scholarly journals The Bidirectional Signal Communication of Microbiota-Gut-Brain Axis in Hypertension

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Xiaoqi Wang ◽  
Zhenzhen Chen ◽  
Bin Geng ◽  
Jun Cai

Hypertension is a critical risk factor of cardiovascular diseases. A new concept of microbiota-gut-brain axis has been established recently, mediating the bidirectional communication between the gut and its microbiome and the brain. Alterations in bidirectional interactions are believed to be involved in the blood pressure regulation. Neuroinflammation and increased sympathetic outflow act as the descending innervation signals from the brain. Increased sympathetic activation plays a recognized role in the genesis of hypertension. The present evidence demonstrates that gut dysbiosis is associated with central nervous system neuroinflammation. However, how the gut influences the brain remains unclear. We reviewed the roles of neuroinflammation and gut microbiota and their interactions in the pathogenesis of hypertension and described the ascending signaling mechanisms behind the microbiota-gut-brain axis in detail. Additionally, the innovative prohypertensive mechanisms of dietary salt through the microbiota-gut-brain axis are summarized. The bidirectional communication mechanisms were proposed for the first time that the descending signals from the brain and the ascending connections from the gut form a vicious circle of hypertension progression, acting as a premise for hypertension therapy.

2020 ◽  
Vol 57 (12) ◽  
pp. 5026-5043 ◽  
Author(s):  
Shan Liu ◽  
Jiguo Gao ◽  
Mingqin Zhu ◽  
Kangding Liu ◽  
Hong-Liang Zhang

Abstract Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term “microbiota-gut-brain axis” from “gut-brain axis” underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer’s disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.


2021 ◽  
pp. 1-10
Author(s):  
Shahul Mujib Kamal ◽  
Norazryana Mat Dawi ◽  
Hamidreza Namazi

BACKGROUND: Walking like many other actions of a human is controlled by the brain through the nervous system. In fact, if a problem occurs in our brain, we cannot walk correctly. Therefore, the analysis of the coupling of brain activity and walking is very important especially in rehabilitation science. The complexity of movement paths is one of the factors that affect human walking. For instance, if we walk on a path that is more complex, our brain activity increases to adjust our movements. OBJECTIVE: This study for the first time analyzed the coupling of walking paths and brain reaction from the information point of view. METHODS: We analyzed the Shannon entropy for electroencephalography (EEG) signals versus the walking paths in order to relate their information contents. RESULTS: According to the results, walking on a path that contains more information causes more information in EEG signals. A strong correlation (p= 0.9999) was observed between the information contents of EEG signals and walking paths. Our method of analysis can also be used to investigate the relation among other physiological signals of a human and walking paths, which has great benefits in rehabilitation science.


2004 ◽  
Vol 380 (3) ◽  
pp. 749-756 ◽  
Author(s):  
Yong-Xin SUN ◽  
Kazuhito TSUBOI ◽  
Yasuo OKAMOTO ◽  
Takeharu TONAI ◽  
Makoto MURAKAMI ◽  
...  

Anandamide (an endocannabinoid) and other bioactive long-chain NAEs (N-acylethanolamines) are formed by direct release from N-acyl-PE (N-acyl-phosphatidylethanolamine) by a PLD (phospholipase D). However, the possible presence of a two-step pathway from N-acyl-PE has also been suggested previously, which comprises (1) the hydrolysis of N-acyl-PE to N-acyl-lysoPE by PLA1/PLA2 enzyme(s) and (2) the release of NAEs from N-acyllysoPE by lysoPLD (lysophospholipase D) enzyme(s). In the present study we report for the first time the characterization of enzymes responsible for this pathway. The PLA1/PLA2 activity for N-palmitoyl-PE was found in various rat tissues, with the highest activity in the stomach. This stomach enzyme was identified as group IB sPLA2 (secretory PLA2), and its product was determined as N-acyl-1-acyl-lysoPE. Recombinant group IB, IIA and V of sPLA2s were also active with N-palmitoyl-PE, whereas group X sPLA2 and cytosolic PLA2α were inactive. In addition, we found wide distribution of lysoPLD activity generating N-palmitoylethanolamine from N-palmitoyl-lysoPE in rat tissues, with higher activities in the brain and testis. Based on several lines of enzymological evidence, the lysoPLD enzyme could be distinct from the known N-acyl-PE-hydrolysing PLD. sPLA2-IB dose dependently enhanced the production of N-palmitoylethanolamine from N-palmitoyl-PE in the brain homogenate showing the lysoPLD activity. N-Arachidonoyl-PE and N-arachidonoyl-lysoPE as anandamide precursors were also good substrates of sPLA2-IB and the lysoPLD respectively. These results suggest that the sequential actions of PLA2 and lysoPLD may constitute another biosynthetic pathway for NAEs, including anandamide.


