Acetylcholinesterase activity in the brain of dystonia musculorum (Dstdt-J) mutant mice

2012 ◽  
Vol 72 (1) ◽  
pp. 79-86 ◽  
Author(s):  
C. Clément ◽  
R. Lalonde ◽  
C. Strazielle
Keyword(s):  
Acetylcholinesterase Activity ◽  
Mutant Mice ◽  
Dystonia Musculorum ◽  
The Brain

Increased dopaminergic innervation in the brain of conditional mutant mice overexpressing Otx2: Effects on locomotor behavior and seizure susceptibility

Neuroscience ◽  
2014 ◽  
Vol 261 ◽  
pp. 173-183 ◽  
Author(s):  
P.P. Tripathi ◽  
L.G. Di Giovannantonio ◽  
E. Sanguinetti ◽  
D. Acampora ◽  
M. Allegra ◽  
...  
Keyword(s):  
Locomotor Behavior ◽  
Mutant Mice ◽  
Seizure Susceptibility ◽  
Conditional Mutant ◽  
The Brain

scholarly journals Aicardi-Goutières syndrome-associated mutation at ADAR1 gene locus activates innate immune response in mouse brain

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Xinfeng Guo ◽  
Clayton A. Wiley ◽  
Richard A. Steinman ◽  
Yi Sheng ◽  
Beihong Ji ◽  
...  
Keyword(s):  
Rna Sequencing ◽  
Rna Editing ◽  
Mouse Brain ◽  
Mutant Mouse ◽  
Cell Types ◽  
Mutant Mice ◽  
Blue Staining ◽  
Sequencing Analysis ◽  
Elevated Type ◽  
The Brain

Abstract Background Aicardi-Goutières syndrome (AGS) is a severe infant or juvenile-onset autoimmune disease characterized by inflammatory encephalopathy with an elevated type 1 interferon-stimulated gene (ISG) expression signature in the brain. Mutations in seven different protein-coding genes, all linked to DNA/RNA metabolism or sensing, have been identified in AGS patients, but none of them has been demonstrated to activate the IFN pathway in the brain of an animal. The molecular mechanism of inflammatory encephalopathy in AGS has not been well defined. Adenosine Deaminase Acting on RNA 1 (ADAR1) is one of the AGS-associated genes. It carries out A-to-I RNA editing that converts adenosine to inosine at double-stranded RNA regions. Whether an AGS-associated mutation in ADAR1 activates the IFN pathway and causes autoimmune pathogenesis in the brain is yet to be determined. Methods Mutations in the ADAR1 gene found in AGS patients were introduced into the mouse genome via CRISPR/Cas9 technology. Molecular activities of the specific p.K999N mutation were investigated by measuring the RNA editing levels in brain mRNA substrates of ADAR1 through RNA sequencing analysis. IFN pathway activation in the brain was assessed by measuring ISG expression at the mRNA and protein level through real-time RT-PCR and Luminex assays, respectively. The locations in the brain and neural cell types that express ISGs were determined by RNA in situ hybridization (ISH). Potential AGS-related brain morphologic changes were assessed with immunohistological analysis. Von Kossa and Luxol Fast Blue staining was performed on brain tissue to assess calcification and myelin, respectively. Results Mice bearing the ADAR1 p.K999N were viable though smaller than wild type sibs. RNA sequencing analysis of neuron-specific RNA substrates revealed altered RNA editing activities of the mutant ADAR1 protein. Mutant mice exhibited dramatically elevated levels of multiple ISGs within the brain. RNA ISH of brain sections showed selective activation of ISG expression in neurons and microglia in a patchy pattern. ISG-15 mRNA was upregulated in ADAR1 mutant brain neurons whereas CXCL10 mRNA was elevated in adjacent astroglia. No calcification or gliosis was detected in the mutant brain. Conclusions We demonstrated that an AGS-associated mutation in ADAR1, specifically the p.K999N mutation, activates the IFN pathway in the mouse brain. The ADAR1 p.K999N mutant mouse replicates aspects of the brain interferonopathy of AGS. Neurons and microglia express different ISGs. Basal ganglia calcification and leukodystrophy seen in AGS patients were not observed in K999N mutant mice, indicating that development of the full clinical phenotype may need an additional stimulus besides AGS mutations. This mutant mouse presents a robust tool for the investigation of AGS and neuroinflammatory diseases including the modeling of potential “second hits” that enable severe phenotypes of clinically variable diseases.

Clinical significance of acetylcholinesterase activity in brain tumors

2021 ◽  
Vol 66 (12) ◽  
pp. 718-721
Author(s):  
Larisa Mikhailovna Obukhova ◽  
I. A. Medyanik ◽  
K. N. Kontorshchikova ◽  
S. A. Simagina ◽  
L. T. Musaelyan ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Clinical Significance ◽  
Whole Blood ◽  
Tumor Tissue ◽  
Acetylcholinesterase Activity ◽  
Bioinformatic Analysis ◽  
Acetyl Cholinesterase ◽  
Primary Tumors ◽  
Grade Ii ◽  
The Brain

