scholarly journals Humoral Recognition-Behavioral Stress-Coping Glycolipids Produced By Mice Given Repeated Electroconvulsive Treatment

2020 ◽  
Vol 3 (2) ◽  

Background: Stress-coping is a core event of mammalians. Depression symptoms are induced by the stress-coping failures. Repeated electroconvulsive treatment gives a strong stress to mammalians, however, the treatment has been used to improve depression symptoms. Mammalians have recognition-behavioral stress-coping neuronal module-system followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid promotes the serotonergic module. GalNAcalpha1-3GalNAc-lipid promotes the adrenergic module. A sulfated Fucalpha1-2Gal-lipid protects the cholinergic module keeping the stress-coping memories from the ischemia-stress. I hypothesized mammalians given repeated electroconvulsive treatment would produce these glycolipids, and would increase the stress-coping ability.Materials and Methods: I examined the glycolipid productions of mice given repeated electroconvulsive treatment under general-anesthesia.Results: I found mice only given the general-anesthesia produced sulfated Galbeta1-4GlcNAc-lipid and GalNAcalpha1-3GalNAc-lipid, and mice given the repeated electroconvulsive treatment under general-anesthesia further produced sulfated Galbeta1-4GlcNAc-lipid and GalNAcalpha1-3GalNAc-lipid, and increased sulfated Fucalpha1-2Gal-lipid production. Conclusion: Depression symptoms are closely related to serotonergic and adrenergic module activities. I understood repeated electroconvulsive treatment would improve depression symptoms via the sulfated Galbeta1-4GlcNAc-lipid and GalNAcalpha1-3GalNAc-lipid productions.

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Yutaka Masuda ◽  
Hiroto Narita ◽  
Hiroaki Hasegawa

Mammalians have recognition-behavioral stress-coping neuronal module system followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid promotes the serotonergic module regulating the emotional behaviors for not-wasting the physical strength; GalNAcalpha1-3GalNAc-lipid promotes the adrenergic module inducing the behaviors escaping from the uneasy situation, and sulfated Fucalpha1-2Gal-lipid protects the cholinergic module keeping the stressor-memory from the ischemia-stress. Mouse given bathing recognizes the stressors to be coped with in the treatment. We previously observed mouse given CO2-microbubble-bathing increased the behavior escaping from the bathing situation. Mouse given CO2-microbubble-bathing would recognize the other stressors to be coped with in the treatment. We examined stress-coping glycolipids produced by mice given controlled bathing treatments, and got the following results. A sulfated Galbeta1-4GlcNAc-lipid production was increased by the acidic bathing condition and the dissolved CO2, GalNAcalpha1-3GalNAc-lipid production was increased by the dissolved CO2, and sulfated Fucalpha1-2Gal-lipid production was increased by the acidic bathing condition. We understood the mice treated with CO2-microbubble-bathing would recognize the acidic bathing condition and the dissolved CO2, but not the microbubble, as the other stressors to be coped.


2020 ◽  
Vol 3 (1) ◽  

Background: Mammalians have the recognition-behavioral stress-coping system regulated via the neuronal modules followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid which promotes the serotonergic module, keeps physical strength by regulating emotional behaviors. GalNAcalpha1-3GalNAc-lipid which promotes the adrenergic module, induces stress-coping behaviors. A sulfated Fucalpha1-2Gal-lipid protects the cholinergic module maintaining stress-coping memories from the ischemic stress. Sialalpha2-3Gal-lipid which promotes the dopaminergic module, integrates these recognition-behaviors. It is considered stresses are closely related to onset of schizophrenia, and the psychotic symptoms are not necessarily deleted after long-time medication. Schizophrenic patients might abnormally produce the humoral recognition-behavioral stress-coping glycolipids even under medication. Materials and Methods: I examined the humoral stress-coping glycolipids of medicated schizophrenic patients and those of medicated manic patients without psychotic symptoms for comparison. Results: The medicated manic patients increased sulfated Galbeta1-4GlcNAc-lipid production. The medicated schizophrenic patients increased sulfated Galbeta1-4GlcNAc-lipid production, and remarkably produced Sialalpha2- 3Gal-lipid. These indicate the manic patients and the schizophrenic patients had a stress to be coped with the serotonergic module activity, and psychotic symptoms of the schizophrenic patients would be induced via stress-coping Sialalpha2-3Gal-lipid production. Conclusion: The stressors are not clear, however, I understood humoral Sialalpha2-3Gal-lipid would be considered as another biomarker of psychotic symptoms of schizophrenia.


