Thallium Induced Changes in Behavioral Patterns: Correlation With Altered Lipid Peroxidation and Lysosomal Enzyme Activity in Brain Regions of Male Rats

1985 ◽  
Vol 1 (1) ◽  
pp. 81-98 ◽  
Author(s):  
David R. Brown ◽  
Barbara G. Callahan ◽  
Mark A. Cleaves ◽  
Robert A. Schatz
Keyword(s):  
Lipid Peroxidation ◽  
Lysosomal Enzyme ◽  
Brain Regions ◽  
Male Rats ◽  
Patterns Of Behavior ◽  
Low Levels ◽  
Behavioral Sequelae ◽  
Human Poisoning ◽  
And Function ◽  
Induced Changes

The effects of exposures to low levels of heavy metals is a complex and serious problem. Thallium is a metal which produces behavioral sequelae in human poisoning and is potentially hazardous with low level exposures. A test battery is presented which utilizes biochemical and behavioral testing to assess the effects of low levels of thallium on central nervous system chemistry and function in rats. The doses of thallium used (4 and 8 mg/kg) produced no overt signs of behavioral toxicity but did produce dose-related increases in lipid peroxidation and activation of the lysosomal enzyme beta-galactosidase in selected brain regions. At these dose levels, thallium also selectively altered the patterns of behavior. The study suggests that the target regions of thallium in the brain include the cortex, the cerebellum and the brainstem. The dose-response relationships, found for certain pairs of behavioral acts, were correlated with biochemical changes in one or more brain regions.

Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions

2005 ◽  
Vol 99 (9) ◽  
pp. 1865-1870 ◽  
Author(s):  
Rosilene R. Kaizer ◽  
Maisa C. Corrêa ◽  
Rosélia M. Spanevello ◽  
Vera M. Morsch ◽  
Cíntia M. Mazzanti ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mouse Brain ◽  
Brain Regions ◽  
Low Levels

Abstract W P263: Alteration In Hippocampal Oscillations After Stroke: A Candidate Biomarker For Stroke-induced Cognitive Impairment

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Ji-Wei He ◽  
Yasuo Nishijima ◽  
Yosuke Akamatsu ◽  
Gratianne Rabiller ◽  
Jialing Liu
Keyword(s):  
Cognitive Impairment ◽  
Extracellular Recording ◽  
Brain Regions ◽  
Network Activity ◽  
Male Rats ◽  
Activation Patterns ◽  
Theta Frequency ◽  
Induced Changes ◽  
Distal Occlusion

Objective: Previously we have found that stroke by distal occlusion of the middle cerebral artery (dMCAO) produced injury restricted to the parietal cortex yet hippocampal impairment. Recent advances in functional connectivity suggest that shared neuronal activation patterns or synchronized brain oscillation define brain networks linking anatomically separate brain regions. Using in vivo electrophysiology, the current study aimed to determine the temporal profile of stroke-induced changes in brain oscillation in the hippocampus, a remote brain region that does not suffer from ischemic injury. Methods: Adult male rats were subjected to either a permanent left MCAO combined with a temporary bilateral occlusion of the common carotid artery (CCAO), or bilateral CCAO alone, for 1 hour. Bilateral extracellular recording was performed under urethane anesthesia using the 32-channel NeuroNexus probes spanning the cortex and CA1 radiatum layer. Results: During reperfusion, a significant decrease in theta-to-delta ratio (T/D) was observed in rats that underwent either dMCAO or CCAO alone. However, a sustained delta predominant state was only observed chronically after dMCAO, suggesting a persistent disruption of hippocampal-neocortical connectivity in the former. In contrast to CCAO, dMCAO also induced a reduced low gamma (30-59 Hz) power, change in dominant theta-frequency and disassociation of theta-gamma coupling. Conclusions: Our results indicate that ischemic stroke induces specific changes in hippocampal oscillations that might underlie the observed cognitive impairment. In contrast to stroke, an episode of mild ischemia by temporary CCAO that does not trigger functional impairment also does not evoke persistent changes in hippocampal oscillations. The observed brain oscillation profile specific to dMCAO offers an integrated measurement of the hippocampal-dependent network activity, and may serve as a candidate biomarker for post-stroke cognitive impairment.

Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner

2006 ◽  
Vol 291 (5) ◽  
pp. E965-E973 ◽  
Author(s):  
Yvonne M. Ulrich-Lai ◽  
Helmer F. Figueiredo ◽  
Michelle M. Ostrander ◽  
Dennis C. Choi ◽  
William C. Engeland ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Zona Glomerulosa ◽  
Male Rats ◽  
Adrenal Weight ◽  
Zona Fasciculata ◽  
Dna And Rna ◽  
Maximal Output ◽  
Increased Sensitivity ◽  
And Function ◽  
Induced Changes

The adrenal gland is an essential stress-responsive organ that is part of both the hypothalamic-pituitary-adrenal axis and the sympatho-adrenomedullary system. Chronic stress exposure commonly increases adrenal weight, but it is not known to what extent this growth is due to cellular hyperplasia or hypertrophy and whether it is subregion specific. Moreover, it is not clear whether increased production of adrenal glucocorticoid after chronic stress is due to increased sensitivity to adrenocorticotropic hormone (ACTH) vs. increased maximal output. The present studies use a 14-day chronic variable stress (CVS) paradigm in adult male rats to assess the effects of chronic stress on adrenal growth and corticosterone steroidogenesis. Exogenous ACTH administration (0–895 ng/100 g body wt) to dexamethasone-blocked rats demonstrated that CVS increased maximal plasma and adrenal corticosterone responses to ACTH without affecting sensitivity. This enhanced function was associated with increased adrenal weight, DNA and RNA content, and RNA/DNA ratio after CVS, suggesting that both cellular hyperplasia and hypertrophy occurred. Unbiased stereological counting of cells labeled for Ki67 (cell division marker) or 4,6-diamidino-2-phenylindole (nuclear marker), combined with zone specific markers, showed that CVS induced hyperplasia in the outer zona fasciculata, hypertrophy in the inner zona fasciculata and medulla, and reduced cell size in the zona glomerulosa. Collectively, these results demonstrate that increased adrenal weight after CVS is due to hyperplasia and hypertrophy that occur in specific adrenal subregions and is associated with increased maximal corticosterone responses to ACTH. These chronic stress-induced changes in adrenal growth and function may have implications for patients with stress-related disorders.

Spinal Cord Edema, 5-Hydroxytryptamine, Lipid Peroxidation, and Lysosomal Enzyme Release After Acute Contusion and Compression Injury in Primates

1985 ◽  
Vol 2 (1) ◽  
pp. 45-58 ◽  
Author(s):  
JACOB ABRAHAM ◽  
AIYLAM S. BALASUBRAMANIAN ◽  
D.R. THEODORE ◽  
SHANMUGAM NAGARAJAN ◽  
C.A. APTE ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Lipid Peroxidation ◽  
Lysosomal Enzyme ◽  
Enzyme Release ◽  
Compression Injury ◽  
Spinal Cord Edema

Steroids during development of genetic hypertension in rats of Lyon strain

1989 ◽  
Vol 257 (2) ◽  
pp. H506-H510 ◽  
Author(s):  
M. Vincent ◽  
C. E. Gomez-Sanchez ◽  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Male Rats ◽  
Hydroxylase Activity ◽  
Full Development ◽  
Genetically Hypertensive Rats ◽  
Low Blood Pressure ◽  
Doc Concentration ◽  
Low Levels ◽  
Genetically Hypertensive

The urinary excretion and the plasma concentration of deoxycorticosterone (DOC), corticosterone, 18-hydroxy-DOC (18-OH-DOC), aldosterone, and 19-nor-DOC were measured by specific radioimmunoassays in genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) male rats of the Lyon strains at two ages that characterize the development of their systolic blood pressure (SBP). When compared with both LN and LL controls, 5-wk-old LH rats exhibited an increased urinary DOC and decreased urinary corticosterone excretions, which were significantly related to the SBP level (r' = 0.618 and -0.520; n = 23; P less than 0.01 for DOC and corticosterone, respectively). In addition, the adrenal synthesis of LH rats was found to rely on an increased 18-hydroxylase activity as indicated by elevated urinary 18-OH-DOC/corticosterone and aldosterone/corticosterone associated with a lower 11-beta-hydroxylase activity shown by the decreased urinary corticosterone/DOC. Twenty-wk-old LH rats with fully developed hypertension exhibited normal urinary excretion of steroids and a decrease in plasma DOC concentration, which negatively correlated with the SBP level (r' = -0.574; n = 25; P less than 0.01). In conclusion, the present study demonstrates that in the Lyon model of genetically hypertensive rats, compared with two genetically different control strains and maintained under physiological unstressed conditions, the development of hypertension is associated with an increased urinary excretion of DOC. After the full development of their hypertension, the mineralocorticoid synthesis in LH rats returns to normal or low levels which could, however, remain inappropriately high for their sodium body content.

