Relevant bibliographies by topics / Mouse brain

Academic literature on the topic 'Mouse brain'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Mouse brain"

1

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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Dissertations / Theses on the topic "Mouse brain"

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Gutierrez, Barragan Daniel. "Brain-wide mapping of fMRI network dynamics in the mouse brain." Doctoral thesis, Università degli studi di Trento, 2018. http://hdl.handle.net/11572/301211.

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Intrinsic brain activity has been widely characterized using the blood-oxygen-level-dependent(BOLD) functional Magnetic Resonance Imaging(fMRI)at rest. There is increasing interest in finding reproducible and robust signatures of large-scale brain synchronization, and pinpointing their neurophysiological substrates and inherent alteration in disease.In this respect, the implementation of dynamic fMRI mapping in laboratory animalsrepresents a major advance, offeringthe opportunity to unravel the elusive drivers of this phenomenon via the use of cell-type specific manipulations that are off limits in humans.Multiple investigations have shown that spontaneous brain activity is non-stationary andinvolves reconfigurationsinto multiple dynamicstates.This research describesa series of studies aimedto map spontaneous fMRI (rsfMRI) network dynamics in the resting mouse brain with voxel resolution. Starting from a proof-of-concept demonstration that canonical resting state fMRI correlations are reliably described by brief instances of regional peak fMRI activity, wedevised a novel frame-wise clustering strategy that allowed us to map recurrent fMRI networks states dynamicsin the mouse brain. We showthat brain-wide patterns of fMRI co-activation can be reliably mapped at the group and subject level, defining a restricted set of recurring brain states characterized by rich network structure. Of particular interest was the observation of opposite co-activation of the mouse default mode network (DMN) and Latero-cortical networks(LCN), two systems that have been proposed to parallel analogous systems of the human brain.Importantly, we also document that these functional states are characterized by contrasting patterns of spontaneous fMRI activity,and exhibit coupled oscillatory dynamics embedded in a common temporal reference marked by infra-slow global fMRI signal oscillations. We next applied this novel framework to a genetic modelof autismand show that aberrant patterns of fMRI connectivity in a genetic model of autism reflect the engagement non-canonical brain states, characterized by altered regional topography and oscillatory dynamics. We finally show that pharmacological stimulation of the cholinergic systems results in reduced large-scale brain synchronization, a finding associated with anew set of oscillating statesin which the involvement of basal forebrain areas is pre-dominant. Collectively,our result demonstrate the possibility of mapping spatio-temporal dynamics of spontaneous brain activity in the living mouse brain with voxel resolution. Our approach reveals a new set of fundamental principles guiding the spatiotemporal organization of resting state fMRI activity, and its disruption in brain disorders.
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Gutierrez, Barragan Daniel. "Brain-wide mapping of fMRI network dynamics in the mouse brain." Doctoral thesis, Università degli studi di Trento, 2018. http://hdl.handle.net/11572/301211.

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Intrinsic brain activity has been widely characterized using the blood-oxygen-level-dependent(BOLD) functional Magnetic Resonance Imaging(fMRI)at rest. There is increasing interest in finding reproducible and robust signatures of large-scale brain synchronization, and pinpointing their neurophysiological substrates and inherent alteration in disease.In this respect, the implementation of dynamic fMRI mapping in laboratory animalsrepresents a major advance, offeringthe opportunity to unravel the elusive drivers of this phenomenon via the use of cell-type specific manipulations that are off limits in humans.Multiple investigations have shown that spontaneous brain activity is non-stationary andinvolves reconfigurationsinto multiple dynamicstates.This research describesa series of studies aimedto map spontaneous fMRI (rsfMRI) network dynamics in the resting mouse brain with voxel resolution. Starting from a proof-of-concept demonstration that canonical resting state fMRI correlations are reliably described by brief instances of regional peak fMRI activity, wedevised a novel frame-wise clustering strategy that allowed us to map recurrent fMRI networks states dynamicsin the mouse brain. We showthat brain-wide patterns of fMRI co-activation can be reliably mapped at the group and subject level, defining a restricted set of recurring brain states characterized by rich network structure. Of particular interest was the observation of opposite co-activation of the mouse default mode network (DMN) and Latero-cortical networks(LCN), two systems that have been proposed to parallel analogous systems of the human brain.Importantly, we also document that these functional states are characterized by contrasting patterns of spontaneous fMRI activity,and exhibit coupled oscillatory dynamics embedded in a common temporal reference marked by infra-slow global fMRI signal oscillations. We next applied this novel framework to a genetic modelof autismand show that aberrant patterns of fMRI connectivity in a genetic model of autism reflect the engagement non-canonical brain states, characterized by altered regional topography and oscillatory dynamics. We finally show that pharmacological stimulation of the cholinergic systems results in reduced large-scale brain synchronization, a finding associated with anew set of oscillating statesin which the involvement of basal forebrain areas is pre-dominant. Collectively,our result demonstrate the possibility of mapping spatio-temporal dynamics of spontaneous brain activity in the living mouse brain with voxel resolution. Our approach reveals a new set of fundamental principles guiding the spatiotemporal organization of resting state fMRI activity, and its disruption in brain disorders.
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Pal, A. (Arup). "Hybrid head cap for mouse brain studies." Master's thesis, University of Oulu, 2019. http://jultika.oulu.fi/Record/nbnfioulu-201909252929.

