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Journal articles on the topic 'Purkinje, Cellules de'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Peirone, S. M., and G. Filogamo. "Caractérisation immunophénotypique des cellules de Purkinje du cœur." Morphologie 88, no. 281 (2004): 90. http://dx.doi.org/10.1016/s1286-0115(04)98072-1.

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2

CALVET, M., and J. CALVET. "Electrophysiologie et analyse d'image du developpement des cellules de Purkinje en culture et sur l'animal entier." Revue d&'apos;Electroencéphalographie et de Neurophysiologie Clinique 17, no. 4 (1987): 437–46. http://dx.doi.org/10.1016/s0370-4475(87)80089-8.

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3

Fazekas, Tamás. "Jan Evangelista Purkinje (1797-1869)." Kaleidoscope history 11, no. 22 (2021): 81–85. http://dx.doi.org/10.17107/kh.2021.22.81-95.

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Being a chairman and professor of physiology in Breslau/Wroclaw till 1850, Jan Evangelista Purkinje (1797-1869) made many crucial discoveries/experiments with the new advanced microscopy and histology techniques. He established the first institute of the physiology of the world (1839) and founded the basic principles and framework of cellular physiology (protoplasmic concept) both in plant and animal tissues. Purkine discovered and described (first in Polish, 1839) the extensive terminal network of the cardiac conduction system. Its paradigmatic discovery was presented in the last two 15-page

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4

Prestori, Francesca, Francesco Moccia, and Egidio D’Angelo. "Disrupted Calcium Signaling in Animal Models of Human Spinocerebellar Ataxia (SCA)." International Journal of Molecular Sciences 21, no. 1 (2019): 216. http://dx.doi.org/10.3390/ijms21010216.

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Spinocerebellar ataxias (SCAs) constitute a heterogeneous group of more than 40 autosomal-dominant genetic and neurodegenerative diseases characterized by loss of balance and motor coordination due to dysfunction of the cerebellum and its efferent connections. Despite a well-described clinical and pathological phenotype, the molecular and cellular events that underlie neurodegeneration are still poorly undaerstood. Emerging research suggests that mutations in SCA genes cause disruptions in multiple cellular pathways but the characteristic SCA pathogenesis does not begin until calcium signaling

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5

McKay, Bruce E., Jordan D. T. Engbers, W. Hamish Mehaffey, et al. "Climbing Fiber Discharge Regulates Cerebellar Functions by Controlling the Intrinsic Characteristics of Purkinje Cell Output." Journal of Neurophysiology 97, no. 4 (2007): 2590–604. http://dx.doi.org/10.1152/jn.00627.2006.

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The contribution of Purkinje cells to cerebellar motor coordination and learning is determined in part by the chronic and acute effects of climbing fiber (CF) afferents. Whereas the chronic effects of CF discharge, such as the depression of conjunctive parallel fiber (PF) inputs, are well established, the acute cellular functions of CF discharge remain incompletely understood. In rat cerebellar slices, we show that CF discharge presented at physiological frequencies substantially modifies the frequency and pattern of Purkinje cell spike output in vitro. Repetitive CF discharge converts a spont

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6

Hernández, Rosendo G., Chris I. De Zeeuw, Ruyan Zhang, Tatyana A. Yakusheva, and Pablo M. Blazquez. "Translation information processing is regulated by protein kinase C-dependent mechanism in Purkinje cells in murine posterior vermis." Proceedings of the National Academy of Sciences 117, no. 29 (2020): 17348–58. http://dx.doi.org/10.1073/pnas.2002177117.

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The cerebellar posterior vermis generates an estimation of our motion (translation) and orientation (tilt) in space using cues originating from semicircular canals and otolith organs. Theoretical work has laid out the basic computations necessary for this signal transformation, but details on the cellular loci and mechanisms responsible are lacking. Using a multicomponent modeling approach, we show that canal and otolith information are spatially and temporally matched in mouse posterior vermis Purkinje cells and that Purkinje cell responses combine translation and tilt information. Purkinje c

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7

Winkler, Sabine C., Etsuko Shimobayashi та Josef P. Kapfhammer. "PKCγ-Mediated Phosphorylation of CRMP2 Regulates Dendritic Outgrowth in Cerebellar Purkinje Cells". Molecular Neurobiology 57, № 12 (2020): 5150–66. http://dx.doi.org/10.1007/s12035-020-02038-6.

