scholarly journals GPER-Deficient Rats Exhibit Lower Serum Corticosterone Level and Increased Anxiety-Like Behavior

2020 ◽  
Vol 2020 ◽  
pp. 1-22 ◽  
Author(s):  
Yi Zheng ◽  
Meimei Wu ◽  
Ting Gao ◽  
Li Meng ◽  
Xiaowei Ding ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Corticosterone Level ◽  
Brain Structures ◽  
Ample Evidence ◽  
Genetic Ablation ◽  
Serum Corticosterone ◽  
Underlying Mechanisms ◽  
G Protein Coupled ◽  
Prolonged Stress

Ample evidence suggests that estrogens have strong influences on the occurrence of stress-related mood disorders, but the underlying mechanisms remain poorly understood. Through multiple approaches, we demonstrate that the G protein-coupled estrogen receptor (GPER) is widely distributed along the HPA axis and in brain structures critically involved in mood control. Genetic ablation of GPER in the rat resulted in significantly lower basal serum corticosterone level but enhanced ACTH release in response to acute restraint stress, especially in the female. GPER-/- rats of either sex displayed increased anxiety-like behaviors and deficits in learning and memory. Additionally, GPER deficiency led to aggravation of anxiety-like behaviors following single-prolonged stress (SPS). SPS caused significant decreases in serum corticosterone in WT but not in GPER-deficient rats. The results highlight an important role of GPER at multiple sites in regulation of the HPA axis and mood.

scholarly journals EPC1/TIP60-Mediated Histone Acetylation Facilitates Spermiogenesis in Mice

2017 ◽  
Vol 37 (19) ◽  
Author(s):  
Yixin Dong ◽  
Kyo-ichi Isono ◽  
Kazuyuki Ohbo ◽  
Takaho A. Endo ◽  
Osamu Ohara ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Germ Cells ◽  
Essential Role ◽  
Critical Role ◽  
Male Germ Cells ◽  
Genetic Ablation ◽  
Histone Hyperacetylation ◽  
Critical Components ◽  
Underlying Mechanisms

ABSTRACT Global histone hyperacetylation is suggested to play a critical role for replacement of histones by transition proteins and protamines to compact the genome during spermiogenesis. However, the underlying mechanisms for hyperacetylation-mediated histone replacement remains poorly understood. Here, we report that EPC1 and TIP60, two critical components of the mammalian nucleosome acetyltransferase of H4 (NuA4) complexes, are coexpressed in male germ cells. Strikingly, genetic ablation of either Epc1 or Tip60 disrupts hyperacetylation and impairs histone replacement, in turn causing aberrant spermatid development. Taking these observations together, we reveal an essential role of the NuA4 complexes for histone hyperacetylation and subsequent compaction of the spermatid genome.

Effect of prolonged stress on NO synthases and IL-1β levels in brain structures and HPA axis activity

2015 ◽  
Vol 67 ◽  
pp. 23
Author(s):  
Anna Gądek-Michalska ◽  
Joanna Tadeusz ◽  
Paulina Rachwalska ◽  
Jan Bugajski
Keyword(s):  
Hpa Axis ◽  
Brain Structures ◽  
Hpa Axis Activity ◽  
Prolonged Stress

Chemical adrenalectomy by aminoglutethimide and the pancreas in suckling rats

1984 ◽  
Vol 247 (4) ◽  
pp. G346-G351 ◽  
Author(s):  
A. Lerner ◽  
P. C. Lee ◽  
E. Lebenthal
Keyword(s):  
Control Level ◽  
Pancreatic Enzyme ◽  
Corticosterone Level ◽  
Suckling Rats ◽  
Serum Corticosterone ◽  
Dna Contents ◽  
Enzyme Development ◽  
Weight Protein ◽  
Pancreatic Exocrine

