P.0843 Pre-gestational stress and antidepressant mirtazapine treatment affect synaptophysin expression of rat offspring in a sex-dependent manner

2021 ◽  
Vol 53 ◽  
pp. S616-S617
Author(s):  
M. Viñas ◽  
K. Belovičová ◽  
M. Dubovický
2018 ◽  
Vol 65 (2) ◽  
pp. 17-22 ◽  
Author(s):  
M. Sasváriová ◽  
B. Tyukos-Kaprinay ◽  
L. Salvaras ◽  
K. Belovičová ◽  
E. Bögi ◽  
...  

Abstract A number of pregnant women all over the world suffer from depression and are treated during gestation with antidepressants, mostly with selective serotonin reuptake inhibitors or selective serotonin and norepinephrine reuptake inhibitors. Exposure to prenatal stress is also a great risk factor for a developing fetus and could be responsible for altered fetal development or various neurobehavioral disturbances of a child. Administration of selective serotonin and norepinephrine reuptake inhibitor venlafaxine is associated with various cardiovascular adverse effects, such as tachycardia, increased blood pressure, arrhythmias and hypertensive crisis. The aim of this study was to focus on the effect of pre-gestational chronic mild unpredictable stress and/or administration of antidepressant venlafaxine (10 mg/kg/day, p. o.) on specific parameters, determining the function of the cardiovascular system of male and female rat offspring. Blood pressure and standard ECG were recorded in the offspring. Exposure to pre-gestational stress did not cause significant changes in the systolic, diastolic blood pressure and pulse frequency either in males or in females, compared to the unexposed control animals. Pre-gestational stress caused the shortening of QT interval and prolongation of QRS complex duration in males. On the other hand, in females, the effects of pre-gestational stress were potentiated by the administration of venlafaxine and resulted in elevated systolic and diastolic blood pressure, prolonged QT interval and shortened QRS complex duration, compared to the control. In conclusion, the female rat offspring are more sensitive to exposure to pre-gestational, to chronic mild unpredictable stress and venlafaxine.


2021 ◽  
pp. 111511
Author(s):  
Diana C. Castro-Rodríguez ◽  
Luis A. Reyes-Castro ◽  
Lilia Vargas-Hernández ◽  
Nozomi Itani ◽  
Peter W. Nathanielsz ◽  
...  

2019 ◽  
Vol 597 (23) ◽  
pp. 5549-5563 ◽  
Author(s):  
Guadalupe L. Rodríguez‐González ◽  
Luis A. Reyes‐Castro ◽  
Claudia J. Bautista ◽  
Azucena A. Beltrán ◽  
Carlos A. Ibáñez ◽  
...  

2019 ◽  
Vol 147 ◽  
pp. 9-16 ◽  
Author(s):  
Libin Liao ◽  
Xueqin Wang ◽  
Xueping Yao ◽  
Bin Zhang ◽  
Lihong Zhou ◽  
...  

Author(s):  
Gemma A.J. Kuijpers ◽  
Harvey B. Pollard

Exocytotic fusion of granules in the adrenal medulla chromaffin cell is triggered by a rise in the concentration of cytosolic Ca2+ upon cell activation. The protein synexin, annexin VII, was originally found in the adrenal medulla and has been shown to cause aggregation and to support fusion of chromaffin granules in a Ca2+-dependent manner. We have previously suggested that synexin may there fore play a role in the exocytotic fusion process. In order to obtain more structural information on synexin, we performed immuno-electron microscopy on frozen ultrathin sections of both isolated chromaffin granules and chromaffin cells.Chromaffin granules were isolated from bovine adrenal medulla, and synexin was isolated from bovine lung. Granules were incubated in the presence or absence of synexin (24 μg per mg granule protein) and Ca2+ (1 mM), which induces maximal granule aggregation, in 0.3M sucrose-40m MMES buffer(pH 6.0). Granules were pelleted, washed twice in buffer without synexin and fixed with 2% glutaraldehyde- 2% para formaldehyde in 0.1 M phosphate buffer (GA/PFA) for 30 min. Chromaffin cells were isolated and cultured for 3-5 days, and washed and incubated in Krebs solution with or without 20 uM nicotine. Cells were fixed 90 sec after on set of stimulation with GA/PFA for 30 min. Fixed granule or cell pellets were washed, infiltrated with 2.3 M sucrose in PBS, mounted and frozen in liquid N2.


2020 ◽  
Vol 64 (2) ◽  
pp. 383-396
Author(s):  
Lara K. Krüger ◽  
Phong T. Tran

Abstract The mitotic spindle robustly scales with cell size in a plethora of different organisms. During development and throughout evolution, the spindle adjusts to cell size in metazoans and yeast in order to ensure faithful chromosome separation. Spindle adjustment to cell size occurs by the scaling of spindle length, spindle shape and the velocity of spindle assembly and elongation. Different mechanisms, depending on spindle structure and organism, account for these scaling relationships. The limited availability of critical spindle components, protein gradients, sequestration of spindle components, or post-translational modification and differential expression levels have been implicated in the regulation of spindle length and the spindle assembly/elongation velocity in a cell size-dependent manner. In this review, we will discuss the phenomenon and mechanisms of spindle length, spindle shape and spindle elongation velocity scaling with cell size.


2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.


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