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Abstract The signalling protein PKCγ is a major regulator of Purkinje cell development and synaptic function. We have shown previously that increased PKCγ activity impairs dendritic development of cerebellar Purkinje cells. Mutations in the protein kinase Cγ gene (PRKCG) cause spinocerebellar ataxia type 14 (SCA14). In a transgenic mouse model of SCA14 expressing the human S361G mutation, Purkinje cell dendritic development is impaired in cerebellar slice cultures similar to pharmacological activation of PKC. The mechanisms of PKCγ-driven inhibition of dendritic growth are still unclear. Using

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8

Tsutsui, Kazuyoshi. "Neurosteroid Biosynthesis and Action in the Purkinje Cell." Journal of Experimental Neuroscience 2 (January 2009): JEN.S2290. http://dx.doi.org/10.4137/jen.s2290.

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It is now clearly established that steroids can be synthesized de novo by the vertebrate brain. Such steroids are called neurosteroids. To understand neurosteroid action in the brain, data on the regio- and temporal-specific synthesis of neurosteroids are needed. In the middle 1990s, the Purkinje cell, an important cerebellar neuron, was identified as a major site for neurosteroid formation in vertebrates. This discovery has allowed deeper insights into neuronal neurosteroidogenesis and biological actions of neurosteroids have become clear by the studies using the Purkinje cell as an excellent

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9

Huang, Tung-Yi, Lung-Sheng Lin, Keng-Chi Cho, et al. "Chronic treadmill exercise in rats delicately alters the Purkinje cell structure to improve motor performance and toxin resistance in the cerebellum." Journal of Applied Physiology 113, no. 6 (2012): 889–95. http://dx.doi.org/10.1152/japplphysiol.01363.2011.

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Although exercise usually improves motor performance, the underlying cellular changes in the cerebellum remain to be elucidated. This study aimed to investigate whether and how chronic treadmill exercise in young rats induced Purkinje cell changes to improve motor performance and rendered the cerebellum less vulnerable to toxin insults. After 1-wk familiarization of treadmill running, 6-wk-old male Wistar rats were divided into exercise and sedentary groups. The exercise group was then subjected to 8 wk of exercise training at moderate intensity. The rotarod test was carried out to evaluate mo

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10

Kageyama, Yusuke, Zhongyan Zhang, Ricardo Roda, et al. "Mitochondrial division ensures the survival of postmitotic neurons by suppressing oxidative damage." Journal of Cell Biology 197, no. 4 (2012): 535–51. http://dx.doi.org/10.1083/jcb.201110034.

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Mitochondria divide and fuse continuously, and the balance between these two processes regulates mitochondrial shape. Alterations in mitochondrial dynamics are associated with neurodegenerative diseases. Here we investigate the physiological and cellular functions of mitochondrial division in postmitotic neurons using in vivo and in vitro gene knockout for the mitochondrial division protein Drp1. When mouse Drp1 was deleted in postmitotic Purkinje cells in the cerebellum, mitochondrial tubules elongated due to excess fusion, became large spheres due to oxidative damage, accumulated ubiquitin a

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11

Cavanagh, J. B., J. L. Holton, C. C. Nolan, D. E. Ray, J. T. Naik, and P. G. Mantle. "The Effects of the Tremorgenic Mycotoxin Penitrem A on the Rat Cerebellum." Veterinary Pathology 35, no. 1 (1998): 53–63. http://dx.doi.org/10.1177/030098589803500105.

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Within 10 minutes of intraperitoneal injection of penitrem A (3 mg/kg), rats develop severe generalized tremors and ataxia that persist for up to 48 hours. These are accompanied by a three- to fourfold increase in cerebellar cortical blood flow. Mitochondrial swelling occurs in cerebellar stellate and basket cells within 30 minutes of dosing and persists for more than 12 hours without leading to cell death. From 2 hours, Purkinje cell dendrites show early cytoplasmic condensation accompanied by fine vacuolation of smooth endoplasmic reticulum and enlargement of perikaryal mitochondria. From 6

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12

Dahmane, N., and A. Ruiz-i-Altaba. "Sonic hedgehog regulates the growth and patterning of the cerebellum." Development 126, no. 14 (1999): 3089–100. http://dx.doi.org/10.1242/dev.126.14.3089.

