>
Chemicals & Drugs
>
Organic Chemical
>
Cuprizone
Cuprizone
Cuprizone is a copper chelating agent used to induce demyelination and serve as an animal model for multiple sclerosis research.
It is typically administered to rodents through the diet, leading to oligodendrocyte death and subsequent myelin loss in the central nervous system.
Cuprizone-induced demyelination is a well-established model that has contributed to our understanding of the mechanisms underlying myelin damage and repair.
Researchers can optimize their Cuprizone studies with PubCompare.ai, an AI-powered platform that enhances reproducibility and accuracy by helping scientists easily locate relevant protocols from literature, pre-prints, and patents, while leveraging AI-driven comparisons to identify the best protocols and products.
Streamlien your Cuprizone reseach and improve your results with this powerful tool.
It is typically administered to rodents through the diet, leading to oligodendrocyte death and subsequent myelin loss in the central nervous system.
Cuprizone-induced demyelination is a well-established model that has contributed to our understanding of the mechanisms underlying myelin damage and repair.
Researchers can optimize their Cuprizone studies with PubCompare.ai, an AI-powered platform that enhances reproducibility and accuracy by helping scientists easily locate relevant protocols from literature, pre-prints, and patents, while leveraging AI-driven comparisons to identify the best protocols and products.
Streamlien your Cuprizone reseach and improve your results with this powerful tool.
Most cited protocols related to «Cuprizone»
Animal Model
Benztropine
Cell Culture Techniques
Cells
Condoms
Cuprizone
Immunoglobulins
Mice, Inbred C57BL
Mus
Optic Nerve
Pharmaceutical Preparations
Saline Solution
Spinal Cord
Therapeutics
Treatment Protocols
Woman
Cuprizone ingestion results in a reproducible pattern of extensive corpus callosum demyelination (12, 13 (link)). Cuprizone treatment was started at 8 weeks of age and only male mice were used. Cuprizone (0.2% (w/w), finely powdered oxalic bis(cyclohexylidenehydrazide) (Sigma-Aldrich, St. Louis, MO), was thoroughly mixed into chow (diet TD.01453; Harlan Teklad, Madison, WI), which was available ad libitum. Mice were maintained on the cuprizone diet until perfused for analysis or returned to normal chow after 6 weeks or 12 weeks of cuprizone ingestion.
Corpus Callosum
Cuprizone
Demyelination
Diet
Males
Mice, Laboratory
Animals
Animals, Laboratory
Cuprizone
Demyelination
Diet
Eating
Food
Males
Mice, House
Pellets, Drug
Remyelination
Rodent
Vacuum
Images of in situ hybridization and immunostaining results were captured with a Spot 2 CCD digital camera using Spot Advanced image acquisition software (Diagnostic Instruments, Sterling Heights, MI) on an Olympus IX-70 microscope. Images were prepared as panels using Adobe Photoshop (San Jose, CA).
For comparing cell densities, all quantification was performed by an investigator blinded to the treatment condition. Cells expressing PLP mRNA were quantified using unbiased stereologic morphometric analysis (12 (link)) (Stereologer System from Systems Planning and Analysis, Inc., Alexandria, VA). Analysis was restricted to the corpus callosum region from the midline and extending laterally to below the cingulum in 15-μm-thick coronal sections. Using the Stereologer System, the specimen thickness contributes to the sampled volume so that measurements reflect cells/mm3. The unbiased stereologic method could not be used appropriately for conditions with relatively few cells of interest in any chosen category. Therefore, quantification of cells in the corpus callosum expressing PDGFαR or Ki-67 required counting all labeled cells and using the Spot 2 CCD camera and software to measure the area sampled, resulting in density units of cells/mm2 (12 (link)).
Quantification of corpus callosum myelination was estimated from MOG immunofluorescence detected with a Spot 2 CCD camera. Using Metamorph software, pixel intensity values were normalized between sections by thresholding to exclude values below the level of immunoreactivity in the dorsal fornix, which was selected as an adjacent white matter tract that is not demyelinated by cuprizone. The percent area of the corpus callosum (midline bilaterally to a point under the cingulum apex) with MOG immunoreactivity above the threshold level was then used as an estimate of the myelinated area.
