Journal articles: 'Mouse brain'

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Calamante, F. "Mouse Brain Kaleidoscope." Neurology 79, no. 17 (October 22, 2012): 1829. http://dx.doi.org/10.1212/wnl.0b013e318270d956.

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Brenner, S. R., F. Calamante, and R. A. Gross. "Mouse Brain Kaleidoscope." Neurology 80, no. 18 (April 29, 2013): 1720. http://dx.doi.org/10.1212/wnl.0b013e318292aa30.

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Melozzi, Francesca, Eyal Bergmann, Julie A. Harris, Itamar Kahn, Viktor Jirsa, and Christophe Bernard. "Individual structural features constrain the mouse functional connectome." Proceedings of the National Academy of Sciences 116, no. 52 (December 11, 2019): 26961–69. http://dx.doi.org/10.1073/pnas.1906694116.

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Whole brain dynamics intuitively depend upon the internal wiring of the brain; but to which extent the individual structural connectome constrains the corresponding functional connectome is unknown, even though its importance is uncontested. After acquiring structural data from individual mice, we virtualized their brain networks and simulated in silico functional MRI data. Theoretical results were validated against empirical awake functional MRI data obtained from the same mice. We demonstrate that individual structural connectomes predict the functional organization of individual brains. Using a virtual mouse brain derived from the Allen Mouse Brain Connectivity Atlas, we further show that the dominant predictors of individual structure–function relations are the asymmetry and the weights of the structural links. Model predictions were validated experimentally using tracer injections, identifying which missing connections (not measurable with diffusion MRI) are important for whole brain dynamics in the mouse. Individual variations thus define a specific structural fingerprint with direct impact upon the functional organization of individual brains, a key feature for personalized medicine.

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Le Bras, Alexandra. "The mouse brain lipidome." Lab Animal 49, no. 11 (October 20, 2020): 313. http://dx.doi.org/10.1038/s41684-020-00678-8.

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Allan Johnson, G., Nian Wang, Robert J. Anderson, Min Chen, Gary P. Cofer, James C. Gee, Forrest Pratson, Nicholas Tustison, and Leonard E. White. "Whole mouse brain connectomics." Journal of Comparative Neurology 527, no. 13 (November 23, 2018): 2146–57. http://dx.doi.org/10.1002/cne.24560.

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Jaeger, Christian, Enrico Glaab, Alessandro Michelucci, Tina M. Binz, Sandra Koeglsberger, Pierre Garcia, Jean-Pierre Trezzi, Jenny Ghelfi, Rudi Balling, and Manuel Buttini. "The Mouse Brain Metabolome." American Journal of Pathology 185, no. 6 (June 2015): 1699–712. http://dx.doi.org/10.1016/j.ajpath.2015.02.016.

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Lee, Hwa Jeong, Yun Zhang, Chunni Zhu, Karen Duff, and William M. Pardridge. "Imaging Brain Amyloid of Alzheimer Disease in Vivo in Transgenic Mice with an Aβ Peptide Radiopharmaceutical." Journal of Cerebral Blood Flow & Metabolism 22, no. 2 (February 2002): 223–31. http://dx.doi.org/10.1097/00004647-200202000-00010.

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Aβ1–40 is a potential peptide radiopharmaceutical that could be used to image the brain Aβ amyloid of Alzheimer disease in vivo, should this peptide be made transportable through the blood–brain barrier in vivo. The blood–brain barrier transport of [125I]-Aβ1–40 in a transgenic mouse model was enabled by conjugation to the rat 8D3 monoclonal antibody to the mouse transferrin receptor. The Aβ1–40–8D3 conjugate is a bifunctional molecule that binds the blood–brain barrier TfR and undergoes transport into brain and binds the Aβ amyloid plaques of Alzheimer disease. App SW/ Psen1 double-transgenic and littermate control mice were administered either unconjugated Aβ1–40 or the Aβ1–40–8D3 conjugate intravenously, and brain scans were obtained 6 hours later. Immunocytochemical analysis showed abundant Aβ immunoreactive plaques in the brains of the App SW/ Psen1 transgenic mice and there was a selective retention of radioactivity in the brains of these mice at 6 hours after intravenous administration of the conjugate. In contrast, there was no selective sequestration either of the conjugate in control littermate mouse brain or of unconjugated Aβ1–40 in transgenic mouse brain. In conclusion, the results show that it is possible to image the Aβ amyloid burden in the brain in vivo with an amyloid imaging agent, provided the molecule is conjugated to a blood–brain barrier drug-targeting system.

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Rehman, Shafiq, Muhammad Ikram, Najeeb Ullah, Sayed Alam, Hyun Park, Haroon Badshah, Kyonghwan Choe, and Myeong Ok Kim. "Neurological Enhancement Effects of Melatonin against Brain Injury-Induced Oxidative Stress, Neuroinflammation, and Neurodegeneration via AMPK/CREB Signaling." Cells 8, no. 7 (July 21, 2019): 760. http://dx.doi.org/10.3390/cells8070760.