The role of corticosterone in the development of pancreatic enzymes of suckling rats was studied through a partial and transient blockade of steroidogenesis by aminoglutethimide. Rats were injected with aminoglutethimide the night before their 14th day of age. Ten hours later they showed a transient decrease of serum total corticosterone level as compared with rats injected only with the vehicle. At 34 and 58 h after injection, their corticosterone levels returned to that of control rats. Pancreatic weight, protein, DNA contents, and total activities of amylase, lipase, and trypsinogen were depressed only in the aminoglutethimide-treated pups 34 h after injection. These pancreatic parameters returned to the control level 58 h after injection. Hydrocortisone given to another group of rats completely abolished the effect of aminoglutethimide on the pancreas. Thus, a transient suppression of serum corticosterone level caused a delay in the developmental accumulation of pancreatic exocrine enzymes that resumed only after the serum corticosterone returned to the control level. These results further confirm that corticosterone is an important modulator of pancreatic enzyme development in the rat.

scholarly journals Recent advances in understanding neuropathic pain: glia, sex differences, and epigenetics

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2743 ◽  
Author(s):  
Halina Machelska ◽  
Melih Ö. Celik
Keyword(s):  
Nervous System ◽  
Neuropathic Pain ◽  
Neuronal Damage ◽  
G Protein Coupled Receptors ◽  
The Central Nervous System ◽  
Non Coding Rnas ◽  
Underlying Mechanisms ◽  
G Protein Coupled ◽  
Epigenetic Processes

Neuropathic pain results from diseases or trauma affecting the nervous system. This pain can be devastating and is poorly controlled. The pathophysiology is complex, and it is essential to understand the underlying mechanisms in order to identify the relevant targets for therapeutic intervention. In this article, we focus on the recent research investigating neuro-immune communication and epigenetic processes, which gain particular attention in the context of neuropathic pain. Specifically, we analyze the role of glial cells, including microglia, astrocytes, and oligodendrocytes, in the modulation of the central nervous system inflammation triggered by neuropathy. Considering epigenetics, we address DNA methylation, histone modifications, and the non-coding RNAs in the regulation of ion channels, G-protein-coupled receptors, and transmitters following neuronal damage. The goal was not only to highlight the emerging concepts but also to discuss controversies, methodological complications, and intriguing opinions.

Suppression of store-operated Ca2+ entry by activation of GPER: contribution to a clamping effect on endothelial Ca2+ signaling

2017 ◽  
Vol 474 (21) ◽  
pp. 3627-3642 ◽  
Author(s):  
Lara E. Terry ◽  
Mark VerMeer ◽  
Jennifer Giles ◽  
Quang-Kim Tran
Keyword(s):  
Endothelial Cells ◽  
Time Course ◽  
Current Data ◽  
Underlying Mechanisms ◽  
Quenching Method ◽  
Reported Data ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
G Protein Coupled

The G protein-coupled estrogen receptor 1 (GPER, formerly also known as GPR30) modulates many Ca2+-dependent activities in endothelial cells. However, the underlying mechanisms are poorly understood. We recently reported that GPER acts to prolong cytoplasmic Ca2+ signals by interacting with and promoting inhibitory phosphorylation of the plasma membrane Ca2+-ATPase. In the present study, we examined the role of GPER activation in modulating store-operated Ca2+ entry (SOCE) via effects on the stromal interaction molecule 1 (STIM1). GPER activation by agonist G-1 reduces the peak but prolongs the plateau of bradykinin-induced Ca2+ signals in primary endothelial cells. G-1 dose-dependently inhibits thapsigargin-induced SOCE measured by the Mn2+ quenching method. GPER heterologous expression reduces SOCE, which is further pronounced by G-1 treatment. Consistently, GPER gene silencing in endothelial cells is associated with an increase in SOCE. Treatment with G-1 reduces puncta formation by STIM1 triggered by the activation of SOCE. The effect of GPER activation to inhibit SOCE is not affected by combined nonphosphorylatable substitutions at serines 486 and 668 on STIM1, but is substantially reduced by similar substitutions at serines 575, 608 and 621. Taken together with our recently reported inhibitory actions of GPER on Ca2+ efflux, the current data contribute to a model in which GPER acts to clamp agonist-induced cytoplasmic Ca2+ signals. Kinetic modeling based on current and reported data is used to estimate the overall effect of GPER activation on point activity of endothelial nitric oxide synthase during the time course of agonist-induced total Ca2+ signals.

scholarly journals The Obligatory Role of the Acetylcholine-Induced Endothelium-Dependent Contraction in Hypertension: Can Arachidonic Acid Resolve this Inflammation?

