scholarly journals Chronic L-Name-Treatment Produces Hypertension by Different Mechanisms in Peripheral Tissues and Brain: Role of Central eNOS

2020 ◽  
Vol 27 (1) ◽  
pp. 46-54
Author(s):  
Olga Pechanova ◽  
Stanislava Vrankova ◽  
Martina Cebova
Keyword(s):  
Time Course ◽  
Nuclear Factor Κb ◽  
Brain Regions ◽  
Prolonged Treatment ◽  
Enos Expression ◽  
Peripheral Tissues ◽  
Male Wistar Rats ◽  
Oxide Synthase ◽  
Nos Isoforms ◽  
The Brain

The goal of our study was to analyze the time course of the effect of NG-nitro-L-arginine methyl ester (L-NAME) on nitric oxide synthase (NOS) isoforms and nuclear factor–κB (NF-κB) protein expression, total NOS activity, and blood pressure (BP) in rats. Adult 12-week-old male Wistar rats were subjected to treatment with L-NAME (40 mg/kg/day) for four and seven weeks. BP was increased after 4- and 7-week L-NAME treatments. NOS activity decreased after 4-week-L-NAME treatment; however, the 7-week treatment increased NOS activity in the aorta, heart, and kidney, while it markedly decreased NOS activity in the brainstem, cerebellum, and brain cortex. The 4-week-L-NAME treatment increased eNOS expression in the aorta, heart, and kidney and this increase was amplified after 7 weeks of treatment. In the brain regions, eNOS expression remained unchanged after 4-week L-NAME treatment and prolonged treatment led to a significant decrease of eNOS expression in these tissues. NF-κB expression increased in both peripheral and brain tissues after 4 weeks of treatment and prolongation of treatment decreased the expression in the aorta, heart, and kidney. In conclusion, decreased expression of eNOS in the brain regions after 7-week L-NAME treatment may be responsible for a remarkable decrease of NOS activity in these regions. Since the BP increase persisted after 7 weeks of L-NAME treatment, we hypothesize that central regulation of BP may contribute significantly to L-NAME-induced hypertension.

scholarly journals Ceramide and Related-Sphingolipid Levels Are Not Altered in Disease-Associated Brain Regions of APPSLand APPSL/PS1M146LMouse Models of Alzheimer's Disease: Relationship with the Lack of Neurodegeneration?

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Laurence Barrier ◽  
Bernard Fauconneau ◽  
Anastasia Noël ◽  
Sabrina Ingrand
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Neuronal Death ◽  
Time Course ◽  
Neuronal Loss ◽  
Brain Regions ◽  
App Processing ◽  
Ceramide Accumulation ◽  
The Brain

There is evidence linking sphingolipid abnormalities, APP processing, and neuronal death in Alzheimer's disease (AD). We previously reported a strong elevation of ceramide levels in the brain of the APPSL/PS1Ki mouse model of AD, preceding the neuronal death. To extend these findings, we analyzed ceramide and related-sphingolipid contents in brain from two other mouse models (i.e., APPSLand APPSL/PS1M146L) in which the time-course of pathology is closer to that seen in most currently available models. Conversely to our previous work, ceramides did not accumulate in disease-associated brain regions (cortex and hippocampus) from both models. However, the APPSL/PS1Ki model is unique for its drastic neuronal loss coinciding with strong accumulation of neurotoxic Aβisoforms, not observed in other animal models of AD. Since there are neither neuronal loss nor toxic Aβspecies accumulation in APPSLmice, we hypothesized that it might explain the lack of ceramide accumulation, at least in this model.

Differential recovery of acetylcholinesterase in guinea pig muscle and brain regions after soman treatment

1998 ◽  
Vol 17 (3) ◽  
pp. 157-162 ◽  
Author(s):  
Maxine C Lintern ◽  
Janet R Wetherell ◽  
Margaret E Smith
Keyword(s):  
Enzyme Activity ◽  
Time Course ◽  
Brain Regions ◽  
Similar Rate ◽  
Molecular Forms ◽  
Similar Degree ◽  
Brain Areas ◽  
Pig Muscle ◽  
Rate Of Recovery ◽  
The Brain

