scholarly journals Anticonvulsant effects of desvenlafaxine on modulating brain monoamine and oxidative stress in mice

2023 ◽  
Vol 83 ◽  
Author(s):  
Khalid Saad Alharbi
Keyword(s):  
Oxidative Stress ◽  
Depressive Disorders ◽  
Motor Coordination ◽  
Maximal Electroshock ◽  
Gamma Aminobutyric Acid ◽  
Major Depressive ◽  
Major Depressive Disorders ◽  
Brain Monoamine ◽  
And Oxidative Stress

Abstract Desvenlafaxine succinate (DVS) inhibits serotonin reuptake selectively and is approved for major depressive disorders. This research investigated influence of DVS on modulating brain monoamine and oxidative stress in mice. The antiepileptic potential of DVS (10, 20, or 30 mg/kg/i.p.) in pentylenetetrazole (PTZ; 85 mg/kg) with i.p. route of administration, strychnine (STR; 75 mg/kg) with i.p. route, pilocarpine (400 mg/kg) with s.c. route and maximal electroshock MES-induced convulsion in mouse models. The activities of oxidative stress, i.e. superoxide dismutase (SOD), glutathione (GSH) and lipid peroxidation (LPO) as well as gamma-aminobutyric acid (GABA) in the brains of PTZ-induced convulsive mice. Treatment with DVS increased the latency to develop siezures and declined mortalities in rodents against PTZ, STR and pilocarpine-induced convulsions. Results of MES-leaded siezures revealed that DVS reduced tonic hind limb extension duration and mortalities significantly. Brain, SOD, GSH and GABA level were significantly (P<0.01) increased and LPO reduced significantly (P<0.01) after DVS treatment. Furthermore, the DVS did not show any motor coordination signs in the rotarod test. We demonstrated that the role of DVS in convulsion genesis in mice under control condition and attenuate the PTZ-induced oxidative damage.

scholarly journals The Role of HPA Axis and Allopregnanolone on the Neurobiology of Major Depressive Disorders and PTSD

2021 ◽  
Vol 22 (11) ◽  
pp. 5495
Author(s):  
Felipe Borges Almeida ◽  
Graziano Pinna ◽  
Helena Maria Tannhauser Barros
Keyword(s):  
Hpa Axis ◽  
Depressive Disorders ◽  
Post Traumatic Stress ◽  
Major Depressive ◽  
Physiological Adaptations ◽  
Suppression Test ◽  
Post Traumatic ◽  
Major Depressive Disorders ◽  
Cortisol Release

Under stressful conditions, the hypothalamic-pituitary-adrenal (HPA) axis acts to promote transitory physiological adaptations that are often resolved after the stressful stimulus is no longer present. In addition to corticosteroids (e.g., cortisol), the neurosteroid allopregnanolone (3α,5α-tetrahydroprogesterone, 3α-hydroxy-5α-pregnan-20-one) participates in negative feedback mechanisms that restore homeostasis. Chronic, repeated exposure to stress impairs the responsivity of the HPA axis and dampens allopregnanolone levels, participating in the etiopathology of psychiatric disorders, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). MDD and PTSD patients present abnormalities in the HPA axis regulation, such as altered cortisol levels or failure to suppress cortisol release in the dexamethasone suppression test. Herein, we review the neurophysiological role of allopregnanolone both as a potent and positive GABAergic neuromodulator but also in its capacity of inhibiting the HPA axis. The allopregnanolone function in the mechanisms that recapitulate stress-induced pathophysiology, including MDD and PTSD, and its potential as both a treatment target and as a biomarker for these disorders is discussed.

scholarly journals Thalamic Gamma Aminobutyric Acid Level Changes in Major Depressive Disorder After a 12-Week Iyengar Yoga and Coherent Breathing Intervention

2021 ◽  
Vol 2 (1) ◽  
pp. 32
Author(s):  
Nishant Dixit
Keyword(s):  
Spiritual Growth ◽  
Depressive Disorders ◽  
Aminobutyric Acid ◽  
Positive Outcomes ◽  
Gamma Aminobutyric Acid ◽  
Gaba Level ◽  
Psychological Benefits ◽  
Major Depressive ◽  
Major Depressive Disorders ◽  
Stimulation Of

Although yoga is considered as a science for spiritual growth of mankind, many studies have shown that various streams of yoga render many physical as well as psychological benefits to the practitioners. Studies based on Yogic intervention (YI) on Major Depressive disorders (MDD) have shown extremely positive outcomes in recent times (1,2). The antidepressant medications which target the monoamine framework were unable to answer to the neurobiological mechanisms of MDD. Gamma aminobutyric acid (GABA), an amino acid neurotransmitter is known to be an important factor in the pathophysiology of mood disorders (3). In this US based study the design was to track the changes in GABA in MDD through a Yogic Intervention based on Iyenger yoga tradition. The study reports that YI does influence the change in GABA level through the stimulation of parasympathetic response.

scholarly journals Reduced Energy Per Cycle, a Marker of Glutamatergic Synaptic Strength, in Individuals Diagnosed with PTSD and Depression

