Relevant bibliographies by topics / Cerebellum model

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Academic literature on the topic 'Cerebellum model'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Cerebellum model"

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Kotani, Osamu, Tadaki Suzuki, Masaru Yokoyama, Naoko Iwata-Yoshikawa, Noriko Nakajima, Hironori Sato, Hideki Hasegawa, Fumihiro Taguchi, Hiroyuki Shimizu, and Noriyo Nagata. "Intracerebral Inoculation of Mouse-Passaged Saffold Virus Type 3 Affects Cerebellar Development in Neonatal Mice." Journal of Virology 90, no. 21 (August 31, 2016): 10007–21. http://dx.doi.org/10.1128/jvi.00864-16.

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ABSTRACTSaffold virus (SAFV), a human cardiovirus, is occasionally detected in infants with neurological disorders, including meningitis and cerebellitis. We recently reported that SAFV type 3 isolates infect cerebellar glial cells, but not large neurons, in mice. However, the impact of this infection remained unclear. Here, we determined the neuropathogenesis of SAFV type 3 in the cerebella of neonatal ddY mice by using SAFV passaged in the cerebella of neonatal BALB/c mice. The virus titer in the cerebellum increased following the inoculation of each of five passaged strains. The fifth passaged strain harbored amino acid substitutions in the VP2 (H160R and Q239R) and VP3 (K62M) capsid proteins. Molecular modeling of the capsid proteins suggested that the VP2-H160R and VP3-K62M mutations alter the structural dynamics of the receptor binding surface via the formation of a novel hydrophobic interaction between the VP2 puff B and VP3 knob regions. Compared with the original strain, the passaged strain showed altered growth characteristics in human-derived astroglial cell lines and greater replication in the brains of neonatal mice. In addition, the passaged strain was more neurovirulent than the original strain, while both strains infected astroglial and neural progenitor cells in the mouse brain. Intracerebral inoculation of either the original or the passaged strain affected brain Purkinje cell dendrites, and a high titer of the passaged strain induced cerebellar hypoplasia in neonatal mice. Thus, infection by mouse-passaged SAFV affected cerebellar development in neonatal mice. This animal model contributes to the understanding of the neuropathogenicity of SAFV infections in infants.IMPORTANCESaffold virus (SAFV) is a candidate neuropathogenic agent in infants and children, but the neuropathogenicity of the virus has not been fully elucidated. Recently, we evaluated the pathogenicity of two clinical SAFV isolates in mice. Similar to other neurotropic picornaviruses, these isolates showed mild infectivity of glial and neural progenitor cells, but not of large neurons, in the cerebellum. However, the outcome of this viral infection in the cerebellum has not been clarified. Here, we examined the tropism of SAFV in the cerebellum. We obtained anin vivo-passaged strain from the cerebella of neonatal mice and examined its genome and its neurovirulence in the neonatal mouse brain. The passaged virus showed high infectivity and neurovirulence in the brain, especially the cerebellum, and affected cerebellar development. This unique neonatal mouse model will be helpful for elucidating the neuropathogenesis of SAFV infections occurring early in life.
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Kiffmeyer, Elizabeth A., Jameson A. Cosgrove, Jenna K. Siganos, Heidi E. Bien, Jade E. Vipond, Karisa R. Vogt, and Alexander D. Kloth. "Deficits in Cerebellum-Dependent Learning and Cerebellar Morphology in Male and Female BTBR Autism Model Mice." NeuroSci 3, no. 4 (November 9, 2022): 624–44. http://dx.doi.org/10.3390/neurosci3040045.

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Recently, there has been increased interest in the role of the cerebellum in autism spectrum disorder (ASD). To better understand the pathophysiological role of the cerebellum in ASD, it is necessary to have a variety of mouse models that have face validity for cerebellar disruption in humans. Here, we add to the literature on the cerebellum in mouse models of autism with the characterization of the cerebellum in the idiopathic BTBR T + Itpr3tf/J (BTBR) inbred mouse strain, which has behavioral phenotypes that are reminiscent of ASD in patients. When we examined both male and female BTBR mice in comparison to C57BL/6J (C57) controls, we noted that both sexes of BTBR mice showed motor coordination deficits characteristic of cerebellar dysfunction, but only the male mice showed differences in delay eyeblink conditioning, a cerebellum-dependent learning task that is known to be disrupted in ASD patients. Both male and female BTBR mice showed considerable expansion of, and abnormal foliation in, the cerebellum vermis—including a significant expansion of specific lobules in the anterior cerebellum. In addition, we found a slight but significant decrease in Purkinje cell density in both male and female BTBR mice, irrespective of the lobule. Finally, there was a marked reduction of Purkinje cell dendritic spine density in both male and female BTBR mice. These findings suggest that, for the most part, the BTBR mouse model phenocopies many of the characteristics of the subpopulation of ASD patients that have a hypertrophic cerebellum. We discuss the significance of strain differences in the cerebellum as well as the importance of this first effort to identify both similarities and differences between male and female BTBR mice with regard to the cerebellum.
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Geminiani, Alice, Claudia Casellato, Alberto Antonietti, Egidio D’Angelo, and Alessandra Pedrocchi. "A Multiple-Plasticity Spiking Neural Network Embedded in a Closed-Loop Control System to Model Cerebellar Pathologies." International Journal of Neural Systems 28, no. 05 (April 19, 2018): 1750017. http://dx.doi.org/10.1142/s0129065717500174.

