scholarly journals Decreased glucorticoid sensitivity as a factor of stressogenic shifts in the activity of monoamine oxidase, lipid peroxidation, and behavior in rats

2003 ◽  
Vol 49 (5) ◽  
pp. 48-51 ◽  
Author(s):  
I. A. Volchegorsky ◽  
V. E. Tseilikman ◽  
D. S. Smirnov ◽  
S. A. Ship ◽  
A. V. Borisenkov
Keyword(s):  
Lipid Peroxidation ◽  
Monoamine Oxidase ◽  
Brain Tissue ◽  
Behavioral Disorders ◽  
Immobilization Stress ◽  
Glucocorticoid Hormones ◽  
And Behavior ◽  
The Brain

Four episodes of immobilization stress cause a decrease in the sensitivity to glucocorticoid hormones, followed by anxiogenic be­havioral disorders, enhanced monoamine oxidase-В (МАО-В) activity and simultaneously increased lipid peroxidation (LPO) in the brain tissue of rats. Concurrently, there is an increase in renal МАО-В activity, as well as renal and hepatic accumulation of LPO products. Administration of kenalog (2 mg/kg), a phar­macological analogue of glucocorticoid hormones, prevents the poststress МАО-В activation and LPO and attenuates anxiogen­ic behavioral disorders in the rats.

scholarly journals Intravital imaging of cerebral microinfarct reveals an astrocyte reaction led to glial scar

2021 ◽  
Author(s):  
Jingu Lee ◽  
Joon-Goon Kim ◽  
Sujung Hong ◽  
Young Seo Kim ◽  
Soyeon Ahn ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Brain Tissue ◽  
Neuronal Death ◽  
Cellular Level ◽  
Intravital Imaging ◽  
Monoamine Oxidase B ◽  
Infarct Area ◽  
The Impact ◽  
The Brain

AbstractCerebral microinfarct increases the risk of dementia. But how microscopic cerebrovascular disruption affects the brain tissue in cellular-level are mostly unknown. Herein, with a longitudinal intravital imaging, we serially visualized in vivo dynamic cellular-level changes in astrocyte, pericyte and neuron as well as microvascular integrity after the induction of cerebral microinfarction for 1 month in mice. At day 2-3, it revealed a localized edema with acute astrocyte loss, neuronal death, impaired pericyte-vessel coverage and extravascular leakage indicating blood-brain barrier (BBB) dysfunction. At day 5, edema disappeared with recovery of pericyte-vessel coverage and BBB integrity. But brain tissue continued to shrink with persisted loss of astrocyte and neuron in microinfarct until 30 days, resulting in a collagen-rich fibrous scar surrounding the microinfarct. Notably, reactive astrocytes appeared at the peri-infarct area early at day 2 and thereafter accumulated in the peri-infarct. Oral administration of a reversible monoamine oxidase B inhibitor significantly decreased the astrocyte reactivity and fibrous scar formation. Our result suggests that astrocyte reactivity may be a key target to alleviate the impact of microinfarction.

scholarly journals Decreased Interleukin-4 Release from the Neurons of the Locus Coeruleus in Response to Immobilization Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Hyun-ju Lee ◽  
Hyun-Jung Park ◽  
Angela Starkweather ◽  
Kyungeh An ◽  
Insop Shim
Keyword(s):  
Locus Coeruleus ◽  
Inverse Relationship ◽  
Immobilization Stress ◽  
Plasma Corticosterone ◽  
Interleukin 4 ◽  
Immune Challenge ◽  
Noradrenergic Neurons ◽  
And Behavior ◽  
The Brain ◽  
Anti Inflammatory Cytokine

It has been demonstrated that immobilization (IMO) stress affects neuroimmune systems followed by alterations of physiology and behavior. Interleukin-4 (IL-4), an anti-inflammatory cytokine, is known to regulate inflammation caused by immune challenge but the effect of IMO on modulation of IL-4 expression in the brain has not been assessed yet. Here, it was demonstrated that IL-4 was produced by noradrenergic neurons in the locus coeruleus (LC) of the brain and release of IL-4 was reduced in response to IMO. It was observed that IMO groups were more anxious than nontreated groups. Acute IMO (2 h/day, once) stimulated secretion of plasma corticosterone and tyrosine hydroxylase (TH) in the LC whereas these increments were diminished in exposure to chronic stress (2 h/day, 21 consecutive days). Glucocorticoid receptor (GR), TH, and IL-4-expressing cells were localized in identical neurons of the LC, indicating that hypothalamic-pituitary-adrenal- (HPA-) axis and sympathetic-adrenal-medullary- (SAM-) axis might be involved in IL-4 secretion in the stress response. Accordingly, it was concluded that stress-induced decline of IL-4 concentration from LC neurons may be related to anxiety-like behavior and an inverse relationship exists between IL-4 secretion and HPA/SAM-axes activation.

