Relevant bibliographies by topics / Calcium channels – Animal models

Academic literature on the topic 'Calcium channels – Animal models'

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Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "Calcium channels – Animal models"

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Kamp, Marcel A., Maxine Dibué, Toni Schneider, Hans-Jakob Steiger, and Daniel Hänggi. "Calcium and Potassium Channels in Experimental Subarachnoid Hemorrhage and Transient Global Ischemia." Stroke Research and Treatment 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/382146.

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Healthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion channel expression and function is initiated, with acute and long-term effects differing from each other. Initial hypoperfusion after exposure of cerebral vessels to oxyhemoglobin correlates with a suppression of voltage-gated potassium channel activity, whereas delayed cerebral vasospasm involves changes in other potassium channel and voltage-gated calcium channels expression and function. Furthermore, expression patterns and function of ion channels appear to differ between main and small peripheral vessels, which may be key in understanding mechanisms behind subarachnoid hemorrhage-induced vasospasm. Here, changes in calcium and potassium channel expression and function in animal models of subarachnoid hemorrhage and transient global ischemia are systematically reviewed and their clinical significance discussed.
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Kazama, Itsuro. "Roles of Lymphocyte Kv1.3-Channels in the Pathogenesis of Renal Diseases and Novel Therapeutic Implications of Targeting the Channels." Mediators of Inflammation 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/436572.

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Delayed rectifier K+-channels (Kv1.3) are predominantly expressed in T lymphocytes. Based on patch-clamp studies, the channels play crucial roles in facilitating the calcium influx necessary to trigger lymphocyte activation and proliferation. Using selective channel inhibitors in experimental animal models,in vivostudies then revealed the clinically relevant relationship between the channel expression and the pathogenesis of autoimmune diseases. In renal diseases, in which “chronic inflammation” or “the overstimulation of cellular immunity” is responsible for the pathogenesis, the overexpression of Kv1.3-channels in lymphocytes promotes their cellular proliferation and thus contributes to the progression of tubulointerstitial fibrosis. We recently demonstrated that benidipine, a potent dihydropyridine calcium channel blocker, which also strongly and persistently inhibits the lymphocyte Kv1.3-channel currents, suppressed the proliferation of kidney lymphocytes and actually ameliorated the progression of renal fibrosis. Based on the recentin vitroevidence that revealed the pharmacological properties of the channels, the most recent studies have revealed novel therapeutic implications of targeting the lymphocyte Kv1.3-channels for the treatment of renal diseases.
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Uchitel, Osvaldo D., Carlota González Inchauspe, and Mariano N. Di Guilmi. "Calcium channels and synaptic transmission in familial hemiplegic migraine type 1 animal models." Biophysical Reviews 6, no. 1 (December 3, 2013): 15–26. http://dx.doi.org/10.1007/s12551-013-0126-y.

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Bakowski, Daniel, Fraser Murray, and Anant B. Parekh. "Store-Operated Ca2+ Channels: Mechanism, Function, Pharmacology, and Therapeutic Targets." Annual Review of Pharmacology and Toxicology 61, no. 1 (January 6, 2021): 629–54. http://dx.doi.org/10.1146/annurev-pharmtox-031620-105135.

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Calcium (Ca2+) release–activated Ca2+ (CRAC) channels are a major route for Ca2+ entry in eukaryotic cells. These channels are store operated, opening when the endoplasmic reticulum (ER) is depleted of Ca2+, and are composed of the ER Ca2+ sensor protein STIM and the pore-forming plasma membrane subunit Orai. Recent years have heralded major strides in our understanding of the structure, gating, and function of the channels. Loss-of-function and gain-of-function mutants combined with RNAi knockdown strategies have revealed important roles for the channel in numerous human diseases, making the channel a clinically relevant target. Drugs targeting the channels generally lack specificity or exhibit poor efficacy in animal models. However, the landscape is changing, and CRAC channel blockers are now entering clinical trials. Here, we describe the key molecular and biological features of CRAC channels, consider various diseases associated with aberrant channel activity, and discuss targeting of the channels from a therapeutic perspective.
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Tano, Jean-Yves, and Maik Gollasch. "Hypoxia and ischemia-reperfusion: a BiK contribution?" American Journal of Physiology-Heart and Circulatory Physiology 307, no. 6 (September 15, 2014): H811—H817. http://dx.doi.org/10.1152/ajpheart.00319.2014.