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The cerebellum plays a crucial role in sensorimotor control and cerebellar disorders compromise adaptation and learning of motor responses. However, the link between alterations at network level and cerebellar dysfunction is still unclear. In principle, this understanding would benefit of the development of an artificial system embedding the salient neuronal and plastic properties of the cerebellum and operating in closed-loop. To this aim, we have exploited a realistic spiking computational model of the cerebellum to analyze the network correlates of cerebellar impairment. The model was modified to reproduce three different damages of the cerebellar cortex: (i) a loss of the main output neurons (Purkinje Cells), (ii) a lesion to the main cerebellar afferents (Mossy Fibers), and (iii) a damage to a major mechanism of synaptic plasticity (Long Term Depression). The modified network models were challenged with an Eye-Blink Classical Conditioning test, a standard learning paradigm used to evaluate cerebellar impairment, in which the outcome was compared to reference results obtained in human or animal experiments. In all cases, the model reproduced the partial and delayed conditioning typical of the pathologies, indicating that an intact cerebellar cortex functionality is required to accelerate learning by transferring acquired information to the cerebellar nuclei. Interestingly, depending on the type of lesion, the redistribution of synaptic plasticity and response timing varied greatly generating specific adaptation patterns. Thus, not only the present work extends the generalization capabilities of the cerebellar spiking model to pathological cases, but also predicts how changes at the neuronal level are distributed across the network, making it usable to infer cerebellar circuit alterations occurring in cerebellar pathologies.
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Pollok, Bettina, Joachim Gross, Daniel Kamp, and Alfons Schnitzler. "Evidence for Anticipatory Motor Control within a Cerebello-Diencephalic-Parietal Network." Journal of Cognitive Neuroscience 20, no. 5 (May 2008): 828–40. http://dx.doi.org/10.1162/jocn.2008.20506.

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The posterior parietal cortex and the cerebellum are assumed to contribute to anticipatory motor control. Thus, it is reasonable that these areas act as a functional unit. To identify a neural signature of anticipatory motor control, 11 healthy volunteers performed a bimanual finger-tapping task with respect to isochronous (i.e., regular) and randomized (i.e., irregular) auditory pacing. Neuromagnetic activity was recorded using a 122-channel whole-head neuromagnetometer. Functional interaction between spatially distributed brain areas was determined by measures of tap-related phase synchronization. Assuming that (i) the cerebellum predicts sensory events by an internal model and (ii) the PPC maintains this prediction, we hypothesized that functional interaction between both structures varies depending on the predictability of the pacing signal. During isochronous pacing, functional connectivity within a cerebello-diencephalic-parietal network before tap onset was evident, suggesting anticipatory motor control. During randomized pacing, however, functional connectivity after tap onset was increased within a parietal-cerebellar loop, suggesting mismatch detection and update of the internal model. Data of the present study imply that anticipatory motor control is implemented in a network-like manner. Our data agree well with the hypothesis that functional connectivity in a cerebello-diencephalic-parietal loop might be crucial for anticipatory motor control, whereas parietal-cerebellar interaction might be critical for feedback processing.
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Omotoso, Gabriel Olaiya, Leviticus Oghenevurinrin Arietarhire, Ileje Inelo Ukwubile, and Ismail Temitayo Gbadamosi. "The Protective Effect of Kolaviron on Molecular, Cellular, and Behavioral Characterization of Cerebellum in the Rat Model of Demyelinating Diseases." Basic and Clinical Neuroscience Journal 11, no. 5 (September 1, 2020): 609–18. http://dx.doi.org/10.32598/bcn.9.10.300.

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Introduction: This study aimed at assessing the protective mechanisms of Kolaviron (KV) on the cerebellum in a rat model of demyelination. Methods: Twenty-eight male Wistar rats were used in the present study. They were randomly divided into 4 groups of 7 rats. Group A (control) received corn oil (0.5 mL/kg/d); group B received 0.2% Cuprizone (CPZ); group C was treated with 200 mg/kg/d of KV, and group D received 0.2% CPZ and 200 mg/kg/d KV for 6 weeks. CPZ powder was mixed with the regular diet while KV was dissolved in corn oil and administered orally. A behavioral test was conducted at the termination of the experiment. Thereafter, the animals were sacrificed and their brains were removed with the excision of the cerebellum. A part of the cerebelli underwent tissue processing with a series of 5 µm thick sections cut from paraffin blocks for histological and immunohistochemical assessment. Besides, the remaining cerebellar tissues were homogenized for the spectrophotometric assays of Oxidative Stress (OS) parameters. Results: The current research findings revealed minimal weight gain following CPZ treatment, but significant weight increase in KV-treated rats. CPZ treatment was associated with a reduction in the number of the line crossed, rearing frequency, rearing duration, center square entry, and center square duration; however, it increased the freezing time, i.e. significantly reversed in the KV-treated animals. Oxidative markers, such as Superoxide Dismutase (SOD) and GPx were reduced in CPZ-treated rats with elevated MDA levels. However, these data were significantly reversed by the co-administration of CPZ and KV. At the tissue level, the cerebellar cortex was characterized by poorly defined layers, cryptic granules, as well as chromatolysis and pyknotic Purkinje cells with the evidence of hypertrophic astrogliosis. Conclusion: CPZ treatment significantly depressed locomotor and exploratory activities. Furthermore, it increased OS and cerebellar toxicity. However, KV intervention significantly enhanced behavioral functions and ameliorated CPZ-induced cerebellar degeneration. Moreover, it considerably regulated OS markers in the cerebellum of the rat model of demyelinating diseases.
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Kim, Jusik, Keeeun Kim, Jung-soon Mo, and Youngsoo Lee. "Atm deficiency in the DNA polymerase β null cerebellum results in cerebellar ataxia and Itpr1 reduction associated with alteration of cytosine methylation." Nucleic Acids Research 48, no. 7 (March 3, 2020): 3678–91. http://dx.doi.org/10.1093/nar/gkaa140.