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Oxidative stress and energy imbalance strongly correlate in neurodegenerative diseases. Repeated concussion is becoming a serious public health issue with uncontrollable adverse effects in the human population, which involve cognitive dysfunction and even permanent disability. Here, we demonstrate that traumatic brain injury (TBI) evokes oxidative stress, disrupts brain energy homeostasis, and boosts neuroinflammation, which further contributes to neuronal degeneration and cognitive dysfunction in the mouse brain. We also demonstrate that melatonin (an anti-oxidant agent) treatment exerts neuroprotective effects, while overcoming oxidative stress and energy depletion and reducing neuroinflammation and neurodegeneration. Male C57BL/6N mice were used as a model for repetitive mild traumatic brain injury (rmTBI) and were treated with melatonin. Protein expressions were examined via Western blot analysis, immunofluorescence, and ELISA; meanwhile, behavior analysis was performed through a Morris water maze test, and Y-maze and beam-walking tests. We found elevated oxidative stress, depressed phospho-5′AMP-activated protein kinase (p-AMPK) and phospho- CAMP-response element-binding (p-CREB) levels, and elevated p-NF-κB in rmTBI mouse brains, while melatonin treatment significantly regulated p-AMPK, p-CREB, and p-NF-κB in the rmTBI mouse brain. Furthermore, rmTBI mouse brains showed a deregulated mitochondrial system, abnormal amyloidogenic pathway activation, and cognitive functions which were significantly regulated by melatonin treatment in the mice. These findings provide evidence, for the first time, that rmTBI induces brain energy imbalance and reduces neuronal cell survival, and that melatonin treatment overcomes energy depletion and protects against brain damage via the regulation of p-AMPK/p-CREB signaling pathways in the mouse brain.

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Chanderkar, L. P., W. K. Paik, and S. Kim. "Studies on myelin-basic-protein methylation during mouse brain development." Biochemical Journal 240, no. 2 (December 1, 1986): 471–79. http://dx.doi.org/10.1042/bj2400471.

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The synthesis and methylation in vivo of myelin basic protein (MBP) during the mouse brain development has been investigated. When mice ranging in age from 13 to 60 days were injected intracerebrally with L-[methyl-3H]methionine, the incorporation of radioactivity into MBP isolated from youngest brain was found to be the highest and declined progressively in mature brains. This pattern of radioactivity incorporation was inversely correlated with the total amount of MBP in the brains, suggesting a higher ratio of MBP methylation to synthesis in younger brain. To differentiate the relative rate of protein synthesis and methylation, animals were given intracerebral injections of a L-[methyl-3H]methionine and L-[35S]methionine mixture and the ratio of 3H/35S (methylation index) was determined. The ratios in the isolated MBP fractions were higher than those of ‘acid extracts’ and ‘breakthrough’ fractions, with a maximal ratio in the youngest brain. This high ratio was well correlated with the higher protein methylase I (PMI) activity in younger brains. The MBP fractions were further separated on SDS/polyacrylamide-gel electrophoresis into several species with apparent Mr ranging from 32,400 to 14,500. The results indicated that each protein species accumulated at a characteristic rate as a function of age. The high-Mr (32,400) species was predominant in younger brain, whereas the smaller MBP was the major species in older brain tissue. The importance of this developmental pattern of MBP synthesis and methylation is discussed in relation to PMI activity.

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O'Connor, Daniel H., Daniel Huber, and Karel Svoboda. "Reverse engineering the mouse brain." Nature 461, no. 7266 (October 2009): 923–29. http://dx.doi.org/10.1038/nature08539.

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Fitzgerald, Richard J. "A microscale mouse-brain model." Physics Today 72, no. 10 (October 1, 2019): 76. http://dx.doi.org/10.1063/pt.3.4328.

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Boschi, Gabrielle, Nicole Launay, Richard Rips, and Jean-Michel Scherrmann. "Brain microdialysis in the mouse." Journal of Pharmacological and Toxicological Methods 33, no. 1 (February 1995): 29–33. http://dx.doi.org/10.1016/1056-8719(94)00054-8.

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13

Brill, David. "Mouse brain map is complete." Nature 443, no. 7110 (September 2006): 380–81. http://dx.doi.org/10.1038/443380c.

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Desestret, Virginie, Olivier Pascual, and Jérôme Honnorat. "A mouse model of autoimmune encephalitis." Brain 138, no. 1 (December 29, 2014): 5–8. http://dx.doi.org/10.1093/brain/awu342.

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Melozzi, Francesca, Marmaduke M. Woodman, Viktor K. Jirsa, and Christophe Bernard. "The Virtual Mouse Brain: A Computational Neuroinformatics Platform to Study Whole Mouse Brain Dynamics." eneuro 4, no. 3 (May 2017): ENEURO.0111–17.2017. http://dx.doi.org/10.1523/eneuro.0111-17.2017.

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Zhang, Rujin, Chaowei Zhuang, Zilin Wang, Guihua Xiao, Kunsha Chen, Hao Li, Li Tong, Weidong Mi, Hao Xie, and Jiangbei Cao. "Simultaneous Observation of Mouse Cortical and Hippocampal Neural Dynamics under Anesthesia through a Cranial Microprism Window." Biosensors 12, no. 8 (July 26, 2022): 567. http://dx.doi.org/10.3390/bios12080567.

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The fluorescence microscope has been widely used to explore dynamic processes in vivo in mouse brains, with advantages of a large field-of-view and high spatiotemporal resolution. However, owing to background light and tissue scattering, the single-photon wide-field microscope fails to record dynamic neural activities in the deep brain. To achieve simultaneous imaging of deep-brain regions and the superficial cortex, we combined the extended-field-of-view microscopy previously proposed with a novel prism-based cranial window to provide a longitudinal view. As well as a right-angle microprism for imaging above 1 mm, we also designed a new rectangular-trapezoidal microprism cranial window to extend the depth of observation to 1.5 mm and to reduce brain injury. We validated our method with structural imaging of microglia cells in the superficial cortex and deep-brain regions. We also recorded neuronal activity from the mouse brains in awake and anesthesitized states. The results highlight the great potential of our methods for simultaneous dynamic imaging in the superficial and deep layers of mouse brains.