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Over the last decades, cardiovascular disease has become the primary cause of death in the Western world, and this trend is expanding throughout the world. In particular, atherosclerosis and the subsequent vessel obliterations are the primary cause of ischemic disease (stroke and coronary heart disease). Excess calcium influx into the cells is one of the major pathophysiological mechanisms important for ischemic injury in the brain and heart in humans. The large-conductance calcium-activated K+ channels (BK) are thus interesting candidates to protect against excess calcium influx and the events leading to ischemic injury. Indeed, the mitochondrial BK channels (mitoBK) have recently been shown to play a protective function against ischemia-reperfusion injury both in vitro and in animal models, although the exact mechanism of this protection is still under scrutiny. In addition, in both the plasma membrane and mitochondrial BK channel, the α-subunit itself is sensitive to hypoxia. This sensitivity is tissue specific and conferred by a highly conserved motif within an alternatively spliced cysteine-rich insert (STREX) in the intracellular C terminus of the channel. This review describes recent developments of the increasing relevance of BK channels in hypoxia and ischemia-reperfusion injury.
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Falcón, Débora, Isabel Galeano-Otero, Marta Martín-Bórnez, María Fernández-Velasco, Isabel Gallardo-Castillo, Juan A. Rosado, Antonio Ordóñez, and Tarik Smani. "TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease." Cells 9, no. 1 (January 10, 2020): 173. http://dx.doi.org/10.3390/cells9010173.

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Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal models of heart infarcts and in vitro experimental models of ischemia and reperfusion. TRPC channel-mediated increase of the intracellular Ca2+ concentration seems to be required for the activation of the signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion and to heart infarction.
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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 (December 27, 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 pathways are disrupted in cerebellar Purkinje cells. Ca2+ signaling in Purkinje cells is important for normal cellular function as these neurons express a variety of Ca2+ channels, Ca2+-dependent kinases and phosphatases, and Ca2+-binding proteins to tightly maintain Ca2+ homeostasis and regulate physiological Ca2+-dependent processes. Abnormal Ca2+ levels can activate toxic cascades leading to characteristic death of Purkinje cells, cerebellar atrophy, and ataxia that occur in many SCAs. The output of the cerebellar cortex is conveyed to the deep cerebellar nuclei (DCN) by Purkinje cells via inhibitory signals; thus, Purkinje cell dysfunction or degeneration would partially or completely impair the cerebellar output in SCAs. In the absence of the inhibitory signal emanating from Purkinje cells, DCN will become more excitable, thereby affecting the motor areas receiving DCN input and resulting in uncoordinated movements. An outstanding advantage in studying the pathogenesis of SCAs is represented by the availability of a large number of animal models which mimic the phenotype observed in humans. By mainly focusing on mouse models displaying mutations or deletions in genes which encode for Ca2+ signaling-related proteins, in this review we will discuss the several pathogenic mechanisms related to deranged Ca2+ homeostasis that leads to significant Purkinje cell degeneration and dysfunction.
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Crotti, Lia, Katja E. Odening, and Michael C. Sanguinetti. "Heritable arrhythmias associated with abnormal function of cardiac potassium channels." Cardiovascular Research 116, no. 9 (May 19, 2020): 1542–56. http://dx.doi.org/10.1093/cvr/cvaa068.

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Abstract Cardiomyocytes express a surprisingly large number of potassium channel types. The primary physiological functions of the currents conducted by these channels are to maintain the resting membrane potential and mediate action potential repolarization under basal conditions and in response to changes in the concentrations of intracellular sodium, calcium, and ATP/ADP. Here, we review the diversity and functional roles of cardiac potassium channels under normal conditions and how heritable mutations in the genes encoding these channels can lead to distinct arrhythmias. We briefly review atrial fibrillation and J-wave syndromes. For long and short QT syndromes, we describe their genetic basis, clinical manifestation, risk stratification, traditional and novel therapeutic approaches, as well as insights into disease mechanisms provided by animal and cellular models.
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Schoepf, Clemens L., Maximilian Zeidler, Lisa Spiecker, Georg Kern, Judith Lechner, Kai K. Kummer, and Michaela Kress. "Selected Ionotropic Receptors and Voltage-Gated Ion Channels: More Functional Competence for Human Induced Pluripotent Stem Cell (iPSC)-Derived Nociceptors." Brain Sciences 10, no. 6 (June 3, 2020): 344. http://dx.doi.org/10.3390/brainsci10060344.