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The molecular bases of brain development and CNS malignancies remain poorly understood. Here we show that Sonic hedgehog (Shh) signaling controls the development of the cerebellum at multiple levels. SHH is produced by Purkinje neurons, it is required for the proliferation of granule neuron precursors and it induces the differentiation of Bergmann glia. Blocking SHH function in vivo results in deficient granule neuron and Bergmann glia differentiation as well as in abnormal Purkinje neuron development. Thus, our findings provide a molecular model for the growth and patterning of the cerebellum

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13

Constaino, Sotelo. "Cell Interactions Underlying Purkinje Cell Replacement by Neural Grafting in the pcd Mutant Cerebellum." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 20, S3 (1993): S43—S52. http://dx.doi.org/10.1017/s0317167100048526.

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ABSTRACT:The results obtained with neuronal grafting in an animal model of heredo-degenerative ataxia (the pcd mutant mouse) have been extremely useful to unmask new aspects of neural plasticity. The grafted embryonic Purkinje cells invade the deficient molecular layer of the host by migrating radially through adult Bergmann fibers. There, they start building their dendritic trees and, by promoting the axonal sprouting of specific adult neuronal population in a timed sequence, they receive appropriate synaptic contacts, starting ten days after grafting. Twenty-one days after grafting, the graf

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14

Liu, Chunyi, Mei Mei, Qiuling Li, et al. "Loss of the golgin GM130 causes Golgi disruption, Purkinje neuron loss, and ataxia in mice." Proceedings of the National Academy of Sciences 114, no. 2 (2016): 346–51. http://dx.doi.org/10.1073/pnas.1608576114.

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The Golgi apparatus lies at the heart of the secretory pathway where it is required for secretory trafficking and cargo modification. Disruption of Golgi architecture and function has been widely observed in neurodegenerative disease, but whether Golgi dysfunction is causal with regard to the neurodegenerative process, or is simply a manifestation of neuronal death, remains unclear. Here we report that targeted loss of the golgin GM130 leads to a profound neurological phenotype in mice. Global KO of mouse GM130 results in developmental delay, severe ataxia, and postnatal death. We further show

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15

Nangoy, Belinda V., Sonny J. R. Kalangi, and Taufiq F. Pasiak. "Gambaran Mikrokopik Serebelum pada Hewan Coba Postmortem." JURNAL BIOMEDIK (JBM) 11, no. 1 (2019): 10. http://dx.doi.org/10.35790/jbm.11.1.2019.23205.

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Abstract: After death, there will be cellular changes that cause definite signs of death. These changes could be used to determine the time of death. This study was aimed to determine the microscopic changes of the cerebellum during 1 hour to 24 hours postmortem. This was a descriptive study. Four domestic pigs of more than 90 kg were used as animal models. After being killed, we made slices in the pig heads to expose and observe cerebellar microscopic changes in several time intervals, as follows: 90 minutes, 2 hours, 3 hours, 4 hours, 5 hours, 6 hours, 7 hours, 8 hours, 9 hours, 10 hours, 11

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16

Chen, K. Amy, Pedro E. Cruz, Derek J. Lanuto, et al. "Cellular fusion for gene delivery to SCA1 affected Purkinje neurons." Molecular and Cellular Neuroscience 47, no. 1 (2011): 61–70. http://dx.doi.org/10.1016/j.mcn.2011.03.003.

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17

Zang, Yunliang, and Erik De Schutter. "The Cellular Electrophysiological Properties Underlying Multiplexed Coding in Purkinje Cells." Journal of Neuroscience 41, no. 9 (2021): 1850–63. http://dx.doi.org/10.1523/jneurosci.1719-20.2020.

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18

Morita, Tetsuo, and Tatsuo Shimada. "Surface morphology of Purkinje cells and myocardial cells following chemical digestion." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (1990): 420–21. http://dx.doi.org/10.1017/s0424820100159643.

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From light and transmission electron microscopic studies, it has been long known that Purkinje cells of mammalian hearts have morphological characteristics different from ordinary myocardial cells. In the present study, not only Purkinje cells and myocardial cells but also connective tissue sheaths surrounding these cells were investigated by combined scanning electron microscopy(SEM) and chemical digestion.The moderator band of adult sheep heart was used because it possessed both Purkinje cells and myocardial cells (Fig.1). Tissue blocks were immersed in Karnovsky’s fixative for 3hr or longer

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19

Gorza, L., S. Schiaffino, and P. Volpe. "Inositol 1,4,5-trisphosphate receptor in heart: evidence for its concentration in Purkinje myocytes of the conduction system." Journal of Cell Biology 121, no. 2 (1993): 345–53. http://dx.doi.org/10.1083/jcb.121.2.345.