scholarly journals Modulatory Effects of Ferulic Acid on Cadmium-Induced Brain Damage

2016 ◽  
Vol 21 (4) ◽  
pp. NP56-NP61 ◽  
Author(s):  
Stephen A. Adefegha ◽  
Olasunkanmi S. Omojokun ◽  
Ganiyu Oboh ◽  
Olasunkanmi Fasakin ◽  
Opeyemi Ogunsuyi
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Monoamine Oxidase ◽  
Oral Administration ◽  
Atpase Activity ◽  
Ferulic Acid ◽  
Brain Damage ◽  
Wistar Strain ◽  
Mda Content ◽  
The Brain

Studies have shown the pharmacological relevance of phenolics like ferulic acid (FA) in promoting health. This study sought to investigate the modulatory effects of FA on cadmium-induced brain damage in rats. Brain damage was induced in Wistar strain rats by oral administration of cadmium (5 mg/kg body weight) for 21 days. Assays for malondialdehyde (MDA) content, acetylcholinesterase (AChE), butyrylcholinesterase (BChE), monoamine oxidase (MAO), and Na+/K+-ATPase activities were carried out. The study revealed significant ( P < .05) increases in the MDA content and all enzymes’ (AChE, BChE, MAO, and Na+/K+-ATPase) activity investigated following cadmium administration. However, rats administered FA (10 and 20 mg/kg body weight) alongside cadmium significantly ( P < .05) protected the brain by reversing the level of lipid peroxidation as measured by the MDA content as well as the enzymes’ activity. This study, therefore, substantiates the neuroprotective potentials of FA especially in the management of cadmium-induced toxicity.

scholarly journals Impact of anxiogenic stress on glucocorticoid sensitivity, glucose tolerance, and alloxan resistance in rats

2002 ◽  
Vol 48 (6) ◽  
pp. 41-44
Author(s):  
I. A. Volchegorsky ◽  
V. E. Tseilikman ◽  
S. A. Ship ◽  
N. V. Bubnov ◽  
A. I. Sinitsky
Keyword(s):  
Behavioral Disorders ◽  
Immobilization Stress ◽  
Acute Hypoxia ◽  
Hypoxia Tolerance ◽  
Behavioral Activity ◽  
Glucose Load ◽  
Mao B ◽  
Load Tolerance ◽  
The Brain ◽  
Hyperglycemic Effect

Four episodes of immobilization stress caused anxiogenic behavioral disorders accompanied by a decrease in sensitivity to glucocorticoid hormones, by an increase in the activity of monoaminooxidase (MAO-B) in the brain tissue, an enhancement in glucose load tolerance, and a reduction in acute hypoxia tolerance in rats. Alloxan-induced diabetes was also associated with a reduction of rat behavioral activity in the open field along with an increase in the cerebral activity of MAO-B. Prior anxiogenic stress potentiated an alloxan-induced increase in cerebral MAO- B activity, enhanced concomitant behavioral disorders in rats, and increased the hyperglycemic effect of alloxan.

scholarly journals Neuroprotective Effects of Tea Against Cadmium Toxicity

2019 ◽  
Vol 2 (12) ◽  
pp. 230
Author(s):  
Francis N. Wachira ◽  
G. O. Areba ◽  
R. M. Ngure ◽  
R. Khalid ◽  
F. Maloba ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Brain Tissue ◽  
Antioxidant Defense ◽  
Neuronal Damage ◽  
Cadmium Toxicity ◽  
Antioxidant Defense System ◽  
Defense System ◽  
Neuroprotective Effects ◽  
Histopathological Studies ◽  
The Brain