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Yao, Hui-Wen, and Chia-Yi Kuan. "Early neutrophil depletion reduces inflammation-sensitized hypoxic-ischemic brain injury in mouse neonates." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 102.10. http://dx.doi.org/10.4049/jimmunol.200.supp.102.10.

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Abstract Hypoxia-ischemia to brain triggers immune responses consisting of activation and recruitment of leukocytes and expression of pro-inflammatory mediators. Inducing neutropenia confers protection against cerebral ischemia in adult and neonatal rats, but it remains unclear if neutrophils enhances neonatal brain damage in inflammation (LPS)-sensitized hypoxic-ischemic (HI) insults to mice. Herein, we demonstrated that following LPS/HI insult, the mRNA expression of C-X-C motif ligands 1 and 2, two potent neutrophil chemoattractants, granulocyte colony-stimulating factor that stimulates the bone marrow to produce and release granulocytes, and pro-inflammatory cytokines, including interleukins 1β and 6 and tumor necrosis factor α, were increased in mouse brains. As early as six hours after insult, neutrophil infiltration was readily detectable in mouse brains and increased with time, especially in those brains with severe damage. Neutrophils either resided within vessel like structures or accumulated within brain parenchyma. In addition, infiltrated neutrophils expressed interleukin 1β and tumor necrosis factor α, as well as citrullinated histones, a marker of neutrophil extracellular traps, in the damaged brains. Importantly, prophylactic depletion of neutrophils from the periphery reduced leukocyte infiltration, the expression of pro-inflammatory mediators in mouse brains, and brain atrophy, whereas post-insult depletion of neutrophils conferred marginal protection. Collectively, our data support the pathogenic roles of neutrophils in the acute phase of inflammation-sensitized hypoxia-ischemia brain injury.

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De Pasquale, Valeria, Michele Costanzo, Rosa Siciliano, Maria Mazzeo, Valeria Pistorio, Laura Bianchi, Emanuela Marchese, Margherita Ruoppolo, Luigi Pavone, and Marianna Caterino. "Proteomic Analysis of Mucopolysaccharidosis IIIB Mouse Brain." Biomolecules 10, no. 3 (February 26, 2020): 355. http://dx.doi.org/10.3390/biom10030355.

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Mucopolysaccharidosis IIIB (MPS IIIB) is an inherited metabolic disease due to deficiency of α-N-Acetylglucosaminidase (NAGLU) enzyme with subsequent storage of undegraded heparan sulfate (HS). The main clinical manifestations of the disease are profound intellectual disability and neurodegeneration. A label-free quantitative proteomic approach was applied to compare the proteome profile of brains from MPS IIIB and control mice to identify altered neuropathological pathways of MPS IIIB. Proteins were identified through a bottom up analysis and 130 were significantly under-represented and 74 over-represented in MPS IIIB mouse brains compared to wild type (WT). Multiple bioinformatic analyses allowed to identify three major clusters of the differentially abundant proteins: proteins involved in cytoskeletal regulation, synaptic vesicle trafficking, and energy metabolism. The proteome profile of NAGLU−/− mouse brain could pave the way for further studies aimed at identifying novel therapeutic targets for the MPS IIIB. Data are available via ProteomeXchange with the identifier PXD017363.

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Nishimura, N., H. Nishimura, A. Ghaffar, and C. Tohyama. "Localization of metallothionein in the brain of rat and mouse." Journal of Histochemistry & Cytochemistry 40, no. 2 (February 1992): 309–15. http://dx.doi.org/10.1177/40.2.1552172.

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Metallothionein (MT) is a low molecular mass protein inducible by heavy metals such as cadmium (Cd), zinc, and copper, and having high affinity for these metals. In the present study, we investigated the immunohistological localization of MT in the brains of rats and mice. In adult rat brain, almost no MT immunostaining was observed, whereas in adult mouse brain strong MT immunostaining was found in the ependymal cells, some glial cells, arachnoid, and pia mater. No immunostaining was detected in neurons and endothelial cells. In younger rats (1-3 weeks old), strong MT immunostaining was observed in ependymal cells, choroid plexus epithelium, arachnoid, and pia mater. The overall MT concentration in adult mouse brain appeared higher than that of the brains of young and adult rats. When adult rats were administered Cd, MT was induced not only in some glial cells, ependymal cells, arachnoid, and pia mater but also in endothelial cells. Although Cd treatment resulted in an increase in the MT immunostaining in the specific cells described above, the MT induction was not great enough to significantly affect the overall MT level in the brain. The present result suggest a possible link of MT with cell growth of choroid plexus epithelium and ependymal cells, as well as a detoxifying role of MT in the blood-brain barrier and the cerebrospinal fluid-brain barrier.

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Steinbach, Karin, Ilena Vincenti, Kristof Egervari, Mario Kreutzfeldt, Franziska van der Meer, Nicolas Page, Bogna Klimek, et al. "Brain-resident memory T cells generated early in life predispose to autoimmune disease in mice." Science Translational Medicine 11, no. 498 (June 26, 2019): eaav5519. http://dx.doi.org/10.1126/scitranslmed.aav5519.