2021 ◽  
Author(s):  
Lynnette Averill ◽  
Lihong Jiang ◽  
Prerana Purohit ◽  
Anastasia Coppoli ◽  
Christopher Averill ◽  
...  
Keyword(s):  
Depressive Disorders ◽  
Antidepressant Treatment ◽  
Synaptic Strength ◽  
Resonance Spectroscopy ◽  
Major Depressive ◽  
Novel Treatments ◽  
Study Results ◽  
Healthy Control ◽  
Major Depressive Disorders

Trauma and chronic stress are believed to induce and exacerbate psychopathology by disrupting glutamate synaptic connectivity. In this pilot study, we utilized energy-per-cycle (EPC), a novel putative biomarker of glutamatergic synaptic strength, to investigate the role of prefrontal neurotransmission in trauma psychopathology. Healthy control (n=18) and patients with comorbid posttraumatic stress and major depressive disorders (PTSD+MDD; n=16) completed 13C-acetate magnetic resonance spectroscopy scans to estimate prefrontal EPC, which is the ratio of neuronal energetic needs per glutamate neurotransmission cycle (VTCA/VCycle). Patients with PTSD+MDD were found to have 28% reduction in prefrontal EPC (t=3.0; df=32, p=0.005). There was no effect of sex on EPC, but age was negatively associated with prefrontal EPC across groups (r=-0.46, n=34, p=0.006). Controlling for age did not affect the study results. Exploratory analyses found antidepressants to have statistically significant effects (F(2,30)=5.3, p=0.01), with the lowest EPC in the unmedicated PTSD+MDD participants (p=0.003). Patients with comorbid PTSD and MDD have reduced prefrontal glutamatergic synaptic strength, as estimated by EPC. Antidepressant treatment appears to partially normalize the prefrontal EPC deficits. These findings suggest that reduced glutamatergic synaptic strength may contribute to the pathophysiology of comorbid PTSD and MDD and might be targeted by novel treatments.

scholarly journals Plasma concentrations of Granulocyte Colony-Stimulating Factor (G-CSF) in Patients with Substance Use Disorders and Comorbid Major Depressive Disorders

2021 ◽  
Author(s):  
Sandra Torres Galván ◽  
María Flóres López ◽  
Pablo Romero Sanchíz ◽  
Nerea Requena Ocaña ◽  
Oscar Porras Perales ◽  
...  
Keyword(s):  
Substance Use ◽  
Substance Use Disorders ◽  
Depressive Disorders ◽  
Plasma Concentrations ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Major Depressive ◽  
Major Depressive Disorders ◽  
Stimulating Factor

Abstract Aims: Granulocyte colony–stimulating factor (G-CSF) has raised much interest due to its role to cocaine addiction in preclinical models. We analyzed the circulating expression of G-CSF in abstinent chronic users of alcohol and/or cocaine with or without comorbid major depressive disorders to investigate the role of this trophic factor with complicated substance use disorders.Methods: We recruited 176 patients and 136 controls. Patients were divided in 50 patients with major depressive disorder (MDD) and 126 abstinent substance use disorders (SUD) patients undergoing treatments for alcohol (N=66) or cocaine (N=60) addiction according to DSM-IV-TR criteria. A blood sample was collected to examine plasma concentrations of G-CSF.Results: The plasma concentrations of G-CSF were significantly decreased in the cocaine group compared with the SUD control group. There was a sex dimorphism in the alcohol group, with lower G-CSF concentrations in women compared with men. Plasma concentrations of G-CSF were associated with abstinence and with the length of alcohol problems. The decrease in G-CSF was associated with comorbid MDD, a finding specific for SUD patients since there were no alterations of G-CSF primary settings MDD outpatients.Conclusions: Circulating G-CSF is reduced in SUD patients, being associated to comorbid MDD. A sex-dependent effect was observed in female AUD. Plasma G-CSF concentrations might be used as a predictor of length of chronic alcohol use and as a stratification role in the dual diagnosis in SUD. Further investigation is needed to explore the role of G-CSF as potential biomarker of pathogenic/prognosis in SUD population.

scholarly journals The Role of Intelligence Quotient as a Risk Factor for Depression: a Literature Review

2021 ◽  
Vol 2 (1) ◽  
pp. 51-54
Author(s):  
Bella Sagita Pratiwi
Keyword(s):  
Risk Factor ◽  
Literature Review ◽  
Intelligence Quotient ◽  
Depressive Disorders ◽  
Cure Rate ◽  
Major Depressive ◽  
Psychomotor Disorders ◽  
Long Time ◽  
Major Depressive Disorders

A B S T R A C TDepression is a mood disorder with general characteristics in the form of changes insleep patterns and appetite, psychomotor disorders, concentration problems,anhedonia, fatigue, hopelessness and helplessness, and suicidal ideation. If thedepressive disorder goes on for a long time (dysthymia), the person is suggested to bemoody, lazy, or withdrawn from relationships because he loses interest in almost allaspects of his life. Depression is a psychiatric disorder that is often found with aprevalence of around 15%. In general, the onset of major depressive disorders is atthe age of 20 to 50 years, but the most often is at the age of 40 years. Cognitive playsa role in the aetiology and prognosis of someone with depression. The higher thecognitive level of a person, the more it will affect the cure rate and prevent recurrencein someone experiencing psychiatric disorders. This literature review will explain therole of intelligence quotient in depressive disorders.

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

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