Each category analyzed included three or more tissue sections per mouse and three or more mice per condition, except where larger sample sizes are noted in text and/or figure legends. One-way analysis of variance (ANOVA) with post hoc Tukey's multiple comparison test was used to determine significant differences among stages of disease progression or treatment. Unpaired Student t-test was used to compare between FGF2 genotypes in nonlesioned mice. Significance of an FGF2 genotype effect across multiple treatment conditions was calculated using a two-way ANOVA. No statistical comparisons were made between mice with different genetic backgrounds (i.e. C57Bl/6 mice and FGF2 mice).
For comparing cell densities, all quantification was performed by an investigator blinded to the treatment condition. Cells expressing PLP mRNA were quantified using unbiased stereologic morphometric analysis (12 (link)) (Stereologer System from Systems Planning and Analysis, Inc., Alexandria, VA). Analysis was restricted to the corpus callosum region from the midline and extending laterally to below the cingulum in 15-μm-thick coronal sections. Using the Stereologer System, the specimen thickness contributes to the sampled volume so that measurements reflect cells/mm3. The unbiased stereologic method could not be used appropriately for conditions with relatively few cells of interest in any chosen category. Therefore, quantification of cells in the corpus callosum expressing PDGFαR or Ki-67 required counting all labeled cells and using the Spot 2 CCD camera and software to measure the area sampled, resulting in density units of cells/mm2 (12 (link)).
Quantification of corpus callosum myelination was estimated from MOG immunofluorescence detected with a Spot 2 CCD camera. Using Metamorph software, pixel intensity values were normalized between sections by thresholding to exclude values below the level of immunoreactivity in the dorsal fornix, which was selected as an adjacent white matter tract that is not demyelinated by cuprizone. The percent area of the corpus callosum (midline bilaterally to a point under the cingulum apex) with MOG immunoreactivity above the threshold level was then used as an estimate of the myelinated area.
Each category analyzed included three or more tissue sections per mouse and three or more mice per condition, except where larger sample sizes are noted in text and/or figure legends. One-way analysis of variance (ANOVA) with post hoc Tukey's multiple comparison test was used to determine significant differences among stages of disease progression or treatment. Unpaired Student t-test was used to compare between FGF2 genotypes in nonlesioned mice. Significance of an FGF2 genotype effect across multiple treatment conditions was calculated using a two-way ANOVA. No statistical comparisons were made between mice with different genetic backgrounds (i.e. C57Bl/6 mice and FGF2 mice).
Cells
Corpus Callosum
Cuprizone
Diagnosis
Disease Progression
Fibroblast Growth Factor 2
Fingers
Fornix, Brain
Genetic Background
Genotype
Immunofluorescence
In Situ Hybridization
Mice, Inbred C57BL
Microscopy
Mus
RNA, Messenger
Student
Tissues
White Matter
PMP were collected from supernatant and suspended as single cells at a final concentration of 100,000 cells per μl in PBS. The cells were then injected into the brains of P0 Rag2−/−hCSF1 immunodeficient mice (C;129S4-Rag2tm1.1FlvCsf1tm1(CSF1)FlvIl2rgtm1.1Flv/J, The Jackson Laboratory). The precise transplantation sites were bilateral from the midline = ±1.0 mm, posterior bregma = −2.0 mm, and dorsoventral depth = −1.5 and −1.2 mm (Fig. 1c ). The mouse pups were placed on ice for 5 min to anesthetize. The pups were injected with 0.5 μl of cells into each site (total four sites), using a digital stereotaxic device (David KOPF Instruments) that was equipped with a neonatal mouse adapter (Stoelting)16 (link). The pups were weaned at 3 weeks and were kept up to 6 months. All animal work was performed without gender bias with approval of the Rutgers University Institutional Animal Care and Use Committee.