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Abstract Genomic instability resulting from defective DNA damage responses or repair causes several abnormalities, including progressive cerebellar ataxia, for which the molecular mechanisms are not well understood. Here, we report a new murine model of cerebellar ataxia resulting from concomitant inactivation of POLB and ATM. POLB is one of key enzymes for the repair of damaged or chemically modified bases, including methylated cytosine, but selective inactivation of Polb during neurogenesis affects only a subpopulation of cortical interneurons despite the accumulation of DNA damage throughout the brain. However, dual inactivation of Polb and Atm resulted in ataxia without significant neuropathological defects in the cerebellum. ATM is a protein kinase that responds to DNA strand breaks, and mutations in ATM are responsible for Ataxia Telangiectasia, which is characterized by progressive cerebellar ataxia. In the cerebella of mice deficient for both Polb and Atm, the most downregulated gene was Itpr1, likely because of misregulated DNA methylation cycle. ITPR1 is known to mediate calcium homeostasis, and ITPR1 mutations result in genetic diseases with cerebellar ataxia. Our data suggest that dysregulation of ITPR1 in the cerebellum could be one of contributing factors to progressive ataxia observed in human genomic instability syndromes.
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Knolle, Franziska, Erich Schröger, Pamela Baess, and Sonja A. Kotz. "The Cerebellum Generates Motor-to-Auditory Predictions: ERP Lesion Evidence." Journal of Cognitive Neuroscience 24, no. 3 (March 2012): 698–706. http://dx.doi.org/10.1162/jocn_a_00167.

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Forward predictions are crucial in motor action (e.g., catching a ball, or being tickled) but may also apply to sensory or cognitive processes (e.g., listening to distorted speech or to a foreign accent). According to the “internal forward model,” the cerebellum generates predictions about somatosensory consequences of movements. These predictions simulate motor processes and prepare respective cortical areas for anticipated sensory input. Currently, there is very little evidence that a cerebellar forward model also applies to other sensory domains. In the current study, we address this question by examining the role of the cerebellum when auditory stimuli are anticipated as a consequence of a motor act. We applied an N100 suppression paradigm and compared the ERP in response to self-initiated with the ERP response to externally produced sounds. We hypothesized that sensory consequences of self-initiated sounds are precisely predicted and should lead to an N100 suppression compared with externally produced sounds. Moreover, if the cerebellum is involved in the generation of a motor-to-auditory forward model, patients with focal cerebellar lesions should not display an N100 suppression effect. Compared with healthy controls, patients showed a largely attenuated N100 suppression effect. The current results suggest that the cerebellum forms not only motor-to-somatosensory predictions but also motor-to-auditory predictions. This extends the cerebellar forward model to other sensory domains such as audition.
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Liu, Qi, Chang Liu, Yu Chen, and Yumei Zhang. "Cognitive Dysfunction following Cerebellar Stroke: Insights Gained from Neuropsychological and Neuroimaging Research." Neural Plasticity 2022 (April 15, 2022): 1–11. http://dx.doi.org/10.1155/2022/3148739.

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Although the cerebellum has been consistently noted in the process of cognition, the pathophysiology of this link is still under exploration. Cerebellar stroke, in which the lesions are focal and limited, provides an appropriate clinical model disease for studying the role of the cerebellum in the cognitive process. This review article targeting the cerebellar stroke population (1) describes a cognitive impairment profile, (2) identifies the cerebellar structural alterations linked to cognition, and (3) reveals possible mechanisms of cerebellar cognition using functional neuroimaging. The data indicates the disruption of the cerebro-cerebellar loop in cerebellar stroke and its contribution to cognitive dysfunctions. And the characteristic of cognitive deficits are mild, span a broad spectrum, dominated by executive impairment. The consideration of these findings could contribute to deeper and more sophisticated insights into the cognitive function of the cerebellum and might provide a novel approach to cognitive rehabilitation. The goal of this review is to spread awareness of cognitive impairments in cerebellar disorders.
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Kurtaj, Lavdim, Vjosa Shatri, and Ilir Limani. "Cerebellar Model Controller with new Model of Granule Cell-golgi Cell Building Blocks and Two-phase Learning Acquires Multitude of Generalization Capabilities in Controlling Robot Joint without Exponential Growth in Complexity." International Journal of Electrical and Computer Engineering (IJECE) 8, no. 6 (December 1, 2018): 4292. http://dx.doi.org/10.11591/ijece.v8i6.pp4292-4309.

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Processing in the cerebellum is roughly described as feed forward processing of incoming information over three layers of the cerebellar cortex that send intermediate output to deep cerebellar nuclei, the only output from the cerebellum. Beside this main picture there are several feedback routes, mainly not included in models. In this paper we use new model for neuronal circuit of the cerebellar granule cell layer, as collection of idealized granule cell–golgi cell building blocks with capability of generating multi-dimensional receptive fields modulated by separate input coming to lower dendrite tree of Golgi cell. Resulting cerebellar model controller with two-phase learning will acquire multitude of generalization capabilities when used as robot joint controller. This will usually require more than one Purkinje cell per output. Functionality of granule cell-Golgi cell building block was evaluated with simulations using Simulink single compartment spiking neuronal model. Trained averaging cerebellar model controller attains very good tracking results for wide range of unlearned slower and faster trajectories, with additional improvements by relearning at faster trajectories. Inclusion of new dynamical effects to the controller results with linear growth in complexity for inputs targeting lower dendrite tree of Golgi cell, important for control applications in robotics, but not only.
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Shiba, Kazuhiro, Takashi Torashima, Hirokazu Hirai, Kazuma Ogawa, Nasima Akhter, Kenichi Nakajima, Seigo Kinuya, and Hirofumi Mori. "Potential Usefulness of D2R Reporter Gene Imaging by IBF as Gene Therapy Monitoring for Cerebellar Neurodegenerative Diseases." Journal of Cerebral Blood Flow & Metabolism 29, no. 2 (November 12, 2008): 434–40. http://dx.doi.org/10.1038/jcbfm.2008.137.