Background: Cadmium (Cd) is a common pollutant and potential neuro-toxicant to humans. The main treatment for heavy metal toxicity is chelation therapy which is however replete with grave side effects. This study was designed to determine the neuroprotective effects of extracts of the tea beverage on experimentally induced cadmium toxicity in the brain of rats. Cadmiumas CdCl2 was administered subcutaneously while tea was given orally.Methods: Healthy Wister rats were used to study the effects of co-administration of Cd and tea extracts on the brain. Cadmium was injected subcutaneously while tea was administered orally to the rats. Brain tissue from euthanized rats was assayed for Zinc Fingers and Homeoboxes Protein 1 (ZHX1), reduced glutathione (GSH), and lipid peroxidation markers Thiobarbituric Acid Reactive Substances (TBARS). Neurohistochemical and histopathological studies were also carried out on the brain tissues of the rats.Results: Cadmium significantly induced neuronal damage exhibited by a significant (p < 0.05) decrease in ZHX1 in the brain tissue, significant (p <0.05) increase in TBARS, as well as significant (p < 0.05) increase in GSH implying an impaired antioxidant defense system. Co-administration of Cd with black or green tea extracts resulted in a significant decrease in lipid peroxidation as well as maintenance of GSH and ZHX1. The neurohistochemical and histopathological studies in the brain of the rats indicated that the tea extracts significantly reduced CdCl2 toxicity and preserved the normal histological architecture of the brain tissues.Conclusion: This paper reports for the first time the efficacy of tea extracts in protecting rats from cadmium induced toxicity and disturbances of antioxidant defense system in the brain.Key words: Tea; flavonoids; Cadmium; neurotoxicity; Chelating agents.

Effects of Radiation on Protein Oxidation and Lipid Peroxidation in the Brain Tissue

2009 ◽  
Vol 41 (10) ◽  
pp. 4394-4396 ◽  
Author(s):  
O. Gulbahar ◽  
A. Aricioglu ◽  
M. Akmansu ◽  
Z. Turkozer
Keyword(s):  
Lipid Peroxidation ◽  
Brain Tissue ◽  
Protein Oxidation ◽  
Effects Of Radiation ◽  
The Brain

Chronic immobilization stress induces anxiety-related behaviors and affects brain essential minerals in male rats

2020 ◽  
pp. 1-8
Author(s):  
Zafer Sahin ◽  
Alpaslan Ozkurkculer ◽  
Omer Faruk Kalkan ◽  
Ahmet Ozkaya ◽  
Aynur Koc ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Central Area ◽  
Essential Elements ◽  
Male Rats ◽  
Control Group ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
The Brain ◽  
Center Area ◽  
Chronic Immobilization Stress

Abstract. Alterations of essential elements in the brain are associated with the pathophysiology of many neuropsychiatric disorders. It is known that chronic/overwhelming stress may cause some anxiety and/or depression. We aimed to investigate the effects of two different chronic immobilization stress protocols on anxiety-related behaviors and brain minerals. Adult male Wistar rats were divided into 3 groups as follows ( n = 10/group): control, immobilization stress-1 (45 minutes daily for 7-day) and immobilization stress-2 (45 minutes twice a day for 7-day). Stress-related behaviors were evaluated by open field test and forced swimming test. In the immobilization stress-1 and immobilization stress-2 groups, percentage of time spent in the central area (6.38 ± 0.41% and 6.28 ± 1.03% respectively, p < 0.05) and rearing frequency (2.75 ± 0.41 and 3.85 ± 0.46, p < 0.01 and p < 0.05, respectively) were lower, latency to center area (49.11 ± 5.87 s and 44.92 ± 8.04 s, p < 0.01 and p < 0.01, respectively), were higher than the control group (8.65 ± 0.49%, 5.37 ± 0.44 and 15.3 ± 3.32 s, respectively). In the immobilization stress-1 group, zinc (12.65 ± 0.1 ppm, p < 0.001), magnesium (170.4 ± 1.7 ppm, p < 0.005) and phosphate (2.76 ± 0.1 ppm, p < 0.05) levels were lower than the control group (13.87 ± 0.16 ppm, 179.31 ± 1.87 ppm and 3.11 ± 0.06 ppm, respectively). In the immobilization stress-2 group, magnesium (171.56 ± 1.87 ppm, p < 0.05), phosphate (2.44 ± 0.07 ppm, p < 0.001) levels were lower, and manganese (373.68 ± 5.76 ppb, p < 0.001) and copper (2.79 ± 0.15 ppm, p < 0.05) levels were higher than the control group (179.31 ± 1.87 ppm, 3.11 ± 0.06 ppm, 327.25 ± 8.35 ppb and 2.45 ± 0.05 ppm, respectively). Our results indicated that 7-day chronic immobilization stress increased anxiety-related behaviors in both stress groups. Zinc, magnesium, phosphate, copper and manganese levels were affected in the brain.

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