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Inositol 1,4,5-trisphosphate (IP3) is one of the second messengers capable of releasing Ca2+ from sarcoplasmic reticulum/ER subcompartments. The mRNA encoding the intracellular IP3 receptor (Ca2+ channel) has been detected in low amounts in the heart of various species by Northern blot analysis. The myocardium, however, is a heterogeneous tissue composed of working myocytes and conduction system cells, i.e., myocytes specialized for the beat generation and stimulus propagation. In the present study, the cellular distribution of the heart IP3 receptor has been investigated. [3H]IP3 binding expe

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20

Gruol, D. L., J. G. Netzeband, and T. E. Nelson. "Somatic Ca2+ signaling in cerebellar Purkinje neurons." Journal of Neuroscience Research 88, no. 2 (2010): 275–89. http://dx.doi.org/10.1002/jnr.22204.

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21

Valenzuela, Fermín, and Mario Vassalle. "Overdrive excitation and cellular calcium load in canine cardiac Purkinje fibers." Journal of Electrocardiology 18, no. 1 (1985): 21–33. http://dx.doi.org/10.1016/s0022-0736(85)80031-5.

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22

Brown, Sherry-Ann, and Leslie M. Loew. "Integration of Cellular Metabolism and Membrane Excitability in Cerebellar Purkinje Neurons." Biophysical Journal 98, no. 3 (2010): 139a. http://dx.doi.org/10.1016/j.bpj.2009.12.751.

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23

Tanaka, Masahiko. "Dendrite Formation of Cerebellar Purkinje Cells." Neurochemical Research 34, no. 12 (2009): 2078–88. http://dx.doi.org/10.1007/s11064-009-0073-y.

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24

Ohashi, Ryo, Shin-ichi Sakata, Asami Naito, Naohide Hirashima, and Masahiko Tanaka. "Dendritic differentiation of cerebellar Purkinje cells is promoted by ryanodine receptors expressed by Purkinje and granule cells." Developmental Neurobiology 74, no. 4 (2013): 467–80. http://dx.doi.org/10.1002/dneu.22139.

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25

DOULAZMI, MOHAMED, NADIA HADJ-SAHRAOUI, FLORENCE FREDERIC, and JEAN MARIANI. "DIMINISHING PURKINJE CELL POPULATIONS IN THE CEREBELLA OF AGING HETEROZYGOUS PURKINJE CELL DEGENERATION BUT NOT HETEROZYGOUS NERVOUS MICE." Journal of Neurogenetics 16, no. 2 (2002): 111–23. http://dx.doi.org/10.1080/01677060213157.

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26

Cougnoux, Antony, Julia C. Yerger, Mason Fellmeth, et al. "Single Cell Transcriptome Analysis of Niemann–Pick Disease, Type C1 Cerebella." International Journal of Molecular Sciences 21, no. 15 (2020): 5368. http://dx.doi.org/10.3390/ijms21155368.

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Niemann–Pick disease, type C1 (NPC1) is a lysosomal disease characterized by endolysosomal storage of unesterified cholesterol and decreased cellular cholesterol bioavailability. A cardinal symptom of NPC1 is cerebellar ataxia due to Purkinje neuron loss. To gain an understanding of the cerebellar neuropathology we obtained single cell transcriptome data from control (Npc1+/+) and both three-week-old presymptomatic and seven-week-old symptomatic mutant (Npc1−/−) mice. In seven-week-old Npc1−/− mice, differential expression data was obtained for neuronal, glial, vascular, and myeloid cells. As

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27

Magat, Julie, Arnaud Fouillet, Marion Constantin, et al. "3D magnetization transfer (MT) for the visualization of cardiac free-running Purkinje fibers: an ex vivo proof of concept." Magnetic Resonance Materials in Physics, Biology and Medicine 34, no. 4 (2021): 605–18. http://dx.doi.org/10.1007/s10334-020-00905-w.