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We investigated a gene expression imaging method to examine the level of therapeutic gene expression in the cerebellum. Using a human immunodeficiency virus derived lentivial vector, we expressed the dopamine D2 receptor (D2R) as a reporter protein to mouse cerebellar Purkinje cells. Biodistribution and ex vivo autoradiography studies were performed by giving [125I]5-iodo-7- N-[(1-ethyl-2-pyrrolidinyl)methyl]carboxamide-2,3-dihydrobenzofuran ([125I]IBF) (1.85MBq), as a radioactive D2R ligand, to model mice expressing the D2R with an HA tag (HA-D2R) in the cerebellum. In this study, [125I]IBF was bound to the D2R expressed in the cerebellum of the model mice selectively. Immunostaining was performed to confirm the HA-D2R expression in the cerebellum of the model mice. A significant correlation ( r = 0.900, P< 0.001) between areas that expressed HA-D2R by immunostaining and areas in which [125I]IBF accumulated by the ex vivo autoradiograms was found. These results indicated that radioiodinated IBF is useful as a reporter probe to detect D2R reporter gene expression, which can be used for monitoring therapeutic gene expression in the cerebellum.
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Dissertations / Theses on the topic "Cerebellum model"

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Gavigan, Thomas. "VOLUMETRIC GROWTH MODEL OF HUMAN MEDULLOBLASTOMA IN THE NUDE MOUSE CEREBELLUM." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/133.

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Medulloblastoma is the most common brain tumor in children, accounting for 10-20% of primary central nervous system (CNS) neoplasms and approximately 40% of all posterior fossa tumors. It is a highly invasive embryonal neuroepithelial tumor that typically arises in the cerebellar vermis and has a tendency to disseminate throughout the CNS early in its course. The molecular mechanisms of the disease largely remain uncharacterized, as the clinical treatment is still associated with mortality and severe side effects. The development of a clinically relevant in vivo model is important not only to further understand the disease but also to provide a method with which to test novel therapeutics. This study quantified the volumetric growth of a human medulloblastoma (VC312) in the athymic nude mouse cerebellum using Gd- enhanced T1-weighed MRI scans. Additionally, a medulloblastoma flank tumor model was used to explore the in vivo effect of the oral anti-cancer agent that inhibits Akt activation in the phosphoinositide 3-kinase (PI3K) pathway. In the orthotopic intracerebellar tumor model, perifosine significantly increased the survival of treated mice while qualitatively reducing leptomeningeal dissemination. In the flank model, perifosine effectively suppressed the volumetric growth, decreased activation of the AKT pathway and reduced cellular proliferation in treated mice.
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Senatore, Rosa. "The role of basal ganglia and cerebellum in motor learning. A computational model." Doctoral thesis, Universita degli studi di Salerno, 2012. http://hdl.handle.net/10556/373.