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Abstract. In this thesis, I present a hybrid head cap in combination with non-invasive multi-channel Electroencephalogram (EEG) and Near-Infrared Spectroscopy (NIRS) to measure brainwaves on mice’s scalps. Laboratory animal research provides insights into multiple potential applications involving humans and other animals. An experimental framework that targets laboratory animals can lead to useful transnational research if it strongly reflects the actual application environment. The non-invasive head cap with three electrodes for EEG and two optodes for NIRS is suggested to measure brainwaves throughout the laboratory mice’s entire brain region without surgical procedures. The suggested hybrid head cap aims to ensure stability in vivo monitoring for mouse brain in a non-invasive way, similarly as the monitoring is performed for the human brain. The experimental part of the work to study the quality of the gathered EEG and fNIRS signals, and usability validation of the head cap, however, was not completed in the planned time frame of the thesis work.
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Kiebish, Michael Andrew. "Mitochondrial lipidome and genome alterations in mouse brain and experimental brain tumors." Thesis, Boston College, 2008. http://hdl.handle.net/2345/27.

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Thesis advisor: Thomas N. Seyfried
Mitochondria are the key regulators of the bioenergetic state of the cell. Damage to mitochondrial protein, DNA, or membrane lipids can result as the cause or affect of disease pathology. Regardless, this damage can impair mitochondrial function resulting in a decreased ability to produce ATP to support cellular viability. This thesis research examined the mitochondrial lipidome by shotgun lipidomics in different populations of C57BL/6J (B6) brain mitochondria (non-synaptic and synaptic) and correlated lipid changes to differences in electron transport chain (ETC) activities. Furthermore, a comparison was made for non-synaptic mitochondria between the B6 and the VM mouse strain. The VM strain has a 1.5% incidence of spontaneous brain tumors, which is 210 fold greater than the B6 strain. I determined that differences in the brain mitochondrial lipidome existed in the VM strain compared to the B6 strain, likely corresponding to an increased rate of spontaneous brain tumor formation. Analysis of the mitochondrial genome in the CT-2A, EPEN, VM-NM1, and VM-M3 brain tumors compared to their syngeneic controls mouse strains, C57BL/6J (B6) and VM mice, was examined to determine if mutations existed in experimental brain cancer models. No pathogenic mtDNA mutations were discovered that would likely cause a decrease in the mitochondrial functionality. A novel hypothesis was devised to examine the tumor mitochondrial lipidome to determine if quantitative or molecular species differences existed that could potentially alter the functionality of the ETC. Brain tumor mitochondria were examined from tumors grown in vivo as well as in vitro. Numerous lipid differences were found in the mitochondria of brain tumors, of which the most interesting involved the unique molecular speciation of cardiolipin. ETC activities were significantly decreased in the primary ETC complexes which contribute protons to the gradient as well as the linked complexes of brain tumor mitochondria compared to controls. Taken together, it is likely that differences in the mitochondrial lipidome of brain tumors results in severe impairment of the mitochondria’s ability to produce ATP through the ETC. This research has provided a new understanding of the role of mitochondrial lipids in brain as well as brain cancer and offers an alternative explanation for metabolic dysfunction in cancer
Thesis (PhD) — Boston College, 2008
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Malak, Ramez. "2D gel analysis on CNP-overexpressing mouse brain." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79041.