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Preclinical research using different rodent model systems has largely contributed to the scientific progress in the pain field, however, it suffers from interspecies differences, limited access to human models, and ethical concerns. Human induced pluripotent stem cells (iPSCs) offer major advantages over animal models, i.e., they retain the genome of the donor (patient), and thus allow donor-specific and cell-type specific research. Consequently, human iPSC-derived nociceptors (iDNs) offer intriguingly new possibilities for patient-specific, animal-free research. In the present study, we characterized iDNs based on the expression of well described nociceptive markers and ion channels, and we conducted a side-by-side comparison of iDNs with mouse sensory neurons. Specifically, immunofluorescence (IF) analyses with selected markers including early somatosensory transcription factors (BRN3A/ISL1/RUNX1), the low-affinity nerve growth factor receptor (p75), hyperpolarization-activated cyclic nucleotide-gated channels (HCN), as well as high voltage-gated calcium channels (VGCC) of the CaV2 type, calcium permeable TRPV1 channels, and ionotropic GABAA receptors, were used to address the characteristics of the iDN phenotype. We further combined IF analyses with microfluorimetric Ca2+ measurements to address the functionality of these ion channels in iDNs. Thus, we provide a detailed morphological and functional characterization of iDNs, thereby, underpinning their enormous potential as an animal-free alternative for human specific research in the pain field for unveiling pathophysiological mechanisms and for unbiased, disease-specific personalized drug development.
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Othman and Hamurtekin. "A New Pain Killer from the Nature: N-Type Calcium Channels Blockers." Proceedings 40, no. 1 (February 8, 2020): 47. http://dx.doi.org/10.3390/proceedings2019040047.

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N-type calcium channels (Neuronal-type Calcium channel, Cav2.2) is a member of high voltage activated calcium channels. There are two native small peptides for N-type calcium channels (NTCC) directly which are derived from cone snail, ω-conotoxin-GVIA isolated from Conus geographus and ω-conotoxin-MVIIA (SNX-111, Ziconotide, PrialtTM), from Conus magus which both directly block the α1-ion conducting pore. NTCCs, have been shown to play a key role in nociceptive transmission due to their strategic location, presynaptically in afferent C & Aᵹ fiber terminals and postsynaptically in descending neuron. NTCCs, which are highly expressed at the pre-synaptic terminals of nociceptive neurons in dorsal horn of the spinal cord regulate release of the key pro-nociceptive neurotransmitters such as glutamate, substance P, neurokinin A, and CGRP. There have been many preclinical studies demonstrating the effect of different NTCC blockers in various acute, inflammatory and neuropathic animal pain models. In 2004 ziconotide has been approved in US and Europe to be used in clinical practice. Furthermore, many clinical trials have been performed in more than 1000 patients studying the efficacy and safety of ziconotide. IT administrated of ziconotide showed significant decrease in pain scores in patients with malignant and nonmalignant pain which are practically in neuropathic pain characteristic and resistant to IT opioids.
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Dissertations / Theses on the topic "Calcium channels – Animal models"

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Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.

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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain damage following cerebral ischaemia is associated with disturbances in intracellular calcium homeostasis, the sodium-calcium exchanger (NCX) is a potential therapeutic target due to its ability to regulate intracellular calcium. Currently, however there is uncertainty as to whether the plasma membrane NCX has a neuroprotective or neurodamaging role following cerebral ischemia. To address this issue I compared hippocampal neuronal injury in NCX3 knockout mice (Ncx3-/-) and wild-type mice (Ncx3+/+) following global cerebral ischaemia. In order to perform this study I first established a bilateral common carotid occlusion (BCCAO) model of global ischaemia in wild-type C57/BlHsnD mice using controlled ventilation. After trials of several ischaemic time points, 17 minutes was established as the optimum duration of ischaemia to produce selective hippocampal CA1 neuronal loss in the wild-type mice. I then subjected NCX3 knockout and wild-type mice to 17 minutes of ischaemia. Following the 17 minute period of ischaemia, wild-type mice exhibited 80% CA1 neuronal loss and 40% CA2 neuronal loss. In contrast, NCX3 knockout mice displayed > 95% CA1 neuronal loss and 95% CA2 neuronal loss. Following experiments using a 17 minute duration of global ischaemia, a 15 minute duration of ischaemia was also evaluated. Wild-type mice exposed to a 15 minute period of ischaemia, did not exhibit any significant hippocampal neuronal loss. In contrast, NCX3 knockout mice displayed 45% CA1 neuronal loss and 25% CA2 neuronal loss. The results clearly demonstrate that mice deficient for the NCX3 protein are more susceptible to global cerebral ischaemia than wild-type mice. My findings showing a neuroprotective role for NCX3 following ischaemia, suggest that the exchanger has a positive role in maintaining neuronal intracellular calcium homeostasis. When this function is disrupted, neurons are more susceptible to calcium deregulation, with resultant cell death via calcium mediated pathways. Therefore, improving NCX activity following cerebral ischaemia may provide a therapeutic strategy to reduce neuronal death.
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Diffley, Leonie. "Calcium regulation and ion channel remodelling in an animal model of heart failure." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493676.