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2010 - 2011
Our research activity investigates the computational processes underlying the execution of complex sequences of movements and aims at understanding how different levels of the nervous system interact and contribute to the gradual improvement of motor performance during learning. Many research areas, from neuroscience to engineering, investigate, from different perspectives and for diverse purposes, the processes that allow humans to efficiently perform skilled movements. From a biological point of view, the execution of voluntary movements requires the interaction between nervous and musculoskeletal systems, involving several areas, from the higher cortical centers to motor circuits in the spinal cord. Understanding these interactions could provide important insights for many research fields, from machine learning to medicine, from the design of robotic limbs to the development of new treatments for movement disorders, such as Parkinson’s disease. This goal could be achieved by finding an answer to the following questions: · How does the central nervous system control and coordinate natural voluntary movements? · Which brain areas are involved in learning a new motor skill? What are the changes that happen in these neural structures? What are the aspects of the movement memorized? · Which is the process that allows people to perform a skilled task, such as playing an instrument, being apparently unaware of the movements they are performing? · What happen when a neurodegenerative disease affects the brain areas involved in executing movements? These questions have been addressed from different perspectives and levels of analysis, from the exploration of the anatomical structure of the neural systems thought to be involved in motor learning (such as the basal ganglia, cerebellum and hippocampus) to the investigation of their neural interaction; from the analysis of the activation of these systems in executing a motor task to the specific activation of a single or a small group of neurons within them. In seeking to understand all the breadth and facets of motor learning, many researchers have used different approaches and methods, such as genetic analysis, neuroimaging techniques (such as fMRI, PET and EEG), animal models and clinical treatments (e.g. drugs administration and brain stimulation). These studies have provided a large body of knowledge that has led to several theories related to the role of the central nervous system in controlling and learning simple and complex movements. These theories envisage the interaction among multiple brain regions, whose cooperation leads to the execution of skilled movements. How can we test these interactions for the purpose of evaluating a theory? Our answer to this question is investigating these interactions through computational models, which provide a valuable complement to the experimental brain research, especially in evaluating the interactions within and among multiple neural systems. Based on these concepts arises our research, which addresses the questions previously pointed out and aims at understanding the computational processes performed by two neural circuits, the Basal Ganglia and Cerebellum, in motor learning. We propose a new hypothesis about the neural processes occurring during acquisition and retention of novel motor skills. According to our hypothesis, a sequence of movements is stored in the nervous system in the form of a spatial sequence of points (composing the trajectory plan associated to the motor sequence) and a sequence of motor commands. We propose that learning novel motor skills requires two phases, in which two different processes take place. Early in learning, when movements are slower, less accurate, and attention demanding, the motor sequence is performed by converting the sequence of target points into the appropriate sequence of motor commands. During this phase, the trajectory plan is acquired and the movements rely on the information provided by the visuo-proprioceptive feedback, which allows to correct the sequence of movements so that the actual trajectory plan corresponds to the desired one and the lowest energy is spent by the muscular subsystem involved. During the late learning phase, when the sequence of movements is performed faster and automatically, with little or no cognitive resources needed to complete it, and is characterized by anticipatory movements, the sequence of motor commands is acquired and thus, the sequence of movements comes to be executed as a single behavior. We suggest that the Basal Ganglia and Cerebellum are involved in learning novel motor sequences, although their role is crucial in different stages of learning. Accordingly, we propose a neural scheme for procedural motor learning, comprising the basal ganglia, cerebellum and cortex, which envisages that the basal ganglia, interacting with the cortex, select the sequence of target points to reach (composing the trajectory plan), whereas the cerebellum, interacting with the cortex, is responsible for converting the trajectory plan into the appropriate sequence of motor commands. Consequently, we suggest that early in learning, task performance is more dependent on the procedural knowledge maintained by the cortex-basal ganglia system, while after a long-term practice, when the sequence of motor commands is acquired within the cerebellum, task performance is more dependent on the motor command sequence maintained by the cortexcerebellar system. We tested the neural scheme (and the hypothesis behind it) through a computational model that incorporates the key anatomical, physiological and biological features of these brain areas in an integrated functional network. Analyzing the behavior of the network in learning novel motor tasks and executing well-known motor tasks, both in terms of the neural activations and motor response provided, we found that the results obtained fit those reported by many neuroimaging and experimental studies presented in the literature. We also carried out further experiments, simulating neurodegenerative disorders (Parkinson's and Huntington disease, which affect the basal ganglia) and cerebellar damages. Results obtained by these experiments validates the proposed hypothesis, showing that the basal ganglia play a key role during the early stage of learning, whereas the cerebellum is crucial for motor skill retention. Our model provides some insights about the learning mechanisms occurring within the cerebellum and gains further understanding of the functional dynamics of information processing within the basal ganglia and cerebellum in normal as well as in diseased brains. Therefore the model provides novel predictions about the role of basal ganglia and cerebellum in motor learning, motivating further investigations of their interactions. [edited by author]
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Babenko, Olena Mykolayivna, and University of Lethbridge Faculty of Arts and Science. "The molecular mechanisms underlying epigenetics of the stress response in the cerebellum in a rat model." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2010, 2010. http://hdl.handle.net/10133/2604.

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Previous findings showed that mild chronic restraint stress causes motor impairments in rats. These behavioural impairments might be related to molecular changes in brain areas that regulate motor functions, such as the cerebellum. Little is known about the role of the cerebellum in stress-induced behavioural alteration. We hypothesized that alteration in animal behaviour after chronic restraint stress is due to brain-specific changes in miRNA and proteins encoding gene expression. Our results revealed that expression of three miRNAs and 39 mRNAs was changed significantly after two weeks of stress. Furthermore, we verified one putative target for one of the changed miRNAs and expression of four randomly selected genes. Changes in gene expression disappeared after two weeks of recovery from stress. These findings provide a novel insight into stress-related mechanisms of gene expression underlying altered behavioural performance. The observations bear implications for the prevention and treatment of stress-related disorders and disease.
xii, 109 leaves. : ill. ; 29 cm
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Chintawar, Satyan. "Neural precursor cells: interaction with blood-brain barrier and neuroprotective effect in an animal model of cerebellar degeneration." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210202.

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Adult neural precursor cells (NPCs) are a heterogeneous population of mitotically active, self-renewing multipotent cells of both adult and developing CNS. They can be expanded in vitro in the presence of mitogens. The B05 transgenic SCA1 mice, expressing human ataxin-1 with an expanded polyglutamine tract in cerebellar Purkinje cells (PCs), recapitulate many pathological and behavioral characteristics of the neurodegenerative disease spinocerebellar ataxia type 1 (SCA1), including progressive ataxia and PC loss. We transplanted neural precursor cells (NPCs) derived from the subventricular zone of GFP-expressing adult mice into the cerebellar white matter of SCA1 mice when they showed absent (5 weeks), initial (13 weeks) and significant PC loss (24 weeks). A stereological count demonstrates that mice with significant cell loss exhibit highest survival of grafted NPCs and migration to the vicinity of PCs as compared to wt and younger grafted animals. These animals showed improved motor skills as compared to sham animals. Confocal analysis and profiling shows that many of implanted cells present in the cerebellar cortex have formed gap junctions with host PCs and express connexin43. Grafted cells did not adopt characteristics of PCs, but stereological and morphometric analysis of the cerebellar cortex revealed that grafted animals had more surviving PCs and a better preserved morphology of these cells than the control groups. Perforated patch clamp recordings revealed a normalization of the PC basal membrane potential, which was abnormally depolarized in sham-treated animals. No significant increase in levels of several neurotrophic factors was observed, suggesting, along with morphological observation, that the neuroprotective effect of grafted NPCs was mediated by direct contact with the host PCs. In this study, evidence for a neuroprotective effect came, in addition to motor behavior improvement, from stereological and electrophysiological analyses and suggest that timing of stem cell delivery is important to determine its therapeutic effect.