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Abstract Objectives We investigate the possibility to exploit high-field MRI to acquire 3D images of Purkinje network which plays a crucial role in cardiac function. Since Purkinje fibers (PF) have a distinct cellular structure and are surrounded by connective tissue, we investigated conventional contrast mechanisms along with the magnetization transfer (MT) imaging technique to improve image contrast between ventricular structures of differing macromolecular content. Methods Three fixed porcine ventricular samples were used with free-running PFs on the endocardium. T1, T2*, T2, and M0 were ev

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28

Lisberger, Stephen G. "Physiologic basis for motor learning in the vestibulo-ocular reflex." Otolaryngology–Head and Neck Surgery 119, no. 1 (1998): 43–48. http://dx.doi.org/10.1016/s0194-5998(98)70172-x.

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The vestibulo-ocular reflex has been used extensively for study of the neural mechanisms of learning that is dependent on an intact cerebellum. Anatomic, physiologic, behavioral, and computational approaches have revealed the neural circuits that are used to generate the vestibulo-ocular reflex and have identified two likely sites of plasticity within those circuits. One site of plasticity is in the vestibular inputs to floccular target neurons, which are located in the vestibular nuclei and receive monosynaptic inhibition from Purkinje cells in the floccular complex of the cerebellar cortex.

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29

Moers, Alexandra, Alexander Nürnberg, Sandra Goebbels, Nina Wettschureck та Stefan Offermanns. "Gα12/Gα13 Deficiency Causes Localized Overmigration of Neurons in the Developing Cerebral and Cerebellar Cortices". Molecular and Cellular Biology 28, № 5 (2007): 1480–88. http://dx.doi.org/10.1128/mcb.00651-07.

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ABSTRACT The heterotrimeric G proteins G12 and G13 link G-protein-coupled receptors to the regulation of the actin cytoskeleton and the induction of actomyosin-based cellular contractility. Here we show that conditional ablation of the genes encoding the α-subunits of G12 and G13 in the nervous system results in neuronal ectopia of the cerebral and cerebellar cortices due to overmigration of cortical plate neurons and cerebellar Purkinje cells, respectively. The organization of the radial glia and the basal lamina was not disturbed, and the Cajal-Retzius cell layer had formed normally in mutan

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30

Sullivan, Megan R., Axel Nimmerjahn, Dmitry V. Sarkisov, Fritjof Helmchen, and Samuel S. H. Wang. "In Vivo Calcium Imaging of Circuit Activity in Cerebellar Cortex." Journal of Neurophysiology 94, no. 2 (2005): 1636–44. http://dx.doi.org/10.1152/jn.01013.2004.

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In vivo two-photon calcium imaging provides the opportunity to monitor activity in multiple components of neural circuitry at once. Here we report the use of bulk-loading of fluorescent calcium indicators to record from axons, dendrites, and neuronal cell bodies in cerebellar cortex in vivo. In cerebellar folium crus IIa of anesthetized rats, we imaged the labeled molecular layer and identified all major cellular structures: Purkinje cells, interneurons, parallel fibers, and Bergmann glia. Using extracellular stimuli we evoked calcium transients corresponding to parallel fiber beam activity. T

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31

Di Gennaro, M., and M. Vassalle. "Relationship between caffeine effects and calcium in canine cardiac Purkinje fibers." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 3 (1985): H520—H533. http://dx.doi.org/10.1152/ajpheart.1985.249.3.h520.

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The actions of caffeine (1-9 mM) on electrical and mechanical events were studied under conditions known to change the intracellular calcium in canine cardiac Purkinje fibers perfused in vitro. It was found that caffeine in a dose-dependent manner 1) shifts the early repolarization to more positive values, 2) shifts the plateau to more negative values, 3) prolongs the terminal phase 3 (induction of a "tail"), 4) transiently increases and then decreases the force of contraction with respect to control values, 5) causes a smaller tail in the presence of agents (local anesthetics, tetrodotoxin, h

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32

Houk, James C., and Simon Alford. "Computational significance of the cellular mechanisms for synaptic plasticity in Purkinje cells." Behavioral and Brain Sciences 19, no. 03 (1996): 457–61. http://dx.doi.org/10.1017/s0140525x00081735.

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33

Moak, Jeffrey P. "Developmental Cellular Electrophysiologic Effects of d-Sotalol on Canine Cardiac Purkinje Fibers." Pediatric Research 29, no. 1 (1991): 104–9. http://dx.doi.org/10.1203/00006450-199101000-00020.