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CHF is a complex disease that results in the remodelling of the heart at every level, from the gross anatomy down to the levels of the ion channel resulting in aberrant signalling and contractile dysfunction. The QT interval of the cardiac ECG is frequently increased in heart failure, suggesting ion channel remodelling which has proarrhythmic consequences. One of the aims of this study was to determine the changes that occur from the in vivo level, down to the level of the ion channel that may contribute to arrhythmogenesis.
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DeRemigio, Hilary. "Markov chain models of instantaneously coupled intracellular calcium channels." W&M ScholarWorks, 2008. https://scholarworks.wm.edu/etd/1539623334.

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Localized calcium elevations known as calcium puffs or sparks are cellular signals arising from cooperative activity of clusters of inositol 1,4,5-trisphosphate receptors (IP3Rs) or ryanodine receptors (RyRs) located at calcium release sites on the endoplasmic or sarcoplasmic reticulum membrane. When Markov chain models of these intracellular calcium-regulated calcium channels are coupled via a mathematical representation of the calcium microdomain, simulated calcium release sites may exhibit the phenomenon of "stochastic calcium excitability" where the IP3Rs or RyRs open and close in a concerted fashion. Although the biophysical theory relating the kinetics of single channels to the collective phenomena of puffs and sparks is only beginning to be developed, Markov chain models of coupled intracellular channels give insight into the dynamics of calcium puffs and sparks.;Interestingly, under some conditions simulated puffs and sparks can be observed even when the single channel model used does not include slow calcium inactivation or any long-lived closed state. In this case termination of the localized calcium elevation occurs when all of the intracellular channels at a release site simultaneously close through a process called stochastic attrition. This dissertation investigates the statistical properties of stochastic attrition viewed as an absorption time on a terminating Markov chain that represents a calcium release site composed of two-state channels that are activated by calcium. Assuming that the local calcium concentration experienced by a channel depends only on the number of open channels at the calcium release site, the probability distribution function for the time until stochastic attrition occurs is derived and an analytical formula for the expectation of this random variable is presented. Also explored is how the contribution of stochastic attrition to the termination of calcium puffs and sparks depends on the number of channels at a release site, the source amplitude of the channels, the background calcium concentration, channel kinetics, and the cooperativity of calcium binding.;This dissertation also studies whether single channel models with calcium inactivation are less sensitive to the details of release site ultrastructure than models that lack a slow calcium-inactivation process. Release site dynamics obtained from simulated calcium release sites composed of instantaneously coupled calcium-regulated calcium channels whose random spatial locations were chosen from a uniform distribution on a disc of specified radius are compared to simulations with channels arranged on hexagonal lattices. Analysis of puff/spark statistics confirms that puffs and sparks are less sensitive to the spatial organization of release sites when the single channel model includes a slow inactivation process. The validity of several different mean-field reductions that do not explicitly account for the details of release site ultrastructure is also investigated.;Calcium release site models are stochastic automata networks that involve many functional transitions, that is, the transition probabilities of each channel depend on the local calcium concentration and thus the state of the other channels. A Kronecker structured representation for calcium release site models is presented and benchmark stationary distribution calculations using both exact and approximate iterative numerical solution techniques that leverage this structure are performed. When it is possible to obtain an exact solution, response measures such as the number of channels in a particular state converge more quickly using the iterative numerical methods than occupation measures calculated via Monte Carlo simulation. When an exact solution is not feasible, iterative approximate methods based on the Power method may be used, with performance similar to Monte Carlo estimates.
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Calcraft, Peter James. "Two-pore channels and NAADP-dependent calcium signalling." Thesis, St Andrews, 2010. http://hdl.handle.net/10023/888.

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Muller, Yunhua Li 1963. "Developmentally regulated expression of the calcium-dependent potassium channel and calcium channels during maturation of the rat cerebellum." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/282231.