2020 ◽  
Vol 26 (30) ◽  
pp. 3723-3732 ◽  
Author(s):  
Jonnelle M. Edwards ◽  
Cameron G. McCarthy ◽  
Camilla F. Wenceslau
Keyword(s):  
Arachidonic Acid ◽  
G Protein ◽  
Vascular Inflammation ◽  
Arachidonic Acid Metabolism ◽  
G Protein Coupled Receptors ◽  
Free Calcium ◽  
Underlying Mechanisms ◽  
Transient Elevation ◽  
G Protein Coupled

The endothelium produces many substances that can regulate vascular tone. Acetylcholine is a widely used pharmacological tool to assess endothelial function. In general, acetylcholine binds to G-protein coupled muscarinic receptors that mediate a transient elevation in intracellular, free calcium. This intracellular rise in calcium is responsible for triggering several cellular responses, including the synthesis of nitric oxide, endothelium- derived hyperpolarizing factor, and eicosanoids derived from arachidonic acid. Endothelial arachidonic acid metabolism is also an important signaling pathway for mediating inflammation. Therefore, in conditions with sustained and excessive inflammation such as hypertension, arachidonic acid serves as a substrate for the synthesis of several vasoconstrictive metabolites, predominantly via the cyclooxygenase and lipoxygenase enzymes. Cyclooxygenase and lipoxygenase products can then activate G-protein coupled receptors expressed on vascular smooth muscle cells to causes contractile responses. As a result, acetylcholine-induced contraction due to arachidonic acid is a commonly observed feature of endothelial dysfunction and vascular inflammation in hypertension. In this review, we will critically analyze the literature supporting this concept, as well as address the potential underlying mechanisms, including the possibility that arachidonic acid signaling is diverted away from the synthesis of pro-resolving metabolites in conditions such as hypertension.

Response Interference as a Mechanism Underlying Implicit Measures

2008 ◽  
Vol 24 (4) ◽  
pp. 218-225 ◽  
Author(s):  
Bertram Gawronski ◽  
Roland Deutsch ◽  
Etienne P. LeBel ◽  
Kurt R. Peters
Keyword(s):  
Task Performance ◽  
Psychological Research ◽  
Implicit Measures ◽  
Mediation Model ◽  
Response Interference ◽  
Relevant Evidence ◽  
Moderated Mediation Model ◽  
Stimulus Features ◽  
Underlying Mechanisms

Over the last decade, implicit measures of mental associations (e.g., Implicit Association Test, sequential priming) have become increasingly popular in many areas of psychological research. Even though successful applications provide preliminary support for the validity of these measures, their underlying mechanisms are still controversial. The present article addresses the role of a particular mechanism that is hypothesized to mediate the influence of activated associations on task performance in many implicit measures: response interference (RI). Based on a review of relevant evidence, we argue that RI effects in implicit measures depend on participants’ attention to association-relevant stimulus features, which in turn can influence the reliability and the construct validity of these measures. Drawing on a moderated-mediation model (MMM) of task performance in RI paradigms, we provide several suggestions on how to address these problems in research using implicit measures.

The More You Say, the Less They Hear

2015 ◽  
Vol 27 (4) ◽  
pp. 159-169 ◽  
Author(s):  
Elsbeth D. Asbeek Brusse ◽  
Marieke L. Fransen ◽  
Edith G. Smit
Keyword(s):  
Hearing Protection ◽  
Entertainment Education ◽  
Mediating Role ◽  
Attitude Measures ◽  
Underlying Mechanisms

Abstract. This study examined the effects of disclosure messages in entertainment-education (E-E) on attitudes toward hearing protection and attitude toward the source. In addition, the (mediating) role of the underlying mechanisms (i.e., transportation, identification, and counterarguing) was studied. In an experiment (N = 336), three different disclosure messages were compared with a no-disclosure condition. The results show that more explicit disclosure messages negatively affect transportation and identification and stimulate the generation of counterarguments. In addition, the more explicit disclosure messages affect both attitude measures via two of these processes (i.e., transportation and counterarguing). Less explicit disclosure messages do not have this effect. Implications of the findings are discussed.

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