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34

Alfaro-Ruíz, Rocío, Carolina Aguado, Alejandro Martín-Belmonte, Ana Esther Moreno-Martínez, and Rafael Luján. "Cellular and Subcellular Localisation of Kv4-Associated KChIP Proteins in the Rat Cerebellum." International Journal of Molecular Sciences 21, no. 17 (2020): 6403. http://dx.doi.org/10.3390/ijms21176403.

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The K+ channel interacting proteins (KChIPs) are a family of cytosolic proteins that interact with Kv4 channels, leading to higher current density, modulation of channel inactivation and faster recovery from inactivation. Using immunohistochemical techniques at the light and electron microscopic level combined with quantitative analysis, we investigated the cellular and subcellular localisation of KChIP3 and KChIP4 to compare their distribution patterns with those for Kv4.2 and Kv4.3 in the cerebellar cortex. Immunohistochemistry at the light microscopic level demonstrated that KChIP3, KChIP4,

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35

Batchelor, Andrew M., and John Garthwaite. "Synaptic integration by mGluRs in cerebellar purkinje cells." Neuropharmacology 35, no. 6 (1996): A2. http://dx.doi.org/10.1016/0028-3908(96)84655-7.

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36

Tempia, F., M. C. Miniaci, D. Anchisi, and P. Strata. "Activation of purkinje cell mGluR by parallel fibres." Neuropharmacology 35, no. 6 (1996): A30. http://dx.doi.org/10.1016/0028-3908(96)84767-8.

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37

Mc Namara, Brian, Simon J. Boniface, Julian Ray, Neil J. Scolding, and Neil Robertson. "Paraneoplastic sensory neuropathy and Purkinje cell antibodies." Muscle & Nerve 22, no. 10 (1999): 1466–67. http://dx.doi.org/10.1002/(sici)1097-4598(199910)22:10<1466::aid-mus20>3.0.co;2-d.

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Lee, Hyang-Ae, Ki-Suk Kim, Sang-Joon Park, and Eun-Joo Kim. "Cellular Mechanism of the QT Prolongation Induced by Sulpiride." International Journal of Toxicology 28, no. 3 (2009): 207–12. http://dx.doi.org/10.1177/1091581809337261.

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In this study, the authors investigated the electrophysiological effect of sulpiride on cardiac repolarization using conventional microelectrode recording techniques in isolated canine Purkinje fibers and a whole-cell patch clamp technique in transiently transfected cells with the hERG, KCNQ1/KCNE1, KCNJ2, and SCN5A cDNA and in rat cardiac myocytes for ICa. In studies of action potential duration, 10 μM, 100 μM, 300 μM, and 1 mM sulpiride prolonged action potential duration in a concentration-dependent manner. In studies of cardiac ion channels, sulpiride did not significantly affect INa, ICa,

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Kapfhammer, Josef P. "Cellular and molecular control of dendritic growth and development of cerebellar Purkinje cells." Progress in Histochemistry and Cytochemistry 39, no. 3 (2004): 131–82. http://dx.doi.org/10.1016/j.proghi.2004.07.002.

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40

Barmack, Neal H., Zuyuan Qian, and Jason Yoshimura. "Regional and cellular distribution of protein kinase C in rat cerebellar purkinje cells." Journal of Comparative Neurology 427, no. 2 (2000): 235–54. http://dx.doi.org/10.1002/1096-9861(20001113)427:2<235::aid-cne6>3.0.co;2-6.

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41

Lordkipanidze, Tamar, and Anna Dunaevsky. "Purkinje cell dendrites grow in alignment with Bergmann glia." Glia 51, no. 3 (2005): 229–34. http://dx.doi.org/10.1002/glia.20200.

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42

Faulstich, M., A. M. van Alphen, C. Luo, S. du Lac, and C. I. De Zeeuw. "Oculomotor Plasticity During Vestibular Compensation Does Not Depend on Cerebellar LTD." Journal of Neurophysiology 96, no. 3 (2006): 1187–95. http://dx.doi.org/10.1152/jn.00045.2006.