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Potassium channels govern the duration and frequency of excitable membrane events, and thus may regulate voltage-dependent signals that are important in neuronal development. This study assesses the developmental expression of two classes of K⁺ channels in vivo and in vitro in the rat cerebellum. In vivo, the level of mslo-related transcript for the Ca²⁺-dependent K⁺ channel (KCa) was shown by Northern analysis to be upregulated during development, whereas transcripts for delayed rectifier (KD) channels remained fairly constant. The same pattern of in vivo development was demonstrated with functional assays by expression in Xenopus oocytes of poly A-enriched RNA isolated from postnatal rat cerebella. In vitro, single channel studies of Purkinje neurons showed that KCa channel activity was increased during development and KD channel activity remained stable. Although the semi-quantitative Reverse Transcription-Polymerase Chain Reaction (RT-PCR) showed that the level of transcripts of the KCa channel sequence remained constant in control culture, the developmental pattern that was seen in vivo was mimicked in vitro when cultures were treated chronically with tetraethylammonium (TEA, 1mM). Chronic treatment with 10 mM extracellular KCl resulted in an upregulation of KCa transcripts similar to that seen with chronic TEA. The stimulatory effects of TEA or KCl were negated in low external calcium (0.1 mM), suggesting that KCa transcript levels were influenced by depolarization and calcium entry. The KCa channels may in part contribute to the mature electrical properties of Purkinje neurons. This was supported by evidence that developmental trends in cellular firing activity were antagonized by decreased KCa channel abundance caused by chronic treatment with TEA. Voltage-gated Ca²⁺ channels (N, R and P type) were developmentally down-regulated at the transcriptional level in control cultures. Chronic treatment with TEA increased the transcript levels for N and R type Ca²⁺ channels, but not for P type, suggesting that the various types of Ca²⁺ channels were differentially regulated. Ca²⁺ signaling plays a key role in neuronal development in many cells. The KCa and Ca²⁺ channels regulate Ca²⁺-entry, and may thus influence the neuronal differentiation.
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Matias, Madeleine Gundayao. "Animal calcium release-activated calcium (CRAC) channels are homologous and derived from the ubiquitous Cation Diffusion Facilitators." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1453033.

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Thesis (M.S.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed June 25, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 48-51).
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Giannattasio, Bartolomeo. "Characterization of ATP receptors and voltage-dependent calcium ion channels in cardiovascular cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=case1060781044.

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Giblin, Kathryn Anne. "Is epilepsy a preventable disorder? New evidence from animal models." Yale University, 2010. http://ymtdl.med.yale.edu/theses/available/etd-03052010-144943/.

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Epilepsy accounts for 0.5% of the global burden of disease, and primary prevention of epilepsy represents one of the three 2007 NINDS Epilepsy Research Benchmarks. Efforts to understand and intervene in the process of epileptogenesis have yielded fruitful preventative strategies in animal models. This article reviews the current understanding of epileptogenesis, introduces the concept of a "critical period" for epileptogenesis, and examines strategies for epilepsy prevention in animal models of both acquired and genetic epilepsies. As proof of principle, we investigated whether early preventative treatment during epileptogenesis in the WAG/Rij rat model of primary generalized epilepsy would persistently suppress the epilepsy phenotype in adulthood. Oral ethosuximide was given from age p21 to 5 months, covering the established period for epileptogenesis in this model. We then assessed the epilepsy phenotype by performing electroencephpalogram (EEG) recordings at serial time points after treatment cessation and by immunocytochemically measuring the cortical expression of ion channels Nav1.1, Nav1.6, and HCN1, which are dysregulated in epileptic WAG/Rij rats. Treatment both persistently suppressed seizures, even up to 3 months after treatment cessation, and blocked ion channel dysregulation. These findings indicated that treatment during epileptogenesis prevented the development of the epileptic phenotype. Subsequently, we investigated the C3H/HeJ mouse model of genetic epilepsy as a candidate for future studies in preventative treatment during epileptogenesis. Serial EEG recordings were performed from p5 to 3 months of age. We found that C3H/HeJ mice underwent three distinct, stereotyped phases of seizure development, which suggests that this model would be an appropriate candidate for future research on prevention of epileptogenesis.
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Rakers, Cordula Marijke [Verfasser]. "The role of glial calcium changes in animal models of stroke / Cordula Marijke Rakers." Bonn : Universitäts- und Landesbibliothek Bonn, 2015. http://d-nb.info/1121105599/34.

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Kaurstad, Guri. "Cardiomyocyte function and calcium handling in animal models of inborn and aquired maximal oxygen uptake." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for sirkulasjon og bildediagnostikk, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-16549.