The protective role of luteolin against the methotrexate-induced hepato-renal toxicity via its antioxidative, anti-inflammatory, and anti-apoptotic effects in rats

2021 ◽  
pp. 096032712199190
Author(s):  
AA Dar ◽  
A Fehaid ◽  
S Alkhatani ◽  
S Alarifi ◽  
WS Alqahtani ◽  
...  
Keyword(s):  
Renal Toxicity ◽  
Histopathological Examination ◽  
Protective Role ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Serum Samples ◽  
Liver And Kidney ◽  
Anti Inflammatory ◽  
Induced Changes ◽  
Apoptotic Effects

Methotrexate (MTX) is frequently used drug in treatment of cancer and autoimmune diseases. Unfortunately, MTX has many side effects including the hepato-renal toxicity. In this study, we hypothesized that Luteolin (Lut) exhibits protective effect against the MTX-induced hepato-renal toxicity. In order to investigate our hypothesis, the experiment was designed to examine the effect of exposure of male rats to MTX (20 mg/kg, i.p., at day 9) alone or together with Lut (50 mg/kg, oral for 14 days) compared to the control rats (received saline). The findings demonstrated that MTX treatment induced significant increases in the liver and kidney functions markers in serum samples including Aspartate transaminase (AST), Alanine transaminase (ALT), creatinine, urea and uric acid. MTX also mediated an oxidative stress expressed by elevated malondialdehyde (MDA) level and decreased level of reduced glutathione (GSH), antioxidant enzyme activities, and downregulation of the Nrf2 gene expression as an antioxidant trigger. Moreover, the inflammatory markers (NF-κB, TNF-α, and IL-1β) were significantly elevated upon MTX treatment. In addition, MTX showed an apoptotic response mediated by elevating the pro-apoptotic (Bax) and lowering the anti-apoptotic (Bcl-2) proteins. All of these changes were confirmed by the observed alterations in the histopathological examination of the hepatic and renal tissues. Lut exposure significantly reversed all the MTX-induced changes in the measured parameters suggesting its potential protective role against the MTX-induced toxicity. Finally, our findings concluded the antioxidative, anti-inflammatory and anti-apoptotic effects of Lut as a mechanism of its protective role against the MTX-induced hepato-renal toxicity in rats.

scholarly journals β-Elemene Suppresses Obesity-Induced Imbalance in the Microbiota-Gut-Brain Axis

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 704
Author(s):  
Yingyu Zhou ◽  
Wanyi Qiu ◽  
Yimei Wang ◽  
Rong Wang ◽  
Tomohiro Takano ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
High Fat Diet ◽  
Brain Regions ◽  
Cerebral Metabolites ◽  
The Central Nervous System ◽  
Cerebral Inflammation ◽  
Regulatory Effects ◽  
Induced Changes ◽  
Pearson Correlations ◽  
Glucose Cycle

As a kind of metabolically triggered inflammation, obesity influences the interplay between the central nervous system and the enteral environment. The present study showed that β-elemene, which is contained in various plant substances, had effects on recovering the changes in metabolites occurring in high-fat diet (HFD)-induced obese C57BL/6 male mice brains, especially in the prefrontal cortex (PFC) and hippocampus (HIP). β-elemene also partially reversed HFD-induced changes in the composition and contents of mouse gut bacteria. Furthermore, we evaluated the interaction between cerebral metabolites and intestinal microbiota via Pearson correlations. The prediction results suggested that Firmicutes were possibly controlled by neuron integrity, cerebral inflammation, and neurotransmitters, and Bacteroidetes in mouse intestines might be related to cerebral aerobic respiration and the glucose cycle. Such results also implied that Actinobacteria probably affected cerebral energy metabolism. These findings suggested that β-elemene has regulatory effects on the imbalanced microbiota-gut-brain axis caused by obesity and, therefore, would contribute to the future study in on the interplay between cerebral metabolites from different brain regions and the intestinal microbiota of mice.

scholarly journals Spine impairment in mice high-expressing neuregulin 1 due to LIMK1 activation

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Peng Chen ◽  
Hongyang Jing ◽  
Mingtao Xiong ◽  
Qian Zhang ◽  
Dong Lin ◽  
...  
Keyword(s):  
Neural Development ◽  
Protein Level ◽  
Brain Regions ◽  
Postmortem Brain ◽  
Pathophysiological Mechanism ◽  
Brain Disorders ◽  
Spine Density ◽  
Genes Encoding ◽  
High Level ◽  
And Function

AbstractThe genes encoding for neuregulin1 (NRG1), a growth factor, and its receptor ErbB4 are both risk factors of major depression disorder and schizophrenia (SZ). They have been implicated in neural development and synaptic plasticity. However, exactly how NRG1 variations lead to SZ remains unclear. Indeed, NRG1 levels are increased in postmortem brain tissues of patients with brain disorders. Here, we studied the effects of high-level NRG1 on dendritic spine development and function. We showed that spine density in the prefrontal cortex and hippocampus was reduced in mice (ctoNrg1) that overexpressed NRG1 in neurons. The frequency of miniature excitatory postsynaptic currents (mEPSCs) was reduced in both brain regions of ctoNrg1 mice. High expression of NRG1 activated LIMK1 and increased cofilin phosphorylation in postsynaptic densities. Spine reduction was attenuated by inhibiting LIMK1 or blocking the NRG1–LIMK1 interaction, or by restoring NRG1 protein level. These results indicate that a normal NRG1 protein level is necessary for spine homeostasis and suggest a pathophysiological mechanism of abnormal spines in relevant brain disorders.

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