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2',3'-Cyclic nucleotide 3 '-phosphodiesterase (CNP) is an early marker for oligodendrocytes, and it is suspected to be implicated in the expansion of membranes during myelination. We have previously generated transgenic mice that overexpress CNP. These mice showed altered oligodendroyte development, produced aberrant myelination, and had less MBP accumulated in myelin. More interestingly, ODCs isolated from those mice had a tremendous increase in the process extension formation. The purpose of the present study is to compare the protein expression pattern in the myelin isolated from control and CNP overexpressing mice (L191), using two-dimensional gel electrophoresis. We found that CNP overexpression increases HSC70, and HSP70, and decreases MAG expression in myelin. We also found that the mRNA for MAG, in L191 brain was identical to control brain during all stages of development. These findings suggest that CNP may be implicated with HSC70 in vesicular transport, and this may explain the mechanism of process extension mediated by CNP.
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Sawiak, Stephen John. "Computational methods for mouse brain phenotyping using MRI." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611550.

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Niranjan, A. "Functional magnetic resonance imaging of the mouse brain." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1543368/.

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Functional magnetic resonance imaging (fMRI) measuring a blood-oxygen-level dependent (BOLD) signal is the most commonly used neuroimaging tool to understand brain function in humans. As mouse models are one of the most commonly used neuroscience experimental models, and with the advent of transgenic mouse models of neurodegenerative pathologies, there has been an increasing push in recent years to apply fMRI techniques to the mouse brain. This thesis focuses on the development and implementation of mouse brain fMRI techniques, in particular to describe the mouse visual system. Multiple studies in the literature have noted several technical challenges in mouse fMRI. In this work I have developed methods which go some way to reducing the impact of these issues, and I record robust and reliable haemodynamic-driven signal responses to visual stimuli in mouse brain regions specific to visual processing. I then developed increasingly complex visual stimuli, approaching the level of complexity used in electrophysiology studies of the mouse visual system, despite the geometric and magnetic field constraints of using a 9.4T pre-clinical MRI scanner. I have also applied a novel technique for measuring high-temporal resolution BOLD responses in the mouse superior colliculus, and I used this data to improve statistical parametric mapping of mouse brain BOLD responses. I also describe the first application of dynamic causal modelling to mouse fMRI data, characterising effective connectivity in the mouse brain visual system. This thesis makes significant contributions to the reverse translation of fMRI to the mouse brain, closing the gap between invasive electrophysiological measurements in the mouse brain and non-invasive fMRI measurements in the human brain.
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Pagani, Marco. "Gray matter covariance networks in the mouse brain." Doctoral thesis, Università degli studi di Trento, 2017. https://hdl.handle.net/11572/368511.

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The presence of networks of correlation between gray matter volumes of brain regions - as measured across subjects in a group of individuals - has been consistently described in several human studies, an approach termed structural covariance MRI (scMRI). Complementary to prevalent brain connectivity modalities like functional and diffusion-weighted imaging, this approach can provide valuable insight into the mutual influence of regional trophic and plastic processes occurring between brain regions. Previous investigations highlighted coordinated growth of these regions within specific structural networks in healthy populations and described their derangement in pathological states. However, a number of fundamental questions about the origin and significance of these couplings remains open and the mechanisms behind the formation of scMRI networks are still poorly understood. To investigate whether analogous scMRI networks are present in lower mammal species amenable to genetic and experimental manipulation such as the laboratory mouse, I coupled high resolution morpho-anatomical MRI with network-based approaches on a large cohort of genetically-homogeneous wild-type mice (C57Bl6/J). To this purpose, I first developed a semi-automated pipeline enabling reliable Voxel Based Morphometry (VBM) of gray matter volumes in the mouse. To validate this approach and its ability to detect plastic changes in brain structures, I applied it to a cohort of aged mice treated with omega-3 polyunsaturated fatty acids (n3-PUFA). This study revealed that treatment with n3PUFA, but not isocaloric olive oil preserved gray matter volume of the hippocampus and frontal cortices, an effect coincident with amelioration of hippocampal-based spatial memory functions. I next employed VBM to investigate scMRI networks in inbred mice using a seed-based approach. In striking resemblance with human findings, I observed the presence of homotopic (i.e. bilateral) architecture in several scMRI cortical and subcortical networks, a finding corroborated by Independent Component Analyses. Subcortical structures also showed highly symmetric inter-hemispheric correlations, with evidence of distributed antero-posterior networks in diencephalic regions of the thalamus and hypothalamus. Hierarchical cluster analysis revealed six identifiable clusters of cortical and sub-cortical regions corresponding to previously described neuroanatomical systems. This work documents for the first time the presence of homotopic cortical and subcortical scMRI networks in the mouse brain, and is poised to pave the way to translational use of this species to investigate the elusive biological and neuroanatomical underpinnings of scMRI network development and its derangement in neuropathological states.
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Pagani, Marco. "Gray matter covariance networks in the mouse brain." Doctoral thesis, University of Trento, 2017. http://eprints-phd.biblio.unitn.it/1916/1/PhD_Thesis_Marco_Pagani.pdf.