In a brain stem cell niche, NSCs reside in a complex cellular and extracellular microenvironment comprising their own progeny, ependymal cells, numerous blood vessels and various extracellular matrix molecules. Recently, it was reported that blood vessel ECs-NSCs crosstalk plays an important role in tissue homeostasis. Bloodstream offers a natural delivery vehicle especially in case of diffuse neurodegenerative diseases which require widespread distribution of exogenous cells. As NSCs are confronted with blood-brain barrier endothelial cells (BBB-ECs) before they can enter into brain parenchyma, we investigated their interaction using primary cultures in an in vitro BBB model. We isolated human fetal neural precursor cells (hfNPCs) from aborted fetal brain tissues and expanded in vitro. We showed that in an in vitro model, human BBB endothelium induces the rapid differentiation of hfNPCs and allows them to cross the endothelial monolayer, with the differentiated progeny remaining in close contact with endothelial cells. These results are not reproduced when using a non-BBB endothelium and are partly dependent on the cytokine MCP1. Our data suggest that, in the presence of attractive signals released by a damaged brain, intravascularly administered NPCs can move across an intact BBB endothelium and differentiate in its vicinity. Overall, our findings have implications for the development of cellular therapies for cerebellar degenerative diseases and understanding of the brain stem cell niche.
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Takagishi, Yoshiko, 芳子 高岸, and Yoshiharu Murata. "Myosin Va mutation in rats is an animal model for the human hereditary neurological disease, Griscelli syndrome type 1." New York Academy of Sciences, 2006. http://hdl.handle.net/2237/10947.

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Hecker, David [Verfasser]. "Migration of interneuronal precursor cells in the developing cerebellum of mice : model-based cell tracking and simulation / David Hecker." Bonn : Universitäts- und Landesbibliothek Bonn, 2010. http://d-nb.info/1016155654/34.

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Klein, de Licona Hannah Washington. "Congenital LCMV virus: mechanism of brain disease in a rat model of congenital viral infection." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/531.

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Lymphocytic choriomeningitis virus (LCMV) infection during pregnancy severely injures the human fetal brain. Neonatal rats inoculated with LCMV are an excellent model of congenital LCMV infection, as they develop neuropathology, including cerebellar injuries, similar to those seen in humans. The goal of this thesis was to determine what underlies brain injury and the differential immune response and to determine the role of T-cells in LCMV induced pathology. First, I examined whether cytokine and chemokine expression after LCMV infection was higher in the cerebellum and olfactory bulbs, which undergo destruction, compared to the hippocampus and septum, which undergo no acute destruction. Second, I used T-cell deficient and T-cell competent animals to evaluate the role of T-lymphocytes in LCMV-induced cerebellar and hippocampus pathology. Finally, I characterized the migration abnormality that develops in the cerebellum after LCMV infection. My results showed that cytokine and chemokine expression is higher in the cerebellum and olfactory bulb than in the hippocampus and septum. Using astrocyte cultures, I determined that astrocytes isolated from the cerebellum have a more robust cytokine response to infection compared to astrocytes from the hippocampus. Furthermore, inoculation of congenitally athymic (rnu/rnu) rats, which are deficient in T-lymphocytes, demonstrated that cerebellar hypoplasia is T-cell independent while cerebellar destruction and abnormal neuron migration is T-cell dependent. In the hippocampus, T-cells protect against loss of dentate granule cells. A study of the migration abnormality determined that LCMV infection disrupts radial glia fibers and extends proliferation of granule cells in a T-cell dependent manner. The findings reported here support a pivotal role of the immune system in regional brain pathology as well as in the disruption of migration.
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Balastik, Martin. "Trim2 mutant mice as a model for cerebellar ataxia." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=975117025.

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MARSHALL, CRAIG ANTHONY. "QUANTITATIVE MEASUREMENT OF THE EXPRESSION OF TWO GENES IN THE CORETX AND CEREBELLUM OF A MOUSE MODEL OF JUVENILE ALZHEIMER’S." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/613283.

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There is a continuing effort in order to connect the two neurodegenerative diseases: Alzheimer’s Disease and Niemann-Pick Type C Disease (NPC1) “Juvenile Alzheimer’s”. Here in this study, we attempted to determine if there was a connection through the gene expression in inflammatory genes, CD14 and ETS-1, in a NPC1 mouse model, Npc1nmf164, using quantitative real time PCR. Hydroxypropyl-beta-cyclodextrin (HPβCD) is reported to provide a beneficial effect on NPC1, and there was interest in seeing if HPβCD treatment could return the expression levels to wildtype levels. Instead, only a significant decrease of the CD14 and ETS-1 in cerebellar tissue of untreated NPC1 affected mice (when compared to wildtype levels), and no significant difference for the treated, affected mice was seen. CD14 p value = 0.026, and ETS-1 p value = 0.014. There was no significant difference found in cortex tissue for either CD14 or ETS-1.
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Parnell, Scott E., Jayanth Ramadoss, Michael D. Delp, Michael W. Ramsey, Wei-Jung A. Chen, James R. West, and Timothy A. Cudd. "Chronic Ethanol Increases Fetal Cerebral Blood Flow Specific to the Ethanol-Sensitive Cerebellum Under Normoxaemic, Hypercapnic and Acidaemic Conditions: Ovine Model." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/4134.