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Hjertemuskelcellefunksjon og kalsiumhåndtering i dyremodeller med medfødt og ervervet maksimalt oksygenopptak Hjerte-karsykdommer er i dag årsaken til flest dødsfall i Europa. Selv om det er kjent at et høyt maksimalt oksygenopptak kan virke beskyttende mot hjerte-karsykdom både hos friske og de med økt risiko, vil studier av de underliggende mekanismene bidra med verdifull informasjon til utvikling av fremtidige retningslinjer for behandling og forebygging av hjertekarsykdom. Maksimalt oksygenopptak er hos de fleste av oss avhengig av hjertets slagvolum som igjen bestemmes av hjertemuskelcellenes kontraksjonsevne. For at hjertemuskelcellene skal kunne kontrahere kraftig er kalsiumhåndteringen i cellene avgjørende. Ett av de proteinene som er med bidrar til å styre dette er kalsium/ kalmodulin avhengig protein kinase II (CaMKII). CaMKII aktiviteten øker når hjertefrekvensen øker og det ser ut til at den økte aktiviteten er viktig for treningsresponsen i hjertemuskelcellene, mens hos hjertesvikt er det motsatt og den økte aktiviteten fører til funksjonsnedsettelse. De overordnede formålene med denne doktorgradsavhandlingen var å undersøke betydningen av et høyt medfødt oksygenopptak på hjertets remodellering etter infarkt, eventuelle forskjeller i treningsrelaterte tilpasninger i hjertemuskelceller fra rotter med ulik medfødt evne til å respondere på trening og om CaMKII er nødvendig for treningsrelaterte forbedringer i maksimalt oksygenopptak, hjertemuskelcellens kontraksjon og kalsiumhåndtering. Resultatene viste at rotter med høyt og rotter med lavt medfødt maksimalt oksygenopptak fikk like stor remodellering av hjerte og funksjonsnedsettelse etter infarkt, men at et høyt utgangspunkt fungerte som en ”buffer” på funksjonsnedsettelsen. Videre fant vi at høy intensitets aerobe intervaller ikke forbedret maksimalt oksygenopptak, hjertemuskelcellefunksjon eller kalsiumhåndtering i rotter med lav medfødt respons til trening. Dette indikerer at mangel på plastisitet i hjertet bidro til å hindre treningsrespons på maksimalt oksygenopptak. Det siste studiet viste at i friske mus er CaMKII nødvendig for å opprettholde kalsiumhomeostase i hjertemuskelcellene og for å oppnå optimal treningsrespons på hjertemuskelcellehypertrofi, funksjon og kalsiumhåndtering. Men paradoksalt nok førte CaMKII inhibering allikevel til en større økning i maksimalt oksygenopptak.
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Books on the topic "Calcium channels – Animal models"

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Rodger, Claire. The anticonvulsant profiles of two calcium channel antagonists in animal models of epilepsy. Manchester: University of Manchester, 1993.

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The effect of calcium antagonists on the normoxic and the ischaemic myocardium: Studies in rat and guinea-pig cardiac preparations. Amsterdam: [s.n.], 1989.

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S, Sideman, Beyar Rafael, Landesberg Amir, and New York Academy of Sciences, eds. Interactive and integrative cardiology. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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Felling, Ryan J. Targets for Neuroprotection in Ischemic Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0111.

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Cerebral ischemia or hypoxia-ischemia initiate a cascade of biochemical events including impaired reuptake of glutamate into perisynaptic glia causing glutamate flooding, calcium fluxing through NMDA glutamate channels, activation of neuronal nitric oxide synthetase, and impaired mitochondrial ATP production. In animal models it is possible to block these steps and protect the brain but the temporal window of protection after the insult lasts only a few hours. Recombinant TPA is clinically protective if given within 3 hours of stroke, but other agents have not been shown to protect brain tissue after stroke. However, total body cooling has also been shown to protect the brain of term infants if initiated within 6 hours of perinatal asphyxia, and a similar level of cooling may provide protection for the brain in adults who have been resuscitated after cardiac arrest.
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Asher, Ornoy, ed. Animal models of human related calcium metabolic disorders. Boca Raton, Fla: CRC Press, 1995.

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(Editor), Stephan Frings, and Jonathan Bradley (Editor), eds. Transduction Channels in Sensory Cells. Wiley-VCH, 2004.

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Bradley, Jonathan, and Stephan Frings. Transduction Channels in Sensory Cells. Wiley & Sons, Incorporated, John, 2006.

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Bradley, Jonathan, and Stephan Frings. Transduction Channels in Sensory Cells. Wiley-VCH Verlag GmbH, 2005.

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Stephan, Frings, and Bradley Jonathan 1961-, eds. Transduction channels in sensory cells. Weinheim: Wiley-VCH, 2004.

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(Editor), H. Leon Bradlow, Jack Fishman (Editor), and Michael P. Osborne (Editor), eds. Cancer Prevention: Novel Nutrient and Pharmaceutical Developments (Annals of the New York Academy of Sciences, V. 889). New York Academy of Sciences, 1999.

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Book chapters on the topic "Calcium channels – Animal models"

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Oh-Hora, Masatsugu, and Xiuyuan Lu. "Function of Orai/Stim Proteins Studied in Transgenic Animal Models." In Calcium Entry Channels in Non-Excitable Cells, 107–26. Boca Raton : Taylor & Francis, 2017. | Series: Methods in signal transduction series: CRC Press, 2017. http://dx.doi.org/10.1201/9781315152592-6.