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Epidemiological studies associate viral infections during childhood with the risk of developing autoimmune disease during adulthood. However, the mechanistic link between these events remains elusive. We report that transient viral infection of the brain in early life, but not at a later age, precipitates brain autoimmune disease elicited by adoptive transfer of myelin-specific CD4+ T cells at sites of previous infection in adult mice. Early-life infection of mouse brains imprinted a chronic inflammatory signature that consisted of brain-resident memory T cells expressing the chemokine (C-C motif) ligand 5 (CCL5). Blockade of CCL5 signaling via C-C chemokine receptor type 5 prevented the formation of brain lesions in a mouse model of autoimmune disease. In mouse and human brain, CCL5+ TRM were located predominantly to sites of microglial activation. This study uncovers how transient brain viral infections in a critical window in life might leave persisting chemotactic cues and create a long-lived permissive environment for autoimmunity.

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Ravindranath, V., and H. K. Ananda Theertha Varada. "High activity of cytochrome P-450-linked aminopyrine N-demethylase in mouse brain microsomes, and associated sex-related difference." Biochemical Journal 261, no. 3 (August 1, 1989): 769–73. http://dx.doi.org/10.1042/bj2610769.

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The presence of cytochrome P-450 and associated mono-oxygenase activities was examined in brain microsomes from male and female mice. Although the cytochrome P-450 level in male mouse brain was very low as compared with mouse liver, the aminopyrine N-demethylase and morphine N-demethylase specific activities in male mouse brain were much higher than those observed in mouse liver. Ethoxycoumarin O-de-ethylase and aniline hydroxylase activities were, however, not detected in mouse brain. Sex-related differences were observed in both the cytochrome P-450 levels and aminopyrine N-demethylase activity in mouse brain, the levels of both being higher in male mouse brain as compared with female mouse brain. Aminopyrine N-demethylase activity in mouse brain microsomes was dependent on the presence of oxygen and NADPH and could be inhibited by piperonyl butoxide, N-octyl imidazole and carbon monoxide. Antiserum raised to the phenobarbital-inducible form of rat liver cytochrome P-450 [P-450(b+e)] inhibited mouse brain aminopyrine N-demethylase activity by around 80+ mouse brain microsomal protein exhibited cross-reactivity against this antiserum when examined by Ouchterlony double diffusion and immunoblotting. The present results indicate the presence of a phenobarbital-inducible form of cytochrome P-450 (or a form of cytochrome P-450 that is similar immunologically) in mouse brain microsomes, which is associated with a sex-related difference.

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Riordan, Ruben. "Brain Cellular Senescence in Mouse Models of Alzheimer's Disease." Innovation in Aging 5, Supplement_1 (December 1, 2021): 929. http://dx.doi.org/10.1093/geroni/igab046.3363.

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Abstract Abstract The accumulation of senescent cells contributes to aging pathologies, including neurodegenerative diseases, and its selective removal improves physiological and cognitive function in wild type mice as well as in Alzheimer’s disease (AD) models. AD models recapitulate some, but not all components of disease and do so at different rates. Whether brain cellular senescence is recapitulated in some or all AD models, and whether the emergence of cellular senescence in AD mouse models occurs before or after the expected onset of AD-like cognitive deficits in these models is not yet known. The goal of this study was to identify mouse models of AD and AD-related dementias that develop measurable markers of cellular senescence in brain and thus may be useful to study the role of cellular senescence in these conditions. We measured levels of cellular senescence markers in brains of P301S(PS19), P301L, hTau, and 3xTg-AD mice that model amyloidopathy and/or tauopathy in AD and related dementias, and in wild type, age-matched control mice for each strain. Expression of cellular senescence markers in brains of transgenic P301L and 3xTg-AD mice was largely indistinguishable from that in WT control age-matched mice. In contrast, markers of cellular senescence were significantly increased in brains of transgenic P301S and hTau mice as compared to WT control mice at the expected time of onset of AD-like cognitive deficits. Taken together, our data suggest that P301S(PS19) and hTau mice may be useful for the study of brain cellular senescence in tauopathies including, but not limited to, AD.

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Tsutsui, Yoshihiro, Hideya Kawasaki, and Isao Kosugi. "Reactivation of Latent Cytomegalovirus Infection in Mouse Brain Cells Detected after Transfer to Brain Slice Cultures." Journal of Virology 76, no. 14 (July 15, 2002): 7247–54. http://dx.doi.org/10.1128/jvi.76.14.7247-7254.2002.

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ABSTRACT Cytomegalovirus (CMV) is the most significant infectious cause of brain disorders in humans involving the developing brain. It is hypothesized that the brain disorders occur after recurrent reactivation of the latent infection in some kinds of cells in the brains. In order to test this hypothesis, we examined the reactivation of latent murine CMV (MCMV) infection in the mouse brain by transfer to brain slice culture. We infected neonatal and young adult mice intracerebrally with recombinant MCMV in which the lacZ gene was inserted into a late gene. The brains were removed 6 months after infection and used to prepare brain slices that were then cultured for up to 4 weeks. Reactivation of latent infection in the brains was detected by β-galactosidase (β-Gal) staining to assess β-galactosidase expression. Viral replication was also confirmed by the plaque assay. Reactivation was observed in about 75% of the mice infected during the neonatal period 6 months after infection. Unexpectedly, reactivation was also observed in 75% of mice infected as young adults, although the infection ratio in the brain slices was significantly lower than that in neonatally infected mice. β-Gal-positive cells were observed in marginal regions of the brains or immature neural cells in the ventricular walls. Immunohistochemical staining showed that the β-Gal-positive reactivated cells were neural stem or progenitor cells. These results suggest that brain disorders may occur long after infection by reactivation of latent infection in the immature neural cells in the brain.

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Cao, Song, Juan Li, Jie Yuan, Dexin Zhang, and Tian Yu. "Fast Localization and Sectioning of Mouse Locus Coeruleus." BioMed Research International 2020 (March 2, 2020): 1–5. http://dx.doi.org/10.1155/2020/4860735.