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Cerebral hypoxia has been proposed as a mechanism by which prenatal ethanol exposure causes fetal alcohol spectrum disorder (FASD) in children, but no study had tested this hypothesis using a chronic exposure model that mimicks a common human exposure pattern. Pregnant sheep were exposed to ethanol, 0.75 or 1.75 g kg−1 (to create blood ethanol concentrations of 85 and 185 mg dl−1, respectively), or saline 3 days per week in succession (a ‘binge drinking’ model) from gestational day (GD) 109 until GD 132. Fetuses were instrumented on GD 119–120 and studied on GD 132. The 1.75 g kg−1 dose resulted in a significant increase in fetal biventricular output (measured by radiolabelled microsphere technique) and heart rate, and a reduction of mean arterial pressure and total peripheral resistance at 1 h, the end of ethanol infusion. The arterial partial pressure of CO2 was increased, arterial pH was decreased and arterial partial pressure of O2 did not change. Fetal whole‐brain blood flow increased by 37% compared with the control group at 1 h, resulting in increased cerebral oxygen delivery. The elevation in brain blood flow was region specific, occurring preferentially in the ethanol‐sensitive cerebellum, increasing by 44% compared with the control group at 1 h. There were no changes in the lower dose group. Assessment of regional differences in the teratogenic effects of ethanol by stereological cell‐counting technique showed a reduced number of cerebellar Purkinje cells in response to the 1.75 g kg−1 dose compared with the control brains. However, no such differences in neuronal numbers were observed in the hippocampus or the olfactory bulb. We conclude that repeated exposure to moderate doses of ethanol during the third trimester alters fetal cerebral vascular function and increases blood flow in brain regions that are vulnerable to ethanol in the presence of acidaemia and hypercapnia, and in the absence of hypoxia.
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Books on the topic "Cerebellum model"

1

David, Rogers, and Research Institute for Advanced Computer Science (U.S.), eds. Temporal learning in the cerebellum: The MicroCircuit model. [Moffett Field, Calif.]: Research Institute for Advanced Computer Science, NASA Ames Research Center, 1990.

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Eskandarian, Azim. A reference model dynamics-CMAC algorithm for simulation and control of robotic manipulators. [S.l.]: George Washington University, 1991.

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Neural transplantation in cerebellar ataxia. Austin, Tex: Landes, 1997.

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Randolph, Raugh Michael, Ames Research Center, Research Institute for Advanced Computer Science (U.S.), and Compcon (34th : 1989 : San Francisco, Calif.), eds. Cerebellar models of associative memory: Three papers from IEEE COMPCON Spring '89. [Moffettt Field, Calif.?]: Research Institute for Advanced Computer Science, NASA Ames Research Center, 1989.

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Ely, Budding Deborah, ed. Subcortical structures and cognition: Implications for neuropsychological assessment. New York: Springer, 2009.

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1946-, Vaina Lucia, ed. From the retina to the neocortex: Selected papers of David Marr. Boston: Birkhäuser, 1991.

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Mason, Peggy. Cerebellum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0024.

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The cerebellum uses sensory feedback and information about intended actions to ensure coordinated and smooth movements despite changing conditions. An analogy between the cerebellum and an orchestral conductor is elaborated. The cerebellum’s involvement in forming and executing motor memories is presented. Cerebellar circuits through the cerebellar cortex and deep nuclei and the dependence of cerebellar learning on climbing fiber input to Purkinje cells are briefly described. Sensory reafference and motor efference copy are defined and their roles in coordinating movement introduced. Cerebellar symptoms including ataxia, dysmetria and dysdiadochokinesia, are discussed and a possible model for dysmetria is considered. The specific inputs to and outputs from the vermis, paravermis, and lateral lobes are detailed in a description of canonical cerebellar loops. Finally, evidence that the cerebellum is involved in modulating nonmotor functions such as language, affect, social cognition, and visceral control is presented for the reader’s consideration.
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Soong, Bing-wen. Trials for Cerebellar Ataxias: From Cellular Models to Human Therapies. Springer International Publishing AG, 2023.

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Berman, Frederick W. Development and characterization of a model of glutamate and domoate toxicity in cultured rat cerebellar granule neurons. 1997.

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Koziol, Leonard F., and Deborah Ely Budding. Subcortical Structures and Cognition: Implications for Neuropsychological Assessment. Springer New York, 2010.

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Book chapters on the topic "Cerebellum model"

1

Koziol, Leonard F., Deborah Ely Budding, and Dana Chidekel. "The Cerebellum." In ADHD as a Model of Brain-Behavior Relationships, 51–53. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8382-3_18.

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Travis, Bryan J. "A Computational Model of the Cerebellum." In Analysis and Modeling of Neural Systems, 131–37. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-4010-6_14.

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Houk, J. C. "Model of the Cerebellum as an Array Of Adjustable Pattern Generators." In Cerebellum and Neuronal Plasticity, 249–60. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0965-9_16.

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Koziol, Leonard F., Deborah Ely Budding, and Dana Chidekel. "The Modular Organization of the Cerebellum." In ADHD as a Model of Brain-Behavior Relationships, 55. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8382-3_19.

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Zhang, Shaobai, and Qun Chen. "Study over Cerebellum Prediction Model During Hand Tracking." In Communications in Computer and Information Science, 159–67. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3966-9_17.

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Antonietti, Alberto, Claudia Casellato, Egidio D’Angelo, and Alessandra Pedrocchi. "Computational Modelling of Cerebellar Magnetic Stimulation: The Effect of Washout." In Lecture Notes in Computer Science, 35–46. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-82427-3_3.