2019 ◽  
Author(s):  
Yutaka Masuda

Abstract Background Mammalians have the recognition-behavioral stress-coping system regulated via the neuronal modules followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid promotes the serotonergic module. GalNAcalpha1-3GalNAc-lipid promotes the adrenergic module. A Fucalpha1-2Glc-lipid protects the cholinergic module. Sialalpha2-3Gal-lipid promotes the dopaminergic module. Methods Major psychoses patients show the emotional and recognition-behavioral symptoms, and long-time medication does not completely delete the symptoms. I examined the recognition-behavioral stress-coping humoral glycolipids produced by medicated major psychoses patients. Results The major depression patients produced the sulfated Galbeta1-4GlcNAc-lipid and the sulfated Fucalpha1-2Glc-lipid, but deduced the GalNAcalpha1-3GalNAc-lipid. The mania patients produced the sulfated Galbeta1-4GlcNAc-lipid. The schizophrenia patients produced the sulfated Galbeta1-4GlcNAc-lipid, and remarkably produced the Sialalpha2-3Gal-lipid. Ruled out the medication-effects, the major depression patients decreased the serotonergic module function and the adrenergic module function, but increased the cholinergic module function. The mania patients increased the serotonergic module function and the adrenergic module function. The schizophrenia patients increased the serotonergic module function, and particularly increased the dopaminergic module function. Conclusion These suggest the stress-coping humoral glycolipids produced by the patients corresponded to the symptoms. Furthermore, I understood the humoral Sialalpha2-3Gal-lipid would be considered as another biomarker identifying schizophrenia.


2019 ◽  
Author(s):  
Alexander C. Goodman ◽  
Ryan Y. Wong

AbstractVariation in stress responses between individuals is linked to factors ranging from stress coping styles to sensitivity of neurotransmitter systems. Many anxiolytic compounds (e.g. ethanol) can increase stressor engagement through modulation of neurotransmitter systems and are used to investigate stress response mechanisms. Here we assessed the role of the GABAA system on the variation of the behavioral stress response by comparing individuals differing in stress coping styles that were chronically treated with ethanol. Specifically, we investigated resulting changes in stress-related behavior and whole-brain GABAA receptor subunits (gabra1, gabra2, gabrd, & gabrg2) in response to a novelty stressor. There were significant main and interaction effects on two stress-related behaviors, where the ethanol-treated proactive individuals showed lower stress-related behaviors than their reactive counterparts. Proactive individuals showed significantly higher expression of gabra1, gabra2, and gabrg2 compared to reactive individuals and ethanol treatment resulted in upregulation of gabra1 and gabrg2 in both stress coping styles. These results show that differences in stress-related behaviors between stress coping styles may be facilitated in part by expression of select GABAA receptor subunits.


2020 ◽  
Vol 5 (4) ◽  
pp. 959-970
Author(s):  
Kelly M. Reavis ◽  
James A. Henry ◽  
Lynn M. Marshall ◽  
Kathleen F. Carlson

Purpose The aim of this study was to examine the relationship between tinnitus and self-reported mental health distress, namely, depression symptoms and perceived anxiety, in adults who participated in the National Health and Nutrition Examinations Survey between 2009 and 2012. A secondary aim was to determine if a history of serving in the military modified the associations between tinnitus and mental health distress. Method This was a cross-sectional study design of a national data set that included 5,550 U.S. community-dwelling adults ages 20 years and older, 12.7% of whom were military Veterans. Bivariable and multivariable logistic regression was used to estimate the association between tinnitus and mental health distress. All measures were based on self-report. Tinnitus and perceived anxiety were each assessed using a single question. Depression symptoms were assessed using the Patient Health Questionnaire, a validated questionnaire. Multivariable regression models were adjusted for key demographic and health factors, including self-reported hearing ability. Results Prevalence of tinnitus was 15%. Compared to adults without tinnitus, adults with tinnitus had a 1.8-fold increase in depression symptoms and a 1.5-fold increase in perceived anxiety after adjusting for potential confounders. Military Veteran status did not modify these observed associations. Conclusions Findings revealed an association between tinnitus and both depression symptoms and perceived anxiety, independent of potential confounders, among both Veterans and non-Veterans. These results suggest, on a population level, that individuals with tinnitus have a greater burden of perceived mental health distress and may benefit from interdisciplinary health care, self-help, and community-based interventions. Supplemental Material https://doi.org/10.23641/asha.12568475


2011 ◽  
Vol 153 (12) ◽  
pp. 553-564 ◽  
Author(s):  
K. Steininger ◽  
A.-S. J. Berli ◽  
R. Jud ◽  
C. C. Schwarzwald

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