Parasitology ◽  
1996 ◽  
Vol 113 (6) ◽  
pp. 559-565 ◽  
Author(s):  
M. K. S. Gustafsson ◽  
A. M. Lindholm ◽  
N. B. Terenina ◽  
M. Reuter

SUMMARYThe free radical nitric oxide (NO), which is synthesized by nitric oxide synthase (NOS), has recently been discovered to function as a neuronal messenger. The presence of NOS was detected in the nervous system of adult Hymenolepis diminuta with NADPH-diaphorase (NADPH-d) histochemistry. The NADPH-d histochemical reaction is regarded as a selective marker for NOS in neuronal tissue. NADPH-d staining was observed in nerve fibres in the main and minor nerve cords and the transverse ring commissures, and in cell bodies in the brain commissure, along the main nerve cords, in the suckers and the rostellar sac. NADPH-d staining was also observed in the wall of the internal seminal vesicle and the genital atrium. The pattern of NADPH-d staining was compared with that of the 5-HT immunoreactive nervous elements. The NADPH-d staining reaction and the 5-HT immunoreactivity occur in separate sets of neurons. This is the first time the NADPH-d reaction has been demonstrated in the nervous system of a flatworm, indicating that NOS is present and that NO can be produced at this level of evolution.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
M. Stankovic ◽  
S. Vucetic-Arsic ◽  
S. Alcaz ◽  
J. Cvejic

Aim:We want to present a polymorphic clinical features like: hallutinations, paranoid ideas, agitation and violence as a result of prolonged cocaine intranasal consumption.Methods:We exposed a 30-year old male patient with ICD-X diagnostic criteria for cocaine dependence (intranasal consumption) that treated in the outpatient unit of Special Hospital of Addicitons, Belgrade, Serbia from April to July 2008. We used the medical records, psychical examination, psychiatric interwievs, standard blood sampling and cocaine urine detections sample (positive).Results:Observations a specific and polymorphic clinical features with presence of psychotic symptoms after cocaine consumptions in our male patient, for the first time after 5 years of cocaine dependence: auditory hallucinations (two- voice speakers), paranoid persecution ideas and suspiciousness, agitation with appearance of vegetative symptomatology (palpitations, sweating, pupil dilatation), extremely violence behavior to other people, complete social reductions (“armed to the outside world”, refused any personal contact and isolated from friends and family, permanent outdoor checking). There was an intensive fear too and impaired judgment.Conclusions:Permanent cocaine consumption can result with produce a numerous of psychiatric symptoms and syndromes as our experience does. It is similar to the findings of other studies and papers reviewed. It is suppose that cocaine has numerous effects on important neurotransmitters in the brain, such as increase as well as the release of dopamine and it related with aggressiveness, hallucinations and other psychiatric symptoms.


2021 ◽  
pp. 1-11
Author(s):  
Najmeh Pakniyat ◽  
Mohammad Hossein Babini ◽  
Vladimir V. Kulish ◽  
Hamidreza Namazi

BACKGROUND: Analysis of the heart activity is one of the important areas of research in biomedical science and engineering. For this purpose, scientists analyze the activity of the heart in various conditions. Since the brain controls the heart’s activity, a relationship should exist among their activities. OBJECTIVE: In this research, for the first time the coupling between heart and brain activities was analyzed by information-based analysis. METHODS: Considering Shannon entropy as the indicator of the information of a system, we recorded electroencephalogram (EEG) and electrocardiogram (ECG) signals of 13 participants (7 M, 6 F, 18–22 years old) in different external stimulations (using pineapple, banana, vanilla, and lemon flavors as olfactory stimuli) and evaluated how the information of EEG signals and R-R time series (as heart rate variability (HRV)) are linked. RESULTS: The results indicate that the changes in the information of the R-R time series and EEG signals are strongly correlated (ρ=-0.9566). CONCLUSION: We conclude that heart and brain activities are related.