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Scheuer, Todd. "Bacterial Sodium Channels: Models for Eukaryotic Sodium and Calcium Channels." In Voltage Gated Sodium Channels, 269–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41588-3_13.

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Kostyuk, Platon, and Sergei Mironov. "Theoretical Models for Calcium Channels in Nerve Cells." In Water and Ions in Biological Systems, 17–26. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4899-0424-9_4.

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Smith-Swintosky, V. L., and M. P. Mattson. "Glutamate, beta-amyloid precursor proteins, and calcium mediated neurofibrillary degeneration." In Cell and Animal Models in Aging and Dementia Research, 29–45. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9350-1_3.

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FOX, LYLE, ATSUSHI UEDA, BRETT BERKE, I.-FENG PENG, and CHUN-FANG WU. "Movement Disorders in Drosophila Mutants of Potassium Channels and Biogenic Amine Pathways." In Animal Models of Movement Disorders, 487–504. Elsevier, 2005. http://dx.doi.org/10.1016/b978-012088382-0/50045-1.

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Khan, Saeed R. "Animal Models of Calcium Oxalate Kidney Stone Formation." In Animal Models for the Study of Human Disease, 483–98. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-415894-8.00021-x.

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Groff, Jeffrey R., Hilary DeRemigio, and Gregory D. Smith. "Markov Chain Models of Ion Channels and Calcium Release Sites." In Stochastic Methods in Neuroscience, 29–64. Oxford University Press, 2009. http://dx.doi.org/10.1093/acprof:oso/9780199235070.003.0002.

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Cohen, Bertram I., and Erwin H. Mosbach. "Effects of Bile Acids and Sterols in Animal Models of Colorectal Cancer." In Calcium, Vitamin D, and Prevention of Colon Cancer, 209–27. CRC Press, 2018. http://dx.doi.org/10.1201/9781351070386-12.

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Baimbridge, K. G., I. Mody, J. A. Shacklock, and J. J. Miller. "CALBINDIN D28k AND ANIMAL MODELS OF EPILEPSY11Supported by a Canadian MRC Program Grant to K.G.B, and J.J.M." In Calcium-Binding Proteins in Health and Disease, 615–17. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-12-521040-9.50115-7.

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Fajmut, Aleš. "Molecular Mechanisms and Targets of Cyclic Guanosine Monophosphate (cGMP) in Vascular Smooth Muscles." In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97708.

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Molecular mechanisms and targets of cyclic guanosine monophosphate (cGMP) accounting for vascular smooth muscles (VSM) contractility are reviewed. Mathematical models of five published mechanisms are presented, and four novel mechanisms are proposed. cGMP, which is primarily produced by the nitric oxide (NO) dependent soluble guanylate cyclase (sGC), activates cGMP-dependent protein kinase (PKG). The NO/cGMP/PKG signaling pathway targets are the mechanisms that regulate cytosolic calcium ([Ca2+]i) signaling and those implicated in the Ca2+-desensitization of the contractile apparatus. In addition to previous mathematical models of cGMP-mediated molecular mechanisms targeting [Ca2+]i regulation, such as large-conductance Ca2+-activated K+ channels (BKCa), Ca2+-dependent Cl− channels (ClCa), Na+/Ca2+ exchanger (NCX), Na+/K+/Cl− cotransport (NKCC), and Na+/K+-ATPase (NKA), other four novel mechanisms are proposed here based on the existing but perhaps overlooked experimental results. These are the effects of cGMP on the sarco−/endo- plasmic reticulum Ca2+-ATPase (SERCA), the plasma membrane Ca2+-ATPase (PMCA), the inositol 1,4,5-trisphosphate (IP3) receptor channels type 1 (IP3R1), and on the myosin light chain phosphatase (MLCP), which is implicated in the Ca2+-desensitization. Different modeling approaches are presented and discussed, and novel model descriptions are proposed.
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Conference papers on the topic "Calcium channels – Animal models"

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DEREMIGIO, HILARY, PETER KEMPER, M. DREW LAMAR, and GREGORY D. SMITH. "MARKOV CHAIN MODELS OF COUPLED INTRACELLULAR CALCIUM CHANNELS: KRONECKER STRUCTURED REPRESENTATIONS AND BENCHMARK STATIONARY DISTRIBUTION CALCULATIONS." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812776136_0035.

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Zhou, Yilu, Lauren Resutek, Liyun Wang, and X. Lucas Lu. "Effects of Bisphosphonate on Long-Term Culture of Cartilage Allografts." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14635.