1 In brain areas of untreated guinea-pigs the highest activity of acetylcholinesterase was seen in the striatum and cerebellum, followed by the midbrain, medulla-pons and cortex, and the lowest in the hippocampus. The activity in diaphragm was sevenfold lower than in the hippocampus. 2 At 1 h after soman (27 mg/kg) administration the activity of the enzyme was dramatically reduced in all tissues studied. In muscle the three major molecular forms (A12, G4 and G1) showed a similar degree of inhibition and a similar rate of recovery and the activity had returned to normal by 7 days. 3 In the brain soman inhibited the G4 form more than the G1 form. The hippocampus, cortex and midbrain showed the greatest reductions in enzyme activity. At 7 days the activity in the cortex, medulla pons and striatum had recovered but in the hippocampus, midbrain and cerebellum it was still inhibited. 4 Thus the effects of soman administration varied in severity and time course in the different tissues studied. However the enzyme activity was still reduced in all tissues at 24 h when the overt signs of poisoning had disappeared.

scholarly journals Genesis of the ultradian rhythm of GH secretion: a new model unifying experimental observations in rats

1998 ◽  
Vol 275 (6) ◽  
pp. E1046-E1054 ◽  
Author(s):  
Clemens Wagner ◽  
S. Roy Caplan ◽  
Gloria S. Tannenbaum
Keyword(s):  
Time Course ◽  
Male Rat ◽  
Peripheral Tissues ◽  
Feedback Mechanisms ◽  
Gh Secretion ◽  
Metabolic Functions ◽  
Neuroendocrine Axis ◽  
Two Peaks ◽  
The Brain ◽  
Gh Receptors

Growth hormone (GH) induces growth in animals and humans and also has important metabolic functions. The GH neuroendocrine axis consists of a signaling cascade from the hypothalamus to the pituitary, the liver, and peripheral tissues, including two major feedback mechanisms. GH is secreted from the pituitary into the circulating blood according to the effect on the somatotrophs of two hypothalamic peptides, GH-releasing hormone (GHRH) and its antagonist, somatostatin (SRIF). The typical GH profile in the male rat shows secretory episodes every 3.3 h, which are subdivided into two peaks. Focusing on the mechanisms for generation of this ultradian GH rhythm, we simulated the time course of GH secretion under a variety of conditions. The model that we propose is based on feedback of GH on its own release mediated both by GH receptors on SRIF neurons in the brain and by a delayed SRIF release into both the brain and portal blood. SRIF, with a resultant periodicity of 3.3 h, affects both the somatotroph cells in the pituitary and the GHRH neurons in the hypothalamus. The secretion of GHRH is postulated to occur in an ∼1-h rhythm modulated by the level of SRIF in the hypothalamus. The model predicts a possible mechanism for the feminization of the male GH rhythm by sex steroids and vice versa, and suggests experiments that might reveal the proposed intrinsic 1-h GHRH rhythm.

scholarly journals Neural Correlates of Group Bias During Natural Viewing

2018 ◽  
Vol 29 (8) ◽  
pp. 3380-3389
Author(s):  
Timothy J Andrews ◽  
Ryan K Smith ◽  
Richard L Hoggart ◽  
Philip I N Ulrich ◽  
Andre D Gouws
Keyword(s):  
Time Course ◽  
Social Groups ◽  
Sensory Information ◽  
Brain Regions ◽  
Group Differences ◽  
Neural Basis ◽  
Brain Responses ◽  
The World ◽  
High Level ◽  
The Brain

Abstract Individuals from different social groups interpret the world in different ways. This study explores the neural basis of these group differences using a paradigm that simulates natural viewing conditions. Our aim was to determine if group differences could be found in sensory regions involved in the perception of the world or were evident in higher-level regions that are important for the interpretation of sensory information. We measured brain responses from 2 groups of football supporters, while they watched a video of matches between their teams. The time-course of response was then compared between individuals supporting the same (within-group) or the different (between-group) team. We found high intersubject correlations in low-level and high-level regions of the visual brain. However, these regions of the brain did not show any group differences. Regions that showed higher correlations for individuals from the same group were found in a network of frontal and subcortical brain regions. The interplay between these regions suggests a range of cognitive processes from motor control to social cognition and reward are important in the establishment of social groups. These results suggest that group differences are primarily reflected in regions involved in the evaluation and interpretation of the sensory input.

Anxiety-related behavior in hyperhomocysteinemia induced by methionine nutritional overload in rats: role of the brain oxidative stress

2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Open Field ◽  
Wistar Rats ◽  
Brain Regions ◽  
Oxidative Status ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light–dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain.