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The locus nucleus (LC) is a multifunctional nucleus which is also the source of norepinephrine in the brain. To date, there is no simple and easy method to locate the small LC in brain sectioning. Here we report a fast, accurate, and easy-to-follow protocol for the localization of mice LC in frozen sectioning. After fixation and dehydration, the intact brains of adult mice were placed on a horizontal surface and vertically cut along the posterior margin of the bilateral cerebral cortex. In the coronal cutting plane, the aqueduct of midbrain can be seen easily with the naked eyes. After embedding the cerebellum part with optimal cutting temperature (OCT) compound, coronal brain slices were cut from the cutting plane, within 1 mm, the aqueduct of midbrain disappeared and the fourth ventricle appeared, then the brain slices contained LC and were collected. From the first collection, at ~200 μm, the noradrenergic neurons’ most enriched brain slices can be collected. The tyrosine hydroxylase immunofluorescence staining confirmed that the localization of LC with this method is accurate and the noradrenergic neuron most abundant slices can be determined with this method.

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Sharma, Kirti, Sebastian Schmitt, Caroline G. Bergner, Stefka Tyanova, Nirmal Kannaiyan, Natalia Manrique-Hoyos, Karina Kongi, et al. "Cell type– and brain region–resolved mouse brain proteome." Nature Neuroscience 18, no. 12 (November 2, 2015): 1819–31. http://dx.doi.org/10.1038/nn.4160.

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Fitzner, Dirk, Jakob M. Bader, Horst Penkert, Caroline G. Bergner, Minhui Su, Marie-Theres Weil, Michal A. Surma, Matthias Mann, Christian Klose, and Mikael Simons. "Cell-Type- and Brain-Region-Resolved Mouse Brain Lipidome." Cell Reports 32, no. 11 (September 2020): 108132. http://dx.doi.org/10.1016/j.celrep.2020.108132.

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Yokoi, Takashi, Naoki Yamamoto, Toyohiro Tada, Masataka Fujita, Akihiko Moriyama, Hitoshi Matsui, Takayuki Takahashi, Hajime Togari, Taiji Kato, and Kiyofumi Asai. "Developmental changes and localization of mouse brain serine proteinase mRNA and protein in mouse brain." Neuroscience Letters 323, no. 2 (April 2002): 133–36. http://dx.doi.org/10.1016/s0304-3940(02)00122-2.

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Chrast, Roman, Hamish S. Scott, Marie Pierre Papasavvas, Colette Rossier, Emmanuel S. Antonarakis, Christine Barras, Muriel T. Davisson, et al. "The Mouse Brain Transcriptome by SAGE: Differences in Gene Expression between P30 Brains of the Partial Trisomy 16 Mouse Model of Down Syndrome (Ts65Dn) and Normals." Genome Research 10, no. 12 (December 1, 2000): 2006–21. http://dx.doi.org/10.1101/gr.158500.

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Trisomy 21, or Down syndrome (DS), is the most common genetic cause of mental retardation. Changes in the neuropathology, neurochemistry, neurophysiology, and neuropharmacology of DS patients' brains indicate that there is probably abnormal development and maintenance of central nervous system structure and function. The segmental trisomy mouse (Ts65Dn) is a model of DS that shows analogous neurobehavioral defects. We have studied the global gene expression profiles of normal and Ts65Dn male and normal female mice brains (P30) using the serial analysis of gene expression (SAGE) technique. From the combined sample we collected a total of 152,791 RNA tags and observed 45,856 unique tags in the mouse brain transcriptome. There are 14 ribosomal protein genes (nine underexpressed) among the 330 statistically significant differences between normal male and Ts65Dn male brains, which possibly implies abnormal ribosomal biogenesis in the development and maintenance of DS phenotypes. This study contributes to the establishment of a mouse brain transcriptome and provides the first overall analysis of the differences in gene expression in aneuploid versus normal mammalian brain cells.

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Lewis, S. A., and N. J. Cowan. "Genetics, evolution, and expression of the 68,000-mol-wt neurofilament protein: isolation of a cloned cDNA probe." Journal of Cell Biology 100, no. 3 (March 1, 1985): 843–50. http://dx.doi.org/10.1083/jcb.100.3.843.

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A 1.2-kilobase (kb) cDNA clone (NF68) encoding the mouse 68,000-mol-wt neurofilament protein is described. The clone was isolated from a mouse brain cDNA library by low-stringency cross-hybridization with a cDNA probe encoding mouse glial fibrillary acidic protein (Lewis et al., 1984, Proc. Natl. Acad. Sci. USA., 81:2743-2746). The identity of NF68 was established by hybrid selection using mouse brain polyA+ mRNA, and cell-free translation of the selected mRNA species. The cell-free translation product co-migrated with authentic 68,000-mol-wt neurofilament protein on an SDS/polyacrylamide gel, and was immunoprecipitable with a monospecific rabbit anti-bovine neurofilament antiserum. In addition, DNA sequence analysis of NF68 showed 90% homology at the amino acid level compared with the sequence of the porcine 68,000-mol-wt neurofilament protein. At high stringency, NF68 detects a single genomic sequence encoding the mouse 68,000-mol-wt neurofilament protein. Two mRNA species of 2.5 kb and 4.0 kb are transcribed from the single gene in mouse brain. The level of expression of these mRNAs remains almost constant in postnatal mouse brains of all ages and, indeed, in the adult. At reduced stringency, NF68 detects a number of mRNAs that are expressed in mouse brain, one of which encodes the 150,000-mol-wt neurofilament protein. The NF68 probe cross-hybridizes at high stringency with genomic sequences in species as diverse as human, chicken, and (weakly) frog, but not with DNA from Drosophila or sea urchin.