Both hiPSC- and hESC-derived PMPs were transplanted into mouse brains. Both engrafted hiPSC- and hESC-derived microglia were analyzed, including characterization of their marker expression (Fig.1 ), morphological changes along brain development (Fig. 2 ), and their phagocytic functions under homeostatic condition (Fig. 3 ), as well as toxin-induced demyelination condition (Fig. 6 ). For the quantification, we pooled the data collected from both hiPSC- and hESC-derived microglia. In the single-cell RNA-sequencing experiment, we only used the animals received transplantation of hiPSC-derived microglia. For cuprizone-induced demyelination, 3-month-old chimeric mice were fed with cuprizone diet (Sigma-Aldrich, 0.2%) or control diet for 4 weeks.
Both hiPSC- and hESC-derived PMPs were transplanted into mouse brains. Both engrafted hiPSC- and hESC-derived microglia were analyzed, including characterization of their marker expression (Fig.
Full text: Click here
Animals
Brain
Cells
Chimera
CSF1 protein, human
Cuprizone
Demyelination
Diet
Fingers
Homeostasis
Human Embryonic Stem Cells
Human Induced Pluripotent Stem Cells
Immunologic Deficiency Syndromes
Infant, Newborn
Institutional Animal Care and Use Committees
Medical Devices
Microglia
Mus
Phagocytes
RAG2 protein, human
Toxins, Biological
Transplantation
Most recents protocols related to «Cuprizone»
The 8–10 week old mice were fed with a standard rodent chow with 0.25% (w/w) cuprizone (bis (cycloheanone) oxaldihydrazone; Sigma) for 5 weeks to induce the demyelination in mouse brains, followed by the switch to the normal chow for 2 additional weeks to allow the recovery from demyelination. The cuprizone-induced demyelinated or remyelinated mice were anesthetized, perfused with PBS, followed by fixation with 4% PFA. The whole mouse brains were removed, post-fixed, sectioned at 30 μm using a vibratome, and subjected for the oil-red O staining, immunohistochemical analysis and electron microcopy analysis. In consideration of the cuprizone induced lesions are in the variability in lesion size and location, the corresponding section every ten serial coronal sections in the corpus callosum of mice was selected and 6–8 sections in one brain were stained for analysis. For the motor coordination assessment, the 8–10 week old mice first received a training of running on a rotating rod at an accelerating speed from 4 to 40 rotations per min for 300 s for 1 week (Harvard apparatus, UK). The mice that could still stay on the rotating cylinder at a speed of 4 rotations/min for 300 s were used for the following motor coordination analysis. The latency to fall off a rotating rod at a speed of 4 rotations/min and the body weight of each mouse were measured every 3 days during the 5 weeks’ cuprizone chow feeding and following 2 weeks’ normal chow feeding.
Full text: Click here
Body Weight
Brain
Corpus Callosum
Cuprizone
Demyelination
Electrons
Mice, House
Rodent
Ten-week-old mice were subjected to nutragel (Bio-Serv) ad libitum containing 0.2% cuprizone (Sigma) for 6 weeks.
Full text: Click here
Cuprizone
Mice, Laboratory
Images were collected on a Zeiss LSM 800 completed system confocal imager. Quantification of immunostaining was done by 1 or 2 blinded investigators using the ImageJ cell counter manually. For corpus callosum imaging, one medial and two lateral images of corpus callosum and cingulum were taken from 3 or 4 sections per slide (n = 3). For motor cortex imaging, a minimum of four images were analyzed from 3 animals. For spinal cord demyelinating lesions, the lesion was located by visualizing the accumulation of Hoechst-positive nuclei within the ventral white matter. A minimum of three lesion sections from 3 mice were analyzed for cell density. For cuprizone, three regions from four sections per animal were analyzed (n = 4). Density per square millimeter was calculated in Microsoft Excel as previously described by Chamberlain et al. (2017) (link). All statistics were performed using Prism. Data are expressed as mean ± SEM. Comparisons were analyzed by two-way ANOVA with Sidak's multiple comparison test, one-way ANOVA with Tukey's multiple comparison test, or two-tailed t test. Diagrams were generated using Mind The Graph.