Differential oxidative stress and DNA damage in rat brain regions and blood following chronic arsenic exposure

2008 ◽  
Vol 24 (4) ◽  
pp. 247-256 ◽  
Author(s):  
D Mishra ◽  
SJS Flora
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Drinking Water ◽  
Wistar Rats ◽  
Arsenic Exposure ◽  
Brain Regions ◽  
Single Strand ◽  
Male Wistar Rats ◽  
Chronic Arsenic Exposure ◽  
The Brain

Chronic arsenic poisoning caused by contaminated drinking water is a wide spread and worldwide problem particularly in India and Bangladesh. One of the possible mechanisms suggested for arsenic toxicity is the generation of reactive oxygen species (ROS). The present study was planned 1) to evaluate if chronic exposure to arsenic leads to oxidative stress in blood and brain – parts of male Wistar rats and 2) to evaluate which brain region of the exposed animals was more sensitive to oxidative injury. Male Wistar rats were exposed to arsenic (50 ppm sodium arsenite in drinking water) for 10 months. The brain was dissected into five major parts, pons medulla, corpus striatum, cortex, hippocampus, and cerebellum. A number of biochemical variables indicative of oxidative stress were studied in blood and different brain regions. Single-strand DNA damage using comet assay was also assessed in lymphocytes. We observed a significant increase in blood and brain ROS levels accompanied by the depletion of GSH/GSSG ratio and glucose-6-phosphate dehydrogenase (G6PD) activity in different brain regions of arsenic-exposed rats. Chronic arsenic exposure also caused significant single-strand DNA damage in lymphocytes as depicted by comet with a tail in arsenic-exposed cells compared with the control cells. On the basis of results, we concluded that the cortex region of the brain was more sensitive to oxidative injury compared with the other regions studied. The present study, thus, leads us to suggest that arsenic induces differential oxidative stress in brain regions with cortex followed by hippocampus and causes single-strand DNA damage in lymphocytes.

scholarly journals The S1 protein of SARS-CoV-2 crosses the blood-brain barrier: Kinetics, distribution, mechanisms, and influence of ApoE genotype, sex, and inflammation

2020 ◽  
Author(s):  
Elizabeth M. Rhea ◽  
Aric F. Logsdon ◽  
Kim M. Hansen ◽  
Lindsey Williams ◽  
May Reed ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Blood Brain Barrier ◽  
Apoe Genotype ◽  
Brain Regions ◽  
Brain Barrier ◽  
Productive Infection ◽  
Peripheral Tissues ◽  
Blood Brain ◽  
Commercial Sources ◽  
The Brain

AbstractEvidence strongly suggests that SARS-CoV-2, the cause of COVID-19, can enter the brain. SARS-CoV-2 enters cells via the S1 subunit of its spike protein, and S1 can be used as a proxy for the uptake patterns and mechanisms used by the whole virus; unlike studies based on productive infection, viral proteins can be used to precisely determine pharmacokinetics and biodistribution. Here, we found that radioiodinated S1 (I-S1) readily crossed the murine blood-brain barrier (BBB). I-S1 from two commercial sources crossed the BBB with unidirectional influx constants of 0.287 ± 0.024 μL/g-min and 0.294 ± 0.032 μL/g-min and was also taken up by lung, spleen, kidney, and liver. I-S1 was uniformly taken up by all regions of the brain and inflammation induced by lipopolysaccharide reduced uptake in the hippocampus and olfactory bulb. I-S1 crossed the BBB completely to enter the parenchymal brain space, with smaller amounts retained by brain endothelial cells and the luminal surface. Studies on the mechanisms of transport indicated that I-S1 crosses the BBB by the mechanism of adsorptive transcytosis and that the murine ACE2 receptor is involved in brain and lung uptake, but not that by kidney, liver, or spleen. I-S1 entered brain after intranasal administration at about 1/10th the amount found after intravenous administration and about 0.66% of the intranasal dose entered blood. ApoE isoform or sex did not affect whole brain uptake, but had variable effects on olfactory bulb, liver, spleen, and kidney uptakes. In summary, I-S1 readily crosses the murine BBB, entering all brain regions and the peripheral tissues studied, likely by the mechanism of adsorptive transcytosis.Graphical Abstract

scholarly journals Endotoxin Stimulates Nitric Oxide Production in the Paraventricular Nucleus of the Hypothalamus through Nitric Oxide Synthase I: Correlation with Hypothalamic-Pituitary-Adrenal Axis Activation1

Endocrinology ◽  
1999 ◽  
Vol 140 (12) ◽  
pp. 5971-5981 ◽  
Author(s):  
Rosa Maria Uribe ◽  
Soon Lee ◽  
Catherine Rivier
Keyword(s):  
Nitric Oxide ◽  
Hpa Axis ◽  
Time Course ◽  
No Production ◽  
No Formation ◽  
Immune Challenges ◽  
Corticosterone Release ◽  
Oxide Synthase ◽  
The Brain ◽  
Pituitary Adrenal Axis