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Tanaka, Sachi, Maki Nishimura, Fumiaki Ihara, Junya Yamagishi, Yutaka Suzuki, and Yoshifumi Nishikawa. "Transcriptome Analysis of Mouse Brain Infected with Toxoplasma gondii." Infection and Immunity 81, no. 10 (July 15, 2013): 3609–19. http://dx.doi.org/10.1128/iai.00439-13.

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ABSTRACTToxoplasma gondiiis an obligate intracellular parasite that invades a wide range of vertebrate host cells. Chronic infections withT. gondiibecome established in the tissues of the central nervous system, where the parasites may directly or indirectly modulate neuronal function. However, the mechanisms underlying parasite-induced neuronal disorder in the brain remain unclear. This study evaluated host gene expression in mouse brain following infection withT. gondii. BALB/c mice were infected with the PLK strain, and after 32 days of infection, histopathological lesions in the frontal lobe were found to be more severe than in other areas of the brain. Total RNA extracted from infected and uninfected mouse brain samples was subjected to transcriptome analysis using RNA sequencing (RNA-seq). In theT. gondii-infected mice, 935 mouse brain genes were upregulated, whereas 12 genes were downregulated. GOstat analysis predicted that the upregulated genes were primarily involved in host immune responses and cell activation. Positive correlations were found between the numbers of parasites in the infected mouse brains and the expression levels of genes involved in host immune responses. In contrast, genes that had a negative correlation with parasite numbers were predicted to be involved in neurological functions, such as small-GTPase-mediated signal transduction and vesicle-mediated transport. Furthermore, differential gene expression was observed between mice exhibiting the clinical signs of toxoplasmosis and those that did not. Our findings may provide insights into the mechanisms underlying neurological changes duringT. gondiiinfection.

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Orsatti, Laura, Maria Vittoria Orsale, Pamela di Pasquale, Andrea Vecchi, Fabrizio Colaceci, Alina Ciammaichella, Ilaria Rossetti, et al. "Turnover rate of coenzyme A in mouse brain and liver." PLOS ONE 16, no. 5 (May 21, 2021): e0251981. http://dx.doi.org/10.1371/journal.pone.0251981.

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Coenzyme A (CoA) is a fundamental cofactor involved in a number of important biochemical reactions in the cell. Altered CoA metabolism results in severe conditions such as pantothenate kinase-associated neurodegeneration (PKAN) in which a reduction of the activity of pantothenate kinase isoform 2 (PANK2) present in CoA biosynthesis in the brain consequently lowers the level of CoA in this organ. In order to develop a new drug aimed at restoring the sufficient amount of CoA in the brain of PKAN patients, we looked at its turnover. We report here the results of two experiments that enabled us to measure the half-life of pantothenic acid, free CoA (CoASH) and acetylCoA in the brains and livers of male and female C57BL/6N mice, and total CoA in the brains of male mice. We administered (intrastriatally or orally) a single dose of a [13C3-15N-18O]-labelled coenzyme A precursor (fosmetpantotenate or [13C3-15N]-pantothenic acid) to the mice and measured, by liquid chromatography-mass spectrometry, unlabelled- and labelled-coenzyme A species appearance and disappearance over time. We found that the turnover of all metabolites was faster in the liver than in the brain in both genders with no evident gender difference observed. In the oral study, the CoASH half-life was: 69 ± 5 h (male) and 82 ± 6 h (female) in the liver; 136 ± 14 h (male) and 144 ± 12 h (female) in the brain. AcetylCoA half-life was 74 ± 9 h (male) and 71 ± 7 h (female) in the liver; 117 ± 13 h (male) and 158 ± 23 (female) in the brain. These results were in accordance with the corresponding values obtained after intrastriatal infusion of labelled-fosmetpantotenate (CoASH 124 ± 13 h, acetylCoA 117 ± 11 and total CoA 144 ± 17 in male brain).

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CENI, Claire, Nathalie POCHON, Virginie BRUN, Hélène MULLER-STEFFNER, Annie ANDRIEUX, Didier GRUNWALD, Francis SCHUBER, et al. "CD38-dependent ADP-ribosyl cyclase activity in developing and adult mouse brain." Biochemical Journal 370, no. 1 (February 15, 2003): 175–83. http://dx.doi.org/10.1042/bj20020604.

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CD38 is a transmembrane glycoprotein that is expressed in many tissues throughout the body. In addition to its major NAD+-glycohydrolase activity, CD38 is also able to synthesize cyclic ADP-ribose, an endogenous calcium-regulating molecule, from NAD+. In the present study, we have compared ADP-ribosyl cyclase and NAD+-glycohydrolase activities in protein extracts of brains from developing and adult wild-type and Cd38-/- mice. In extracts from wild-type brain, cyclase activity was detected spectrofluorimetrically, using nicotinamide—guanine dinucleotide as a substrate (GDP-ribosyl cyclase activity), as early as embryonic day 15. The level of cyclase activity was similar in the neonate brain (postnatal day 1) and then increased greatly in the adult brain. Using [14C]NAD+ as a substrate and HPLC analysis, we found that ADP-ribose is the major product formed in the brain at all developmental stages. Under the same experimental conditions, neither NAD+-glycohydrolase nor GDP-ribosyl cyclase activity could be detected in extracts of brains from developing or adult Cd38-/- mice, demonstrating that CD38 is the predominant constitutive enzyme endowed with these activities in brain at all developmental stages. The activity measurements correlated with the level of CD38 transcripts present in the brains of developing and adult wild-type mice. Using confocal microscopy we showed, in primary cultures of hippocampal cells, that CD38 is expressed by both neurons and glial cells, and is enriched in neuronal perikarya. Intracellular NAD+-glycohydrolase activity was measured in hippocampal cell cultures, and CD38-dependent cyclase activity was higher in brain fractions enriched in intracellular membranes. Taken together, these results lead us to speculate that CD38 might have an intracellular location in neural cells in addition to its plasma membrane location, and may play an important role in intracellular cyclic ADP-ribose-mediated calcium signalling in brain tissue.