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Zoledronic acid (ZA), an FDA approved bisphosphonate (BP) medicine, is widely used for the treatment of osteoclast-related bone loss diseases [1]. Our previous study has found that systemic administration of ZA could dramatically suppress the development of post-traumatic osteoarthritis (PTOA) in the DMM (destabilization of the medial meniscus) mouse model, a model recapitulating the altered joint loading associated with PTOA [2]. This finding is consistent with a few similar studies using different animal models [3]. However, little is known about the cellular and biochemical mechanisms of BP mediated chondro-protection in PTOA pathogenesis. Studies have shown that PTOA often initiates from the apoptosis and altered metabolism of cartilage chondrocytes. In this study, we will investigate the direct effects of ZA on the metabolisms of chondrocytes using long-term in vitro culture of cartilage allografts. As one of the earliest responses of chondrocytes to mechanical stimulation, intracellular calcium ([Ca 2+] i) signaling is the upstream of numerous mechanotransduction pathways [4]. We hypothesize that the chondro-protective mechanisms of ZA could be represented by the characteristics of [Ca 2+] i signaling of in situ chondrocytes. Our specific aims were to: (i) compare the in situ spontaneous [Ca 2+] i responses of chondrocytes cultured in non-ZA and ZA supplemented environments, and (ii) compare the biomechanical properties of cartilage allografts under the two culture conditions.
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Marshall, Lauren, Andra Frost, Tim Fee, and Joel Berry. "Assembly and Characterization of 3D, Vascularized Breast Cancer Tissue Mimics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14199.

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Drug development platforms such as two-dimensional (2D) in vitro cell culture systems and in vivo animal studies do not accurately predict human in vivo effectiveness of candidate therapeutics [1]. Cell culture systems have limited similarities to primary human cells and tissues as only one cell type is employed and animal studies have a generally limited ability to recapitulate human drug response as different species have differences in metabolism, physiology, and behavior. Mike Leavitt, a former U.S. Secretary of Health and Human Services, has stated that “currently, nine out of ten experimental drugs fail in clinical studies because we cannot accurately predict how they will behave in people based on laboratory and animal studies” [2]. Therefore, this research project is focused on developing an in vitro platform to test candidate therapeutics for more efficacious predictions of human response. We have fabricated a three-dimensional (3D) breast cancer tissue volume containing a vascular network. This vascular network is necessary because current in vitro systems (e.g., rotating bioreactors, suspension of spheroids, and growth on a porous scaffold) are limited in size (1–2 mm) by their absence of micrometer-scale blood flow micro-channels that allow for oxygen and nutrient diffusion into the tissue [4]. The extracellular matrix scaffold has been developed to mimic the native extracellular matrix and includes relevant cell types (e.g., human breast cancer epithelial cells and human breast fibroblasts) along with the prefabricated vascular network (prevascularization). These systems are intended to support long-term growth, recapitulate physiological tissue function, and accurately model response to treatment. It is hypothesized that the development of reproducible tissue volumes will transform breast cancer drug development by providing reliable, cost-effective models that can more accurately predict therapeutic efficacy than current preclinical in vivo and in vitro models.
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Emerson, David R., and Robert W. Barber. "Designing Efficient Microvascular Networks Using Conventional Microfabrication Techniques." In ASME 2009 Second International Conference on Micro/Nanoscale Heat and Mass Transfer. ASMEDC, 2009. http://dx.doi.org/10.1115/mnhmt2009-18312.

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The ability to fabricate networks of micro-channels that obey the biological properties of bifurcating structures found in nature suggests that it is possible to construct artificial vasculatures or bronchial structures. These devices could aid in the desirable objective of eliminating many forms of animal testing. In addition, the ability to precisely control hydraulic conductance could allow designers to create specific concentration gradients that would allow biologists to correlate the behavior of cells. In 1926, Murray found that there was an optimum branching ratio between the diameters of the parent and daughter vessels at a bifurcation. For biological vascular systems, this is referred to as Murray’s law and its basic principle has been found to be valid in many plant and mammalian organisms. An important consequence arises from this law: when the successive generations consist of regular dichotomies, the tangential shear stress at the wall remains constant throughout the network. This simple concept forms an elegant biomimetic design rule that will allow designers to create complex sections with the desired hydraulic conductance or resistance. The paper presents a theoretical analysis of how biomimetic networks of constant-depth rectangular channels can be fabricated using standard photolithographic techniques. In addition, the design rule developed from Murray’s law is extended to a simple power-law fluid to investigate whether it is feasible to design biomimetic networks for non-Newtonian liquids. Remarkably, Murray’s law is obeyed for power-law fluids in cylindrical pipes. Although highly promising, the extension of the analysis to rectangular or trapezoidal channels requires much further work. Moreover, it is unclear at this stage whether Murray’s law holds for other non-Newtonian models.
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