1999 ◽  
Vol 277 (6) ◽  
pp. E965-E970 ◽  
Author(s):  
Phyllis M. Wise

The menopause marks the permanent end of fertility in women. It was once thought that this dramatic physiological change could be explained simply by the exhaustion of the reservoir of ovarian follicles. New data from studies performed in women and animal models make us reassess this assumption. An increasing body of evidence suggests that there are multiple pacemakers that contribute to the transition to irregular cycles, decreasing fertility, and the timing of the menopause. We will present evidence that lends credence to the possibility that a dampening and desynchronization of the precisely orchestrated neural signals lead to miscommunication between the brain and the pituitary-ovarian axis, and that this constellation of hypothalamic-pituitary-ovarian events leads to the deterioration of regular cyclicity and heralds menopausal transition.


2021 ◽  
Author(s):  
Kristen K Baumann ◽  
Wei-Shan Sandy Liang ◽  
Daniel V Quaranta ◽  
Miranda L Wilson ◽  
Helina S Asrat ◽  
...  

Ozone (O3) is an air pollutant which primarily damages the lungs, but growing evidence supports that O3 exposure can also affect the brain. Serum amyloid A (SAA) and kynurenine have been identified as circulating factors that are upregulated by O3, and both can contribute to depressive-like behaviors in mice. However, little is known about the relations of O3 exposure to sickness and depressive-like behaviors in experimental settings. In this study, we evaluated O3 dose-, time- and sex- dependent changes in circulating SAA in context of pulmonary inflammation and damage, sickness and depressive-like behavioral changes, and systemic changes in kynurenine and indoleamine 2,3-dioxygenase (IDO), an enzyme that regulates kynurenine production and contributes to inflammation-induced depressive-like behaviors. Our results in Balb/c and CD-1 mice showed that 3ppm O3, but not 2 or 1ppm O3, caused elevations in serum SAA and pulmonary neutrophils, and these responses resolved by 48 hours. Sickness and depressive-like behaviors were observed at all O3 doses (1-3ppm), although the detection of certain behavioral changes varied by dose. We also found that Ido1 mRNA expression was increased in the brain and spleen 24 hours after 3ppm O3, and that kynurenine was increased in blood. Together, these findings indicate that acute O3 exposure induces transient symptoms of sickness and depressive-like behaviors which may occur in the presence or absence of overt pulmonary neutrophilia and systemic increases of SAA. We also present evidence that the IDO/kynurenine pathway is upregulated systemically following an acute exposure to O3 in mice.


2021 ◽  
Author(s):  
Felipe Lemos ◽  
Caio Prins ◽  
Raul Carpi-Santos ◽  
Ingrid Waclawiak ◽  
Sofia Santos ◽  
...  

Abstract Galectin-3 stabilizes cell-cell junctions and regulates inflammatory pathways in the gut-liver axis. Galectin-3 knockout (Lgals3−/−) mice have atypical behaviors by obscure mechanisms. Given that BALB/c mice naturally develop low-sociability, stereotypies and restrict interest, they have been included as autism experimental model. Our major aims were to investigate whether galectin-3 in the gut-liver axis interferes with autistic-like behaviors analyzing BALB/c Lgals3−/− mice or under partial inhibition of galectin-3 oral intake of cow’s milk for 7 days. Behavioral patterns were assessed using a three-chambers test, open field, and self-grooming. Histological analysis and immunohistochemistry (Galectin-3, NOS-2, Iba-1, Ki-67, Dll-4, Shank-3, Synaptophysin and Drebrin) were performed in gut, liver, and/or brain. Lgals3−/− mice amplified stereotypies, social retraction and restrict interest associated with reduction of cerebral Shank-3+ cells. In Lgals3+/+ mice, cow’s milk intake also amplified atypical behaviors, reduced galectin-3 in enterocytes and Kupffer cells, and disturbed niches of intestinal KI67+ and Dll-4+ cells and hepatic NOS2+ cells. In the brain of milk-treated mice, Iba-1+ microglial cells and NOS2+ Purkinje cells were increased whereas Shank-3+ and Drebrin+Synaptophysin+ cells were reduced suggesting, for the first time, that galectin-3 interferes with autistic behavior. Perhaps, a perspective to new therapies in genetically predisposed individuals to atypical behaviors.


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