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TORRES, L. F. B., and L. W. DUCHEN. "THE MUTANT mdx: INHERITED MYOPATHY IN THE MOUSE." Brain 110, no. 2 (1987): 269–99. http://dx.doi.org/10.1093/brain/110.2.269.

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Iwami, Kenichiro, Hiroyuki Momota, Atsushi Natsume, Sayano Kinjo, Tetsuya Nagatani, and Toshihiko Wakabayashi. "A novel method of intracranial injection via the postglenoid foramen for brain tumor mouse models." Journal of Neurosurgery 116, no. 3 (March 2012): 630–35. http://dx.doi.org/10.3171/2011.10.jns11852.

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Object Mouse models have been widely used in developing therapies for human brain tumors. However, surgical techniques such as bone drilling and skin suturing to create brain tumors in adult mice are still complicated. The aim of this study was to establish a simple and accurate method for intracranial injection of cells or other materials into mice. Methods The authors performed micro CT scans and skull dissection to assess the anatomical characteristics of the mouse postglenoid foramen. They then used xenograft and genetically engineered mouse models to evaluate a novel technique of percutaneous intracranial injection via the postglenoid foramen. They injected green fluorescent protein–labeled U87MG cells or virus-producing cells into adult mouse brains via the postglenoid foramen and identified the location of the created tumors by using bioluminescence imaging and histological analysis. Results The postglenoid foramen was found to be a well-conserved anatomical structure that allows percutaneous injection into the cerebrum, cerebellum, brainstem, and basal cistern in mice. The mean (± SD) time for the postglenoid foramen injection technique was 88 ± 15 seconds. The incidence of in-target tumor formation in the xenograft model ranged from 80% to 100%, depending on the target site. High-grade gliomas were successfully developed by postglenoid foramen injection in the adult genetically engineered mouse using virus-mediated platelet-derived growth factor B gene transfer. There were no procedure-related complications. Conclusions The postglenoid foramen can be used as a needle entry site into the brain of the adult mouse. Postglenoid foramen injection is a less invasive, safe, precise, and rapid method of implanting cells into the adult mouse brain. This method can be applied to both orthotopic xenograft and genetically engineered mouse models and may have further applications in mice for the development of therapies for human brain tumors.

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Arévalo, Lena, and Polly Campbell. "Placental effects on the maternal brain revealed by disrupted placental gene expression in mouse hybrids." Proceedings of the Royal Society B: Biological Sciences 287, no. 1918 (January 15, 2020): 20192563. http://dx.doi.org/10.1098/rspb.2019.2563.

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The mammalian placenta is both the physical interface between mother and fetus, and the source of endocrine signals that target the maternal hypothalamus, priming females for parturition, lactation and motherhood. Despite the importance of this connection, the effects of altered placental signalling on the maternal brain are insufficiently studied. Here, we show that placental dysfunction alters gene expression in the maternal brain, with the potential to affect maternal behaviour. Using a cross between the house mouse and the Algerian mouse, in which hybrid placental development is abnormal, we sequenced late-gestation placental and maternal medial preoptic area transcriptomes and quantified differential expression and placenta-maternal brain co-expression between normal and hybrid pregnancies. The expression of Fmn1 and Drd3 was significantly altered in the brains of females exposed to hybrid placentas. Most strikingly, expression patterns of placenta-specific gene families and Drd3 in the brains of house mouse females carrying hybrid litters matched those of female Algerian mice, the paternal species in the cross. Our results indicate that the paternally derived placental genome can influence the expression of maternal–fetal communication genes, including placental hormones, suggesting an effect of the offspring's father on the mother's brain.

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Semenov, Mikhail. "Proliferative Capacity of Adult Mouse Brain." International Journal of Molecular Sciences 22, no. 7 (March 26, 2021): 3449. http://dx.doi.org/10.3390/ijms22073449.

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We studied cell proliferation in the postnatal mouse brain between the ages of 2 and 30 months and identified four compartments with different densities of proliferating cells. The first identified compartment corresponds to the postnatal pallial neurogenic (PPN) zone in the telencephalon; the second to the subpallial postnatal neurogenic (SPPN) zone in the telencephalon; the third to the white matter bundles in the telencephalon; and the fourth to all brain parts outside of the other three compartments. We estimated that about 3.4 million new cells, including 0.8 million in the subgranular zone (SGZ) in the hippocampus, are produced in the PPN zone. About 21 million new cells, including 10 million in the subependymal zone (SEZ) in the lateral walls of the lateral ventricle and 2.7 million in the rostral migratory stream (RMS), are produced in the SPPN zone. The third and fourth compartments together produced about 31 million new cells. The analysis of cell proliferation in neurogenic zones shows that postnatal neurogenesis is the direct continuation of developmental neurogenesis in the telencephalon and that adult neurogenesis has characteristics of the late developmental process. As a developmental process, adult neurogenesis supports only compensatory regeneration, which is very inefficient.