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AbstractNowadays, clinicians have multiple tools that they can use to stimulate the brain, by means of electric or magnetic fields that can interfere with the bio-electrical behaviour of neurons. However, it is still unclear which are the neural mechanisms that are involved and how the external stimulation changes the neural responses at network-level. In this paper, we have exploited the simulations carried out using a spiking neural network model, which reconstructed the cerebellar system, to shed light on the underlying mechanisms of cerebellar Transcranial Magnetic Stimulation affecting specific task behaviour. Namely, two computational studies have been merged and compared. The two studies employed a very similar experimental protocol: a first session of Pavlovian associative conditioning, the administration of the TMS (effective or sham), a washout period, and a second session of Pavlovian associative conditioning. In one study, the washout period between the two sessions was long (1 week), while the other study foresaw a very short washout (15 min). Computational models suggested a mechanistic explanation for the TMS effect on the cerebellum. In this work, we have found that the duration of the washout strongly changes the modification of plasticity mechanisms in the cerebellar network, then reflected in the learning behaviour.
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Sotelo, Constantino. "Cerebellar Transplantation: A Potential Model to Study Repair and Development of Neurons and Circuits in the Cerebellum." In Development of the Cerebellum from Molecular Aspects to Diseases, 465–93. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59749-2_22.

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Pessac, Bernard, and Françoise Alliot. "Do Mouse Cerebellum Astrocytes Play a Role in Neuronal Survival and Differentiation?" In Model Systems of Development and Aging of the Nervous System, 201–8. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2037-1_14.

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Sotelo, Constantino. "Cerebellar Transplantation: A Potential Model to Study Repair and Development of Neurons and Circuits in the Cerebellum." In Contemporary Clinical Neuroscience, 605–33. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23104-9_26.

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Shim, Vui Ann, Chris Stephen Naveen Ranjit, Bo Tian, and Huajin Tang. "A Simplified Cerebellum-Based Model for Motor Control in Brain Based Devices." In Neural Information Processing, 520–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-42054-2_65.

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Conference papers on the topic "Cerebellum model"

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Kawato, M., and H. Gomi. "Model of four regions of the cerebellum." In 1991 IEEE International Joint Conference on Neural Networks. IEEE, 1991. http://dx.doi.org/10.1109/ijcnn.1991.170436.

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"Brain-inspired Sensorimotor Robotic Platform - Learning in Cerebellum-driven Movement Tasks through a Cerebellar Realistic Model." In Special Session on Challenges in Neuroengineering. SCITEPRESS - Science and and Technology Publications, 2013. http://dx.doi.org/10.5220/0004659305680573.

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Zhang Shao-bai, Ruan Xiao-gang, and Cheng Xiefeng. "A new constructing method of cerebellum model applying to DIVA model." In 2009 Chinese Control and Decision Conference (CCDC). IEEE, 2009. http://dx.doi.org/10.1109/ccdc.2009.5192809.

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Zhou, Chenye, and Shaobai Zhang. "Research on timing function of cerebellum in DIVA model." In International Conference on Communication Technology. Southampton, UK: WIT Press, 2014. http://dx.doi.org/10.2495/icct130381.

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Mathew, Seema, Parimal Giri, and Manjusha Agwan. "A Simulink Implementation of the Cerebellum Model Articulation Controller." In 2010 Second International Conference on Advances in Computing, Control and Telecommunication Technologies (ACT). IEEE, 2010. http://dx.doi.org/10.1109/act.2010.47.

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Presannan, Anandhu, Arathi Rajendran, Bipin Nair, and Shyam Diwakar. "Reproducing the Firing Properties of a Cerebellum Deep Cerebellar Nucleus with a Multi-Compartmental Morphologically Realistic Biophysical Model." In 2018 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2018. http://dx.doi.org/10.1109/icacci.2018.8554491.

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Luo, Junwen, Graeme Coapes, Patrick Degenaar, Tadashi Yamazaki, Terrence Mak, and Chung Tin. "A real-time silicon cerebellum spiking neural model based on FPGA." In 2014 International Symposium on Integrated Circuits (ISIC). IEEE, 2014. http://dx.doi.org/10.1109/isicir.2014.7029586.

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Yoosef, Afila, Harilal Parasuram, Chaitanya Medini, Sergio Solinas, Egidio D'Angelo, Bipin Nair, and Shyam Diwakar. "Parallelization of a Computational Model of a Biophysical Neuronal Circuitry of Rat Cerebellum." In the 2014 International Conference. New York, New York, USA: ACM Press, 2014. http://dx.doi.org/10.1145/2660859.2660962.

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Geminiani, Alice, Aurimas Mockevicius, Egidio D'Angelo, and Claudia Casellato. "Cerebellum involvement in dystonia: insights from a spiking neural network model during associative learning." In 2022 44th Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2022. http://dx.doi.org/10.1109/embc48229.2022.9871205.

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Reyes López, Misael, Fernando Arámbula Cosío, Boris Escalante Ramírez, and Jimena Olveres Montiel. "Shape model and Hermite features for the segmentation of the cerebellum in fetal ultrasound." In 14th International Symposium on Medical Information Processing and Analysis, edited by Eduardo Romero, Natasha Lepore, and Jorge Brieva. SPIE, 2018. http://dx.doi.org/10.1117/12.2511411.

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Reports on the topic "Cerebellum model"

1

Gambello, Michael. Behavioral Analysis and Rescue of a Novel Cerebellar Mouse Model of Tuberous Sclerosis Complex. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada566012.

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