Abstract Nitric oxide (NO) is an unstable gas that is produced in brain tissues involved in the control of the activity of the hypothalamus-pituitary-adrenal (HPA) axis. Transcripts for constitutive neuronal NO synthase (NOS I), one of the enzymes responsible for NO formation in the brain, is up-regulated by systemic endotoxin[ lipopolysaccharide (LPS)] injection. However, this change is delayed compared with LPS induced-ACTH release, which makes it difficult to determine whether it is functionally important for the hormonal response. To obtain a more resolutive time course of the NO response, we first measured NO in microdialysates of the paraventricular (PVN) nucleus of the hypothalamus. The iv injection of 100 μg/kg LPS induced a rapid and short-lived increase in concentrations of this gas, which corresponded to the initiation of the ACTH response. LPS-induced Ca2+-dependent NOS activity in the PVN as well as the number of PVN cells expressing citrulline (a compound produced stoichiometrically with NO) also increased significantly over a time course that corresponded to ACTH and corticosterone release. Finally, blockade of NO production with the arginine derivative Nω-nitro-l-arginine-methylester (L-NAME; 50 mg/kg, sc), which attenuated the ACTH response to LPS, virtually abolished basal NOS activity in the PVN, as well as anterior and neurointermediate lobes of the pituitary, and prevented the appearance of citrulline in the PVN of rats injected with LPS. Collectively, these results show that LPS-induced activation of the HPA axis correlates with the activation of the PVN NOergic system, and supports a stimulatory role for NO in the modulation of the HPA axis in response to immune challenges.

The Sources of Sequential Modulations of Control Processes in Arithmetic Strategies: A Magnetoencephalography Study

2017 ◽  
Vol 29 (6) ◽  
pp. 1033-1043 ◽  
Author(s):  
Thomas Hinault ◽  
Jean-Michel Badier ◽  
Sylvain Baillet ◽  
Patrick Lemaire
Keyword(s):  
Executive Control ◽  
Time Course ◽  
Cognitive Strategies ◽  
Brain Regions ◽  
Strategy Execution ◽  
Estimation Task ◽  
Cognitive Domains ◽  
Computational Estimation ◽  
Control Processes ◽  
The Brain

In a wide variety of cognitive domains, performance is determined by the selection and execution of cognitive strategies to solve problems. We used magnetoencephalography to identify the brain regions involved and specify the time course of dynamic modulations of executive control processes during strategy execution. Participants performed a computational estimation task in which they were instructed to execute a poorer or better strategy to estimate results of two-digit multiplication problems. When participants were asked to execute the poorer strategy, two distinct sets of brain activations were identified, depending on whether the poorer strategy (engaging the left inferior frontal junction) or the better strategy (engaging ACC) had been executed on the immediately preceding items. Our findings also revealed the time course of activations in regions involved in sequential modulations of cognitive control processes during arithmetic strategy execution. These findings point at processes of proactive preparation on items after poorer strategy items and dynamics of reactive adjustments after better strategy items.

Running the Female Power Grid Across Lifespan Through Brain Estrogen Signaling

2021 ◽  
Vol 84 (1) ◽  
Author(s):  
Holly A. Ingraham ◽  
Candice B. Herber ◽  
William C. Krause
Keyword(s):  
Brain Regions ◽  
Estrogen Signaling ◽  
Annual Review ◽  
Publication Date ◽  
Drug Induced ◽  
Peripheral Tissues ◽  
Hormone Sensitive ◽  
The Brain ◽  
Female Power

The role of central estrogen in cognitive, metabolic, and reproductive health has long fascinated the lay public and scientists alike. In the last two decades, insight into estrogen signaling in the brain and its impact on female physiology is beginning to catch up with the vast information already established for its actions on peripheral tissues. Using newer methods to manipulate estrogen signaling in hormone-sensitive brain regions, neuroscientists are now identifying the molecular pathways and neuronal subtypes required to establish crucial sex differences in energy allocation. However, the immense cellular complexity of these hormone-sensitive brain regions makes it clear that more research is needed to fully appreciate how estrogen modulates neural circuits to regulate physiological and behavioral end points. Such insight is essential for understanding how natural or drug-induced hormone fluctuations across lifespan affect women's health. Expected final online publication date for the Annual Review of Physiology, Volume 84 is February 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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