hormones during Xe session went down: STH- from 4.8 ± 0.9 ng / ml to 1.9 ± 0.5 ng / ml (p <0.001); Ko - from 375.5 ± 23.6 nmol / L to 303.2 ± 20.7 nmol / L (p <0.0001); insulin - from 19.9 ± 3.6 pmol / L to 11.7 ± 2.7 pmol / L (p <0.001). To restore sleep, 2 - 3 sessions were needed; to relief PS - 5 sessions, to refuse of painkillers in phantom pains - 12 sessions. Conclusion. 20-30% Xe with oxygen therapy has a pronounced analgesic, sedative and anti-stress effect in children with severe injuries.


2011 ◽  
Vol 109 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Luis A. Méndez-Cuesta ◽  
Berenice Márquez-Valadez ◽  
Verónica Pérez-De la Cruz ◽  
Perla D. Maldonado ◽  
Ricardo A. Santana ◽  
...  

2015 ◽  
Vol 308 (6) ◽  
pp. H612-H622 ◽  
Author(s):  
Benedek Erdos ◽  
Iara Backes ◽  
Michael L. McCowan ◽  
Linda F. Hayward ◽  
Deborah A. Scheuer

Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) in response to hypertensive stimuli including stress and hyperosmolarity. However, it is unclear whether BDNF in the PVN contributes to increases in blood pressure (BP). We tested the hypothesis that increased BDNF levels within the PVN would elevate baseline BP and heart rate (HR) and cardiovascular stress responses by altering central angiotensin signaling. BP was recorded using radiotelemetry in male Sprague-Dawley rats after bilateral PVN injections of adeno-associated viral vectors expressing green fluorescent protein (GFP) or myc epitope-tagged BDNF fusion protein. Cardiovascular responses to acute stress were evaluated 3 to 4 wk after injections. Additional GFP and BDNF-treated animals were equipped with osmotic pumps for intracerebroventricular infusion of saline or the angiotensin type-1 receptor (AT1R) inhibitor losartan (15 μg·0.5 μl−1·h−1). BDNF treatment significantly increased baseline BP (121 ± 3 mmHg vs. 99 ± 2 mmHg in GFP), HR (394 ± 9 beats/min vs. 314 ± 4 beats/min in GFP), and sympathetic tone indicated by HR- and BP-variability analysis and adrenomedullary tyrosine hydroxylase protein expression. In contrast, body weight and BP elevations to acute stressors decreased. BDNF upregulated AT1R mRNA by ∼80% and downregulated Mas receptor mRNA by ∼50% in the PVN, and losartan infusion partially inhibited weight loss and increases in BP and HR in BDNF-treated animals without any effect in GFP rats. Our results demonstrate that BDNF overexpression in the PVN results in sympathoexcitation, BP and HR elevations, and weight loss that are mediated, at least in part, by modulating angiotensin signaling in the PVN.


1996 ◽  
Vol 63 (2) ◽  
pp. 166-172 ◽  
Author(s):  
Maria Luisa Barbaccia ◽  
Gianna Roscetti ◽  
Marco Trabucchi ◽  
Maria Cristina Mostallino ◽  
Alessandra Concas ◽  
...  

Author(s):  
Ildiko Rita Dunay ◽  
Rainer Hellweg ◽  
Björn H. Schott ◽  
Golo Kronenberg ◽  
Ulrike Schmidt ◽  
...  

Abstract Background Brain-derived neurotrophic factor (BDNF) exerts its effects on neural plasticity via 2 distinct receptor types, the tyrosine kinase TrkB and the p75 neurotrophin receptor (p75NTR). The latter can promote inflammation and cell death while TrkB is critically involved in plasticity and memory, particularly in the hippocampus. Acute and chronic stress have been associated with suppression of hippocampal BDNF expression and impaired hippocampal plasticity. We hypothesized that p75NTR might be involved in the hippocampal stress response, in particular in stress-induced BDNF suppression, which might be accompanied by increased neuroinflammation. Method We assessed hippocampal BDNF protein concentrations in wild-type mice compared that in mice lacking the long form of the p75NTR (p75NTRExIII−/−) with or without prior exposure to a 1-hour restraint stress challenge. Hippocampal BDNF concentrations were measured using an optimized ELISA. Furthermore, whole-brain mRNA expression of pro-inflammatory interleukin-6 (Il6) was assessed with RT-PCR. Results Deletion of full-length p75NTR was associated with higher hippocampal BDNF protein concentration in the stress condition, suggesting persistently high hippocampal BDNF levels in p75NTR-deficient mice, even under stress. Stress elicited increased whole-brain Il6 mRNA expression irrespective of genotype; however, p75NTRExIII−/− mice showed elevated baseline Il6 expression and thus a lower relative increase. Conclusions Our results provide evidence for a role of p75NTR signaling in the regulation of hippocampal BDNF levels, particularly under stress. Furthermore, p75NTR signaling modulates baseline but not stress-related Il6 gene expression in mice. Our findings implicate p75NTR signaling as a potential pathomechanism in BDNF-dependent modulation of risk for neuropsychiatric disorders.


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