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The presence of networks of correlation between gray matter volumes of brain regions - as measured across subjects in a group of individuals - has been consistently described in several human studies, an approach termed structural covariance MRI (scMRI). Complementary to prevalent brain connectivity modalities like functional and diffusion-weighted imaging, this approach can provide valuable insight into the mutual influence of regional trophic and plastic processes occurring between brain regions. Previous investigations highlighted coordinated growth of these regions within specific structural networks in healthy populations and described their derangement in pathological states. However, a number of fundamental questions about the origin and significance of these couplings remains open and the mechanisms behind the formation of scMRI networks are still poorly understood. To investigate whether analogous scMRI networks are present in lower mammal species amenable to genetic and experimental manipulation such as the laboratory mouse, I coupled high resolution morpho-anatomical MRI with network-based approaches on a large cohort of genetically-homogeneous wild-type mice (C57Bl6/J). To this purpose, I first developed a semi-automated pipeline enabling reliable Voxel Based Morphometry (VBM) of gray matter volumes in the mouse. To validate this approach and its ability to detect plastic changes in brain structures, I applied it to a cohort of aged mice treated with omega-3 polyunsaturated fatty acids (n3-PUFA). This study revealed that treatment with n3PUFA, but not isocaloric olive oil preserved gray matter volume of the hippocampus and frontal cortices, an effect coincident with amelioration of hippocampal-based spatial memory functions. I next employed VBM to investigate scMRI networks in inbred mice using a seed-based approach. In striking resemblance with human findings, I observed the presence of homotopic (i.e. bilateral) architecture in several scMRI cortical and subcortical networks, a finding corroborated by Independent Component Analyses. Subcortical structures also showed highly symmetric inter-hemispheric correlations, with evidence of distributed antero-posterior networks in diencephalic regions of the thalamus and hypothalamus. Hierarchical cluster analysis revealed six identifiable clusters of cortical and sub-cortical regions corresponding to previously described neuroanatomical systems. This work documents for the first time the presence of homotopic cortical and subcortical scMRI networks in the mouse brain, and is poised to pave the way to translational use of this species to investigate the elusive biological and neuroanatomical underpinnings of scMRI network development and its derangement in neuropathological states.
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Tunca, Cansu 1977. "Synaptic plasticity in the MyosinVa mutant mouse." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/46662.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2009.
Includes bibliographical references (leaves 32-41).
The trafficking of essential proteins into spines is an important aspect of synaptic plasticity. MyosinVa, an actin-based motor protein, has been implicated in the synaptic delivery of AMPARs during LTP [1]. However an earlier study showed that LTP and LTD were unaffected in the MyosinVa-null dilute-lethal mice [2]. To evaluate the role of MyosinVa in synaptic plasticity, we studied different forms of LTP and LTD in the CA1 region of the hippocanmpus from MyosinVa dominant negative mutant flailer mouse using field potential recordings. Flailer mice showed no impairment of LTP or NMDAR-dependent LTD, consistent with the findings of the study on dilute-lethal. In addition, MyosinVa has been implicated in the transport of an RNA-binding protein into the spines upon mGluR activation [3]. We explored protein synthesis and mGluR-dcpendent LTD in flailer. The preliminary data we obtained show a transient impairment in mGluR.-LTD, suggesting a role for MyosinVa in protein synthesis dependent plasticity.
by Cansu Tunca.
S.M.
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Books on the topic "Mouse brain"

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Goffinet, André M., and Pasko Rakic, eds. Mouse Brain Development. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-540-48002-0.

