Regulation of metallothionein concentrations in rat brain: effect of glucocorticoids, zinc, copper, and endotoxin

1994 ◽  
Vol 266 (5) ◽  
pp. E760-E767 ◽  
Author(s):  
T. Gasull ◽  
M. Giralt ◽  
J. Hernandez ◽  
P. Martinez ◽  
I. Bremner ◽  
...  

The effects of known inducers of liver metallothionein (MT) synthesis on MT concentrations in the rat brain have been determined using antibodies that are specific for MT I and II and do not cross-react with MT III. There were substantial differences in the MT concentrations in different areas of the brain. Dexamethasone increased MT levels after 24 h in the frontal cortex, cortex, medulla oblongata plus pons, midbrain, striatum, hippocampus, and cerebellum but not in the hypothalamus. Corticosterone produced similar results except in the hippocampus. Long-lasting adrenocorticotropic hormone increased MT concentrations after 12 h in midbrain and striatum but not in the liver. Adrenalectomy decreased MT concentrations after 6 days in the medulla oblongata plus pons, striatum, hippocampus, and hypothalamus but increased concentrations in the liver and kidneys; these effects were reversed by corticosterone. The role of glucocorticoids in the regulation of MT levels therefore differs between tissues and within specific areas of the brain. Injection of zinc or copper intracerebroventricularly and the use of a zinc-deficient diet increased and decreased MT levels, respectively, in some but not all brain areas. Endotoxin increased liver MT but not brain MT I levels after 8 h.

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Valeria Hansberg-Pastor ◽  
Ana Gabriela Piña-Medina ◽  
Aliesha González-Arenas ◽  
Ignacio Camacho-Arroyo

The CCAAT/enhancer-binding protein beta (C/EBPβ) is a transcription factor expressed in different areas of the brain that regulates the expression of several genes involved in cell differentiation and proliferation. This protein has three isoforms (LAP1, LAP2, and LIP) with different transcription activation potential. The role of female sex hormones in the expression pattern of C/EBPβisoforms in the rat brain has not yet been described. In this study we demonstrate by western blot that the expression of the three C/EBPβisoforms changes in different brain areas during the estrous cycle. In the cerebellum, LAP2 content diminished on diestrus and proestrus and LIP content diminished on proestrus and estrus days. In the prefrontal cortex, LIP content was higher on proestrus and estrus days. In the hippocampus, LAP isoforms presented a switch on diestrus day, since LAP1 content was the highest while that of LAP2 was the lowest. The LAP2 isoform was the most abundant one in all the three brain areas. The LAP/LIP ratio changed throughout the cycle and was tissue specific. These results suggest that C/EBPβisoforms expression changes in a tissue-specific manner in the rat brain due to the changes in sex steroid hormone levels presented during the estrous cycle.


Author(s):  
Tomas T. Roos ◽  
Megg G. Garcia ◽  
Isak Martinsson ◽  
Rana Mabrouk ◽  
Bodil Israelsson ◽  
...  

AbstractThe amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer’s disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its prion-like spread. We demonstrate that an intracellular source of Aβ can induce amyloid plaques in vivo via hippocampal injection. We show that hippocampal injection of mouse AD brain homogenate not only induces plaques, but also damages interneurons and affects intracellular Aβ levels in synaptically connected brain areas, paralleling cellular changes seen in AD. Furthermore, in a primary neuron AD model, exposure of picomolar amounts of brain-derived Aβ leads to an apparent redistribution of Aβ from soma to processes and dystrophic neurites. We also observe that such neuritic dystrophies associate with plaque formation in AD-transgenic mice. Finally, using cellular models, we propose a mechanism for how intracellular accumulation of Aβ disturbs homeostatic control of Aβ levels and can contribute to the up to 10,000-fold increase of Aβ in the AD brain. Our data indicate an essential role for intracellular prion-like Aβ and its synaptic spread in the pathogenesis of AD.


2021 ◽  
Vol 86 (6) ◽  
pp. 704-715
Author(s):  
Sofie D. Shirenova ◽  
Nadezhda N. Khlebnikova ◽  
Nataliya A. Krupina

Abstract Early-life stress is a risk factor for the development of behavioral and cognitive disorders in humans and animals. Such stressful situations include social isolation in early postnatal ontogenesis. Behavioral and cognitive impairments associated with neuroplastic changes in brain structures. We have found that after ten weeks of social isolation, male Wistar rats show behavioral abnormalities and cognitive deficit, accompanied by an increase in the relative expression of gene encoding serine protease prolyl endopeptidase (PREP, EC 3.4.21.26) in the brain frontal cortex. The present study aimed to assess synaptophysin (SYP), brain-derived neurotrophic factor precursor (proBDNF), and PREP expression using Western blot in the brain structures – the hippocampus, frontal cortex, and striatum of the rats subjected to prolonged social isolation compared with group-housed animals. Twenty Wistar rats were used for this study (10 males and 10 females). Experimental animals (5 males and 5 females) were kept one per cage for nine months, starting from the age of one month. Ten-month-old socially isolated rats showed memory deficit in passive avoidance paradigm and Morris Water Maze and reactivity to novelty reduction. We used monoclonal antibodies for the Western blot analysis of the expression of SYP, proBDNF, and PREP in the rat brain structures. Social isolation caused a proBDNF expression reduction in the frontal cortex in females and a reduction in PREP expression in the striatum in males. These data suppose that neurotrophic factors and PREP are involved in the mechanisms of behavioral and cognitive impairments observed in the rats subjected to prolonged social isolation with an early life onset.