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Vestibular paradigms are widely used for investigating mechanisms underlying cerebellar motor learning. These include adaptation of the vestibuloocular reflex (VOR) after visual-vestibular mismatch training and vestibular compensation after unilateral damage to the vestibular apparatus. To date, various studies have shown that VOR adaptation may be supported by long-term depression (LTD) at the parallel fiber to Purkinje cell synapse. Yet it is unknown to what extent vestibular compensation may depend on this cellular process. Here we investigated adaptive gain changes in the VOR and optokinet

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McFarland, Rebecca, Hadi S. Zanjani, Jean Mariani та Michael W. Vogel. "Changes in the Distribution of theα3 Na+/K+ATPase Subunit in Heterozygous Lurcher Purkinje Cells as a Genetic Model of Chronic Depolarization during Development". International Journal of Cell Biology 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/152645.

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A common assumption of excitotoxic mechanisms in the nervous system is that the ionic imbalance resulting from overstimulation of glutamate receptors and increased Na+and Ca++influx overwhelms cellular energy metabolic systems leading to cell death. The goal of this study was to examine how a chronic Na+channel leak current in developing Purkinje cells in the heterozygous Lurcher mutant (+/Lc) affects the expression and distribution of theα3 subunit of the Na+/K+ATPase pump, a key component of the homeostasis system that maintains ionic equilibrium in neurons. The expression pattern of the cat

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Yang, Guang, Rod M. Feddersen, Fangyi Zhang, H. Brent Clark, Alvin J. Beitz, and Costantino Iadecola. "Cerebellar vascular and synaptic responses in normal mice and in transgenics with Purkinje cell dysfunction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 2 (1998): R529—R540. http://dx.doi.org/10.1152/ajpregu.1998.274.2.r529.

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We used transgenic mice with Purkinje cell dysfunction (PO3 line) to study the role of these neurons in the increase in cerebellar blood flow (BFcrb) produced by stimulation of the cerebellar parallel fibers (PF). Mice (age 8–10 wk) were anesthetized (halothane) and artificially ventilated. Arterial pressure and end-tidal CO2 were monitored continuously. Arterial blood gases were measured. The PF were stimulated electrically (100 μA, 30 Hz; 40 s), and the increases in BFcrb were monitored by a laser-Doppler flow probe. First, we characterized the increases in BFcrb and the field potentials pro

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Fozzard, H. A., D. A. Hanck, J. C. Makielski, B. E. Scanley, and M. F. Sheets. "Sodium channels in cardiac Purkinje cells." Experientia 43, no. 11-12 (1987): 1162–68. http://dx.doi.org/10.1007/bf01945516.

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Wuenschell, C. W., A. Messer, and A. J. Tobin. "Lurcher purkinje cells express glutamic acid decarboxylase and calbindin mRNAs." Journal of Neuroscience Research 27, no. 1 (1990): 65–70. http://dx.doi.org/10.1002/jnr.490270110.

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Gilmour, R. F., N. F. Otani, and M. A. Watanabe. "Memory and complex dynamics in cardiac Purkinje fibers." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 4 (1997): H1826—H1832. http://dx.doi.org/10.1152/ajpheart.1997.272.4.h1826.

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The contribution of cumulative changes in action potential duration (memory) to complex cellular electrophysiological behavior was investigated in canine cardiac Purkinje fibers. Complex behavior induced during constant pacing was caused by reciprocal interactions between the time to full repolarization (TFR), where TFR = response duration + latency, and the diastolic interval (DI). The relationship between TFR and the preceding DI during complex behavior differed from that obtained using a standard restitution protocol. In particular, higher-order periodicities and chaos were produced in fibe

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Zanjani, Hadi S., Rebecca McFarland, Pauline Cavelier, et al. "Death and survival of heterozygous Lurcher Purkinje cellsIn vitro." Developmental Neurobiology 69, no. 8 (2009): 505–17. http://dx.doi.org/10.1002/dneu.20715.

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Hamling, Kyla R., Zachary J. C. Tobias, and Tamily A. Weissman. "Mapping the development of cerebellar Purkinje cells in zebrafish." Developmental Neurobiology 75, no. 11 (2015): 1174–88. http://dx.doi.org/10.1002/dneu.22275.

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Kaprielian, Zaven, A. Malcolm Campbell, and Douglas M. Fambrough. "Identification of a Ca2+-ATPase in cerebellar Purkinje cells." Molecular Brain Research 6, no. 1 (1989): 55–60. http://dx.doi.org/10.1016/0169-328x(89)90028-4.

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