It has been established that the non-neuronal cholinergic system is related to the oncogenesis which increases the attractiveness of its components as the promising markers of oncologic diseases. The purpose of this work is to evaluate the clinical significance of the analysis of the activity of acetyl cholinesterase as a new marker of gliomas. The activity of acetyl cholinesterase was assessed by photo colorimetric analysis according to the Hestrin method recalculating the activity of the enzyme in the tumor tissue per 1 g of protein, and in the blood - by 0.1 g of hemoglobin. The data obtained in the primary tumors of the brain (28) in the tissue of the brain of persons who died as a result of injury (6) and in whole blood of patients with gliomas (28) and practically healthy people (10) were compared with the use of a number of statistical programs. A significant decrease in the activity of acetyl cholinesterase in tumor tissue and in whole blood is revealed as the degree of anaplasia of tumors increases, starting with Grade II. It is for the first time that a significant direct correlation was noted showing the consistency between the decrease in the activity of acetyl cholinesterase in the tumor tissue of the brain and blood. Bioinformatic analysis showed the connection of the enzyme of acetyl cholinesterase with proteins of the PI3K-AKT and Notch signaling pathways providing antiapoptotic and proliferative effects. The found dependences provide new insights into understanding of the mechanisms of gliomas genesis and can be used for selection of new diagnostic markers of brain tumors.

scholarly journals Biomarker Effects in Carassius auratus Exposure to Ofloxacin, Sulfamethoxazole and Ibuprofen

2019 ◽  
Vol 16 (9) ◽  
pp. 1628 ◽  
Author(s):  
Xiaofan Yang ◽  
Xiaoping Xu ◽  
Xueyu Wei ◽  
Jie Wan ◽  
Yu Zhang
Keyword(s):  
Ache Activity ◽  
Carassius Auratus ◽  
Crucian Carp ◽  
Hazard Quotient ◽  
Acetylcholinesterase Activity ◽  
Response To Treatment ◽  
Aquatic Environments ◽  
Combined Effects ◽  
Adverse Impacts ◽  
The Brain

Ofloxacin, sulfamethoxazole and ibuprofen are three commonly used drugs which can be detected in aquatic environments. To assess their ecotoxicity, the effects of these three pharmaceuticals and their mixture on AChE (acetylcholinesterase) activity in the brain, and EROD (7-ethoxyresorufin-O-deethylase) and SOD (superoxide dismutase) activities in the liver of the freshwater crucian carp Carassius auratus were tested after exposure for 1, 2, 4 and 7 days. The results showed that treatments with 0.002–0.01 mg/L ofloxacin and 0.0008–0.004 mg/L sulfamethoxazole did not significantly change AChE, EROD and SOD activities. AChE activity was significantly inhibited in response to treatment with >0.05mg/L ofloxacin and >0.02 mg/L sulfamethoxazole. All three biomarkers were induced significantly in treatments with ibuprofen and the mixture of the three pharmaceuticals at all the tested concentrations. The combined effects of ofloxacin, sulfamethoxazole and ibuprofen were compared with their isolated effects on the three biomarkers, and the results indicated that exposure to ibuprofen and the mixture at environmentally relevant concentrations could trigger adverse impacts on Carassius auratus. The hazard quotient (HQ) index also demonstrated a high risk for ibuprofen. Moreover, the present study showed that the effects of ofloxacin, sulfamethoxazole and ibuprofen might be additive on the physiological indices of Carassius auratus.

Characterization of novel dystonia musculorum mutant mice: Implications for central nervous system abnormality

2016 ◽  
Vol 96 ◽  
pp. 271-283 ◽  
Author(s):  
Masao Horie ◽  
Kazuyuki Mekada ◽  
Hiromi Sano ◽  
Yoshiaki Kikkawa ◽  
Satomi Chiken ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mutant Mice ◽  
Dystonia Musculorum

scholarly journals Walnut Oil Prevents Scopolamine-Induced Memory Dysfunction in a Mouse Model

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1630
Author(s):  
Jianqiao Liao ◽  
Yifan Nai ◽  
Li Feng ◽  
Yimeng Chen ◽  
Mei Li ◽  
...  
Keyword(s):  
Body Weight ◽  
Memory Impairment ◽  
Acetylcholinesterase Activity ◽  
Walnut Oil ◽  
Histological Changes ◽  
Hippocampal Ca1 ◽  
Malondialdehyde Content ◽  
Wet Weight ◽  
The Brain ◽  
Total Superoxide Dismutase

For thousands of years, it has been widely believed that walnut is a kind of nut that has benefits for the human body. Walnut oil, accounting for about 70% of walnut, mainly consists of polyunsaturated fatty acids. To investigate the effect of walnut oil on memory impairment in mice, scopolamine (3 mg/kg body weight/d) was used to establish the animal model during Morris Water Maze (MWM) tests. Walnut oil was administrated orally at 10 mL/kg body weight/d for 8 consecutive weeks. The results showed that walnut oil treatment ameliorated the behavior of the memory-impaired mice in the MWM test. Additionally, walnut oil obviously inhibited acetylcholinesterase activity (1.26 ± 0.12 U/mg prot) (p = 0.013) and increased choline acetyltransferase activity (129.75 ± 6.76 U/mg tissue wet weight) in the brains of scopolamine-treated mice (p = 0.024), suggesting that walnut oil could prevent cholinergic function damage in mice brains. Furthermore, walnut oil remarkably prevented the decrease in total superoxide dismutase activity (93.30 ± 5.50 U/mg prot) (p = 0.006) and glutathione content (110.45 ± 17.70 mg/g prot) (p = 0.047) and the increase of malondialdehyde content (13.79 ± 0.96 nmol/mg prot) (p = 0.001) in the brain of scopolamine-treated mice, indicating that walnut oil could inhibit oxidative stress in the brain of mice. Furthermore, walnut oil prevented histological changes of neurons in hippocampal CA1 and CA3 regions induced by scopolamine. These findings indicate that walnut oil could prevent memory impairment in mice, which might be a potential way for the prevention of memory dysfunctions.

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