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Schambra, Uta. Prenatal Mouse Brain Atlas. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-47093-1.

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J, Franklin Keith B., ed. The mouse brain in stereotaxic coordinates. 3rd ed. Oxford: Academic, 2007.

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Franklin, Keith B. J. The mouse brain in stereotaxic coordinates. San Diego: Academic Press, 1997.

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M, Lauder Jean, and Silver Jerry, eds. Atlas of the prenatal mouse brain. San Diego: Academic Press, 1992.

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J, Franklin Keith B., ed. The mouse brain in stereotaxic coordinates. 2nd ed. Amsterdam ; Boston: Elsevier Academic Press, 2004.

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Schambra, Uta. Atlas of the Prenatal Mouse Brain. San Diego: Academic Press, 1992.

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Valverde, Facundo. Golgi Atlas of the Postnatal Mouse Brain. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6501-0.

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Jacobowitz, David M. Chemoarchitectonic atlas of the developing mouse brain. Boca Raton: CRC Press, 1998.

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Valverde, Facundo. Golgi atlas of the postnatal mouse brain. Wien: Springer-Verlag, 1998.

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Book chapters on the topic "Mouse brain"

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Johnson, Jennifer, Brian DelGiudice, Dinesh S. Bangari, Eleanor Peterson, Gregory Ulinski, Susan Ryan, and Beth L. Thurberg. "Brain." In The Laboratory Mouse, edited by Gayle Callis, 3–4. Boca Raton, Florida : CRC Press, [2019]: CRC Press, 2019. http://dx.doi.org/10.1201/9780429057755-2.

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Morgan, Kevin T., and Winslow G. Sheldon. "Lipoma, Brain, Mouse." In Nervous System, 130–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83516-2_23.

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Barthold, Stephen W. "Mouse Hepatitis Virus Infection, Brain, Mouse." In Nervous System, 180–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83516-2_31.

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Johnson, Jennifer, Brian DelGiudice, Dinesh S. Bangari, Eleanor Peterson, Gregory Ulinski, Susan Ryan, and Beth L. Thurberg. "Brain - Trimming for Coronal Sections." In The Laboratory Mouse, edited by Gayle Callis, 5–6. Boca Raton, Florida : CRC Press, [2019]: CRC Press, 2019. http://dx.doi.org/10.1201/9780429057755-3.

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Johnson, Jennifer, Brian DelGiudice, Dinesh S. Bangari, Eleanor Peterson, Gregory Ulinski, Susan Ryan, and Beth L. Thurberg. "Brain - Trimming for Sagittal Sections." In The Laboratory Mouse, edited by Gayle Callis, 7–8. Boca Raton, Florida : CRC Press, [2019]: CRC Press, 2019. http://dx.doi.org/10.1201/9780429057755-4.

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Schröder, Hannsjörg, Natasha Moser, and Stefan Huggenberger. "Macroscopic Anatomy of the Mouse Brain." In Neuroanatomy of the Mouse, 45–57. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-19898-5_4.

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Gao, Xing, Limeng Wu, Raquel D. Thalheimer, Jie Chen, Yao Sun, Grace Y. Lee, Scott R. Plotkin, and Lei Xu. "Assessing Neurological Function in Brain Tumor Mouse Model." In Brain Tumors, 199–220. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0856-2_9.

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Archontidi, Sofia, Sandra Joppé, Yanis Khenniche, Chiara Bardella, and Emmanuelle Huillard. "Mouse Models of Diffuse Lower-Grade Gliomas of the Adult." In Brain Tumors, 3–38. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0856-2_1.

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Klomp, Dennis W. J., and W. Klaas Jan Renema. "Spectroscopic Imaging of the Mouse Brain." In Methods in Molecular Biology, 337–51. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-219-9_18.

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Lee, Jae-Kyung, and Malú G. Tansey. "Microglia Isolation from Adult Mouse Brain." In Microglia, 17–23. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-520-0_3.

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Conference papers on the topic "Mouse brain"

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Yao, Junjie, Joon-Mo Yang, Lidai Wang, Jun Zou, and Lihong V. Wang. "Fast Functional Photoacoustic Microscopy of Mouse Brain." In Optics and the Brain. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/brain.2015.brm4b.3.