Full text: Click here
Animals
Cell Nucleus
Cells
Corpus Callosum
Cuprizone
Motor Cortex
Mus
neuro-oncological ventral antigen 2, human
prisma
Spinal Cord
Vaginal Diaphragm
White Matter
All animals were fed a creatine-deficient amino acid diet (Envigo; TD.01084) unless otherwise specified. Demyelination was induced in 8-week-old male and female mice by adding 0.2% cuprizone (bis(cyclohexanone)oxaldihydrazone) into normal chow (LabDiet 5053) or creatine-deficient diet for 5 weeks. Cuprizone diet was replaced every 3 d to prevent stability concerns. All recovery diets used TD.01084 and added creatine or cyclocreatine (Sigma). Recovery diets after cuprizone were one of the following: normal chow, creatine-deficient diet, 2% creatine, or 0.1% cyclocreatine. Animals were weighed once every 2 d to ensure animals did not lose more than 10% body weight.
Full text: Click here
Amino Acids
Animals
Body Weight
Creatine
Cuprizone
cyclocreatine
cyclohexanone
Demyelination
Diet
Females
Males
Mice, House
Eight-week-old C57BL/6 J, Trem2em1Aduci (i.e. Trem2R47H NSS), Trem2em1Adiuj (i.e. Trem2R47H CSS), and Trem2em2Adiuj (i.e. Trem2-KO) mice (Jackson Laboratory stock number: 000664, 034,036, 027,918, 027,197 respectively) were used. Each mouse model consisted of 2 groups of 4 male mice. Control mice were supplied standard chow for 6 weeks while the CPZ groups were fed 0.3% cuprizone chow also for 6 weeks (Envigo, Indianapolis, IN). Mice within the same experiment group (i.e., same genotype and diet) were housed together for the duration of feeding. Weights of individual mouse and chow consumptions of each cage were recorded, and chow was changed every 3 or 4 days to monitor expected weight loss as well as ensuring freshness of cuprizone chow. Brains were collected and fixed in 4% paraformaldehyde for 24 h followed by cryoprotection by immersion in 5% sucrose for 24 h then 30% sucrose for 5 days, all at 4 °C.
Full text: Click here
Brain
Cuprizone
Diet
Genotype
Men
Mice, House
paraform
Submersion
Sucrose
TREM2 protein, human
Top products related to «Cuprizone»
Sourced in United States, Germany, Macao, China
Cuprizone is a laboratory equipment product manufactured by Merck Group. It is a chemical compound that is primarily used in research applications. The core function of Cuprizone is to induce demyelination in animal models, which is a condition where the protective myelin sheath around nerve fibers is damaged or lost.
Sourced in United States, Germany, Sao Tome and Principe, United Kingdom, Switzerland, Macao, China, Australia, Canada, Japan, Spain, Belgium, France, Italy, New Zealand, Denmark
Tamoxifen is a drug used in the treatment of certain types of cancer, primarily breast cancer. It is a selective estrogen receptor modulator (SERM) that can act as both an agonist and antagonist of the estrogen receptor. Tamoxifen is used to treat and prevent breast cancer in both men and women.
Sourced in United States
Bis-cyclohexanone oxaldihydrazone is a chemical compound used as a laboratory reagent. It functions as a chelating agent, capable of forming stable complexes with various metal ions.
Sourced in United States
Cuprizone is a chemical compound used in research applications. It is a copper-chelating agent that has been shown to induce demyelination in the central nervous system of rodents. The product is primarily used in the study of animal models of multiple sclerosis and other neurodegenerative diseases.
Sourced in United States, Montenegro, Canada, China, France, United Kingdom, Japan, Germany
C57BL/6 mice are a widely used inbred mouse strain commonly used in biomedical research. They are known for their black coat color and are a popular model organism due to their well-characterized genetic and physiological traits.
Sourced in United States
Cuprizone (CPZ) is a laboratory chemical compound primarily used in research applications. It serves as a tool for researchers to induce demyelination in animal models, particularly in the study of multiple sclerosis and other demyelinating disorders. Cuprizone functions by disrupting the process of myelin sheath formation in the central nervous system, leading to the loss of myelin. This property makes it a valuable resource for researchers investigating the mechanisms and potential treatments related to demyelination.
Sourced in United States, United Kingdom, Germany, Macao
Luxol fast blue is a staining dye commonly used in histological and neuroanatomical research. It is a soluble copper-based dye that selectively stains the myelin sheath of nerve fibers, allowing for the visualization and analysis of the myelination in tissue samples.