2018 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Nagapuri Kiran Kumar ◽  
Mesram Nageshwar ◽  
Karnati Pratap Reddy

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.


2021 ◽  
Vol 10 (24) ◽  
pp. 5859
Author(s):  
Katarzyna Wachowska ◽  
Piotr Gałecki

The authors aim to present a narrative review of research on the inflammatory aetiology of depression. Depression is a psychiatric disorder, constituting the most common reason of disability due to a health condition. It has been estimated that at least one in six people suffer from depression at some point of their lives. The aetiology of depression, although researched extensively all around the world, still remains unclear. Authors discuss the possible role of inflammation in depression, the neurodevelopmental theory of depression as well as associations between cognition and depression. Possible associations between memory dysfunction among depressive patients and inflammatory markers are included. The associations between the immune system, depression and cognition are observed. Possible mediating factors between these areas include personality traits, hormonal imbalance and functioning of the brain areas. The question as to what mediating factors are involved is still open to research.


2022 ◽  
Author(s):  
Joana Cabral ◽  
Francesca Castaldo ◽  
Jakub Vohryzek ◽  
Vladimir Litvak ◽  
Christian Bick ◽  
...  

A rich repertoire of oscillatory signals is detected from human brains with electro- and magnetoencephalography (EEG/MEG). However, the principles underwriting coherent oscillations and their link with neural activity remain unclear. Here, we hypothesise that the emergence of transient brain rhythms is a signature of weakly stable synchronization between spatially distributed brain areas, occurring at network-specific collective frequencies due to non-negligible conduction times. We test this hypothesis using a phenomenological network model to simulate interactions between neural mass potentials (resonating at 40Hz) in the structural connectome. Crucially, we identify a critical regime where metastable oscillatory modes emerge spontaneously in the delta (0.5-4Hz), theta (4-8Hz), alpha (8-13Hz) and beta (13-30Hz) frequency bands from weak synchronization of subsystems, closely approximating the MEG power spectra from 89 healthy individuals. Grounded in the physics of delay-coupled oscillators, these numerical analyses demonstrate the role of the spatiotemporal connectome in structuring brain activity in the frequency domain.


Author(s):  
R.F. Butterworth ◽  
M. Gonce ◽  
A. Barbeau

SUMMARY:We have studied the brain regional distribution of methyl mercury following intravenous administration of CH3203HgCl in rat. Early peak levels were obtained in cerebellum, medulla oblongata and midbrain. The efficacy of removal of 203Hg by different chelators is also region dependent. The most efficient chelator for brain mercury proved to be mesodimercaptosuccinic acid.


Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1445
Author(s):  
Svetlana Demyanenko ◽  
Valentina Dzreyan ◽  
Svetlana Sharifulina

Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed. The ischemic stroke generally reduces the gene expression due to suppression of acetylation of histones H3 and H4. Histone deacetylases inhibitors have been shown to be effective in protecting the brain from ischemic damage. Histone deacetylases inhibitors induce neurogenesis and angiogenesis in damaged brain areas promoting functional recovery after cerebral ischemia. However, the role of different histone deacetylases isoforms in the survival and death of brain cells after stroke is still controversial. This review aims to analyze the data on the neuroprotective activity of nonspecific and selective histone deacetylase inhibitors in ischemic stroke.


2019 ◽  
Author(s):  
Yu Liu ◽  
Shuhua Qi ◽  
Fridtjof Thomas ◽  
Brittany L. Correia ◽  
Angela P. Taylor ◽  
...  

ABSTRACTRespiration is controlled by central pattern generating circuits in the brain stem, whose activity can be modulated by inputs from other brain areas to adapt respiration to autonomic and behavioral demands. The cerebellum is known to be part of the neuronal circuitry activated during respiratory challenges, such as hunger for air, but has not been found to be involved in the control of unobstructed breathing at rest (eupnea). Here we applied a measure of intrinsic rhythmicity, the CV2, which evaluates the similarity of subsequent intervals and is thus sensitive to changes in rhythmicity at the temporal resolution of individual respiratory intervals. The variability of intrinsic respiratory rhythmicity was reduced in a mouse model of cerebellar ataxia compared to their healthy littermates. Irrespective of that difference, the average respiratory rate and the average coefficient of variation (CV) were comparable between healthy and ataxic mice. We argue that these findings are consistent with a proposed role of the cerebellum in the coordination of respiration with other rhythmic orofacial movements, such as fluid licking and swallowing.


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