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Gong, Hui, Jing Yuan, Anan Li, Xiangning Li, and Qingming Luo. "Visible whole mouse brain at single neuron resolution." In Optics and the Brain. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/brain.2015.brm3b.5.

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Cao, Rui, Bo Ning, Naidi Sun, Jun Li, Tianxiong Wang, Zhiyi Zuo, and Song Hu. "Multi-parametric Photoacoustic Microscopy of the Awake Mouse Brain." In Optics and the Brain. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/brain.2016.bth2d.4.

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Ning, Bo, Rui Cao, Jun Li, Naidi Sun, Zhiyi Zuo, and Song Hu. "Multi-parametric Photoacoustic Microscopy of Photothrombotic Stroke in the Mouse Brain." In Optics and the Brain. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/brain.2016.bth3d.4.

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Rahn, Rachel M., Annie R. Bice, Lindsey M. Brier, Joseph D. Dougherty, and Joseph P. Culver. "Optical Imaging of Functional Connectivity Across Development in the Mouse Cortex." In Optics and the Brain. Washington, D.C.: OSA, 2018. http://dx.doi.org/10.1364/brain.2018.btu2c.6.

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He, Qinghua, Yuandong Li, and Ruikang K. Wang. "Imaging photoplethysmography for assessing stimulus-evoked hemodynamics in mouse barrel cortex." In Optics and the Brain. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/brain.2023.bth1b.5.

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We use imaging photoplethysmography (iPPG) to assess cerebral hemodynamics of mice under whisker stimulation. The spatial blood pulsation changes measured by iPPG is in consistence with optical coherence tomography angiography (OCTA) measurements.
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Shao, Ling-Xiao, Clara Liao, Ian Gregg, Pasha A. Davoudian, Neil K. Savalia, Kristina Delagarza, and Alex C. Kwan. "Visualizing drug actions on dendrites: psilocybin and other classic psychedelics." In Optics and the Brain. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/brain.2023.btu2b.2.

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To determine effects of psychedelics on neuronal architecture, we used two-photon microscopy to image dendritic spines in mouse frontal cortex after administering psilocybin (Neuron, 109, 2535, 2021) and compared with other psychoactive drugs.
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Zilpelwar, Sharvari, Xiaojun Cheng, and David A. Boas. "Interferometric dynamic laser speckle imaging." In Optics and the Brain. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/brain.2023.bth1b.2.

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We developed interferometric dynamic laser speckle imaging (iDLSI) capable of three-dimensional volumetric measurements of the blood flow. Here, we present the numerical and analytical model for g2,iDLSI(τ) and perform preliminary measurement in the mouse brain.
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Xu, Dongli, Jun B. Ding, and Leilei Peng. "Synaptic resolution two-photon stimulation and imaging of neural activity with Bessel beam light-sheet microscopy." In Optics and the Brain. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/brain.2023.bw4b.3.

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We report combining two-photon Bessel beam light-sheet microscopy with two-photon uncaging to perform all-optical neural stimulation and imaging at synaptic resolution. Imaging results from mouse brain slices under 2P uncaging of glutamate will be presented.
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Xu, Gang, Philip V. Bayly, and Larry A. Taber. "Residual Stress in the Mouse Brain." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192205.

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Proper folding of the cerebral cortex is critical to normal human brain function. The mechanisms of cortical folding, however, remain incompletely understood, although they have intrigued neuroscientists for more than a century. Clearly a biomechanical problem, cortical folding has been speculated to result from stresses induced by differential or constrained growth [1]. More recently, investigators have postulated that tension in neural axons of cerebral white matter causes specific folding patterns [2]. However, it is uncertain if sustained tension exists in axons in both the developing and mature brain.
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Reports on the topic "Mouse brain"

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Manley, N. B., J. I. Fabrikant, and E. L. Alpen. Cell and tissue kinetics of the subependymal layer in mouse brain following heavy charged particle irradiation. Office of Scientific and Technical Information (OSTI), December 1988. http://dx.doi.org/10.2172/7191328.

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Yang, Ruoting, Jr Daigle, Muhie Bernie J., Hammamieh Seid Y., Jett Rasha, Petzold Marti, Doyle Linda, and Francis J. III. Core Modular Blood and Brain Biomarkers in Social Defeat Mouse Model for Post Traumatic Stress Disorder. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada596945.

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