Sourced in United States, China
The C57BL/6 mouse is a widely used inbred strain that serves as a standard laboratory mouse model. It is a common control strain in many studies due to its well-characterized genetic background. These mice can be used for a variety of research applications, including but not limited to immunology, neuroscience, and metabolic studies.
Sourced in United States
Cuprizone is a laboratory chemical compound used in scientific research. It is a copper chelator that has been utilized in various studies, particularly in the field of neuroscience. The core function of Cuprizone is to induce demyelination, a process in which the protective myelin sheath surrounding nerve fibers is damaged or removed. This research tool is commonly employed to create animal models for the study of demyelinating diseases, such as multiple sclerosis.
Sourced in United States
Cuprizone (bis-cyclohexanone oxaldihydrazone) is a chemical compound used in laboratory research. It is a copper chelator, capable of binding and sequestering copper ions. The primary function of Cuprizone is to facilitate the study of demyelination and remyelination processes in various experimental models.
More about "Cuprizone"
Cuprizone is a copper chelating agent commonly used in animal models to study demyelination, a hallmark of multiple sclerosis (MS) and other neurological disorders.
When administered to rodents, typically through the diet, Cuprizone leads to the death of oligodendrocytes, the cells responsible for the production and maintenance of myelin in the central nervous system (CNS).
This Cuprizone-induced demyelination model has been instrumental in advancing our understanding of the mechanisms underlying myelin damage and repair, providing valuable insights for MS research.
To optimize Cuprizone studies and improve reproducibility, researchers can leverage the power of PubCompare.ai, an AI-powered platform that enhances research efficiency.
PubCompare.ai helps scientists easily locate relevant protocols from literature, preprints, and patents, while utilizing AI-driven comparisons to identify the best protocols and products for their Cuprizone experiments.
By streamlining the research process and leveraging the latest advancements in protocol optimization, PubCompare.ai empowers researchers to enhance the accuracy and reproducibility of their Cuprizone-related studies.
In addition to Cuprizone, other chemical agents like Tamoxifen and Bis-cyclohexanone oxaldihydrazone (also known as Cuprizone or CPZ) have been used to induce demyelination in animal models.
Furthermore, the C57BL/6 mouse strain is commonly utilized in Cuprizone studies due to its susceptibility to Cuprizone-induced demyelination.
Researchers may also employ Luxol fast blue staining to visualize and quantify myelin loss in the CNS during Cuprizone experiments.
By harnessing the insights gained from the Cuprizone model and leveraging the capabilities of PubCompare.ai, scientists can streamline their research, improve their results, and contribute to the advancement of our understanding of demyelinating diseases like multiple scleraosis.
When administered to rodents, typically through the diet, Cuprizone leads to the death of oligodendrocytes, the cells responsible for the production and maintenance of myelin in the central nervous system (CNS).
This Cuprizone-induced demyelination model has been instrumental in advancing our understanding of the mechanisms underlying myelin damage and repair, providing valuable insights for MS research.
To optimize Cuprizone studies and improve reproducibility, researchers can leverage the power of PubCompare.ai, an AI-powered platform that enhances research efficiency.
PubCompare.ai helps scientists easily locate relevant protocols from literature, preprints, and patents, while utilizing AI-driven comparisons to identify the best protocols and products for their Cuprizone experiments.
By streamlining the research process and leveraging the latest advancements in protocol optimization, PubCompare.ai empowers researchers to enhance the accuracy and reproducibility of their Cuprizone-related studies.
In addition to Cuprizone, other chemical agents like Tamoxifen and Bis-cyclohexanone oxaldihydrazone (also known as Cuprizone or CPZ) have been used to induce demyelination in animal models.
Furthermore, the C57BL/6 mouse strain is commonly utilized in Cuprizone studies due to its susceptibility to Cuprizone-induced demyelination.
Researchers may also employ Luxol fast blue staining to visualize and quantify myelin loss in the CNS during Cuprizone experiments.
By harnessing the insights gained from the Cuprizone model and leveraging the capabilities of PubCompare.ai, scientists can streamline their research, improve their results, and contribute to the advancement of our understanding of demyelinating diseases like multiple scleraosis.