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Hines, Pamela J. "Gliogenesis in the adult mouse brain." Science 372, no. 6547 (June 10, 2021): 1162.15–1164. http://dx.doi.org/10.1126/science.372.6547.1162-o.

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Lake, Evelyn M. R. "Consciousness: Mapping the awake mouse brain." Current Biology 32, no. 3 (February 2022): R138—R140. http://dx.doi.org/10.1016/j.cub.2021.11.033.

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Travis, J. "Brain Chemical May Aid Mouse Mothering." Science News 152, no. 23 (December 6, 1997): 358. http://dx.doi.org/10.2307/3980832.

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MARUYAMA, Etsuko. "Biochemical characterization of mouse brain necdin." Biochemical Journal 314, no. 3 (March 15, 1996): 895–901. http://dx.doi.org/10.1042/bj3140895.

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Necdin is a protein encoded by neural differentiation-specific mRNA derived from embryonal carcinoma cells (P19). Necdin of mouse brain was characterized by Western blotting and silver-staining analysis by using affinity purified antibodies to 17 synthetic peptides of deduced C-terminal amino acids. Necdin exhibits a molecular mass of 51 kDa on SDS/PAGE, and is localized in the S1 and S2 nucleosomal fractions. Sonicated necdin is found in all fractions of Sephacryl S-300 gel filtration chromatography, with a peak at 700 kDa. Necdin is released on micrococcal nuclease digestion, which is essential for electrophoretic migration on acetic acid/urea/Triton gels, suggesting that it could be a DNA-binding protein. Nucleosomal necdin shows two peaks at approx. 10 S and approx. 20 S on sucrose gradient centrifugation in the presence of 0.6 M NaCl, and a single peak in the presence of 2.0 M NaCl. Necdin forms a huge complex through chemical cross-linking with glutaraldehyde or dimethyl sulphate. The silver-staining intensity of the 51 kDa band corresponds to the decrease in the immuno-staining in a reagent concentration-dependent manner. Necdin binds tightly to a double-stranded DNA affinity chromatography column, and can be eluted from it with 2.0 M NaCl after washing with 0.6 M NaCl (approx. 100 ng per ml of gel). This purified necdin exhibits a pI of 9.1 on isoelectric focusing. The nucleosomal necdin complex (> 200 kDa) was adsorbed on an organomercurial agarose affinity chromatography column and was eluted with 10 mM DTT, revealing that necdin is possibly involved in the transactive nucleosomal complex. These data show that necdin is a nuclear basic DNA-binding protein that associates with other molecules to regulate transcriptionally active genes and nuclear function.

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Ang, Siew-Lan, Aitana Perca-Gomez, Emmanuel Lacroix, and Muriel Rhinn. "Genetic analysis of mouse brain patterning." Biochemical Society Transactions 28, no. 5 (October 1, 2000): A138. http://dx.doi.org/10.1042/bst028a138c.

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LOMBROSO, PAUL J., and DANIEL GOLDOWITZ. "Brain Development, VIII: The Reeler Mouse." American Journal of Psychiatry 155, no. 12 (December 1998): 1660. http://dx.doi.org/10.1176/ajp.155.12.1660.

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Vogt, Nina. "The mouse reference brain in 3D." Nature Methods 17, no. 7 (July 2020): 655. http://dx.doi.org/10.1038/s41592-020-0899-4.

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Brumwell, Craig L., and Tom Curran. "Developmental mouse brain gene expression maps." Journal of Physiology 575, no. 2 (August 24, 2006): 343–46. http://dx.doi.org/10.1113/jphysiol.2006.112607.

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Guo, Shuzhen, Yiming Zhou, Changhong Xing, Josephine Lok, Angel T. Som, MingMing Ning, Xunming Ji, and Eng H. Lo. "The Vasculome of the Mouse Brain." PLoS ONE 7, no. 12 (December 20, 2012): e52665. http://dx.doi.org/10.1371/journal.pone.0052665.

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Berning, S., K. I. Willig, H. Steffens, P. Dibaj, and S. W. Hell. "Nanoscopy in a Living Mouse Brain." Science 335, no. 6068 (February 2, 2012): 551. http://dx.doi.org/10.1126/science.1215369.

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Self, J., H. M. Haitchi, H. Griffiths, S. T. Holgate, D. E. Davies, and A. Lotery. "Frmd7 expression in developing mouse brain." Eye 24, no. 1 (March 6, 2009): 165–69. http://dx.doi.org/10.1038/eye.2009.44.

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Zhu, Fei, Mélissa Cizeron, Zhen Qiu, Ruth Benavides-Piccione, Maksym V. Kopanitsa, Nathan G. Skene, Babis Koniaris, et al. "Architecture of the Mouse Brain Synaptome." Neuron 99, no. 4 (August 2018): 781–99. http://dx.doi.org/10.1016/j.neuron.2018.07.007.

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Cecchi, Chiara, and Edoardo Boncinelli. "Emx homeogenes and mouse brain development." Trends in Neurosciences 23, no. 8 (August 2000): 347–52. http://dx.doi.org/10.1016/s0166-2236(00)01608-8.

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Pagliusi, S. R., M. Schachner, P. H. Seeburg, and B. D. Shivers. "AMOG expression pattern in mouse brain." Cell Differentiation and Development 27 (August 1989): 199. http://dx.doi.org/10.1016/0922-3371(89)90607-2.

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Journal articles on the topic 'Mouse brain'

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