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

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

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1

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 chan

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2

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 overexpressi

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3

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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4

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

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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 event

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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 mode

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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

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8

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

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9

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 chara

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10

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 descendin

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11

Honoré, Per Hartvig, Anna Basnet, Pernille Kristensen, Lene Munkholm Andersen, Signe Neustrup, Pia Møllgaard, Laila Eljaja, and Ole J. Bjerrum. "Predictive validity of pharmacologic interventions in animal models of neuropathic pain." Scandinavian Journal of Pain 2, no. 4 (October 1, 2011): 178–84. http://dx.doi.org/10.1016/j.sjpain.2011.06.002.

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AbstractIntroductionThe pathophysiologic and neurochemical characteristics of neuropathic pain must be considered in the search for new treatment targets. Breakthroughs in the understanding of the structural and biochemical changes in neuropathy have opened up possibilities to explore new treatment paradigms. However, long term sequels from the damage are still difficult to treat.Aim of the studyTo examine the validity of pharmacological treatments in humans and animals for neuropathic pain.MethodAn overview from the literature and own experiences of pharmacological treatments employed to inte

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DE, VRY J., K. R. JENTZSCH, and G. ECKEL. "EFFECTS OF THE L-TYPE CALCIUM CHANNEL ANTAGONIST NIMODIPINE IN ANIMAL MODELS OF DEPRESSION." Behavioural Pharmacology 7, Supplement 1 (May 1996): 28. http://dx.doi.org/10.1097/00008877-199605001-00062.

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13

Mason, W. T., S. R. Rawlings, P. Cobbett, S. K. Sikdar, R. Zorec, S. N. Akerman, C. D. Benham, M. J. Berridge, T. Cheek, and R. B. Moreton. "Control of secretion in anterior pituitary cells--linking ion channels, messengers and exocytosis." Journal of Experimental Biology 139, no. 1 (September 1, 1988): 287–316. http://dx.doi.org/10.1242/jeb.139.1.287.

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Normal anterior pituitary cells, in their diversity and heterogeneity, provide a rich source of models for secretory function. However, until recently they have largely been neglected in favour of neoplastic, clonal tumour cell lines of pituitary origin, which have enabled a number of studies on supposedly homogeneous cell types. Because many of these lines appear to lack key peptide and neurotransmitter receptors, as well as being degranulated with accompanying abnormal levels of secretion, we have developed a range of normal primary anterior pituitary cell cultures using dispersion and enric

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14

Ripsch, Matthew, Carrie Ballard, May Khanna, Joyce Hurley, Fletcher White, and Rajesh Khanna. "A peptide uncoupling CRMP-2 from the presynaptic Ca2+ channel complex demonstrates efficacy in animal models of migraine and AIDS therapy-induced neuropathy." Translational Neuroscience 3, no. 1 (January 1, 2012): 1–8. http://dx.doi.org/10.2478/s13380-012-0002-4.

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AbstractBiological, genetic, and clinical data provide compelling proof for N-type voltage-gated calcium channels (CaV2.2) as therapeutic targets for chronic pain. While decreasing channel function is ultimately anti-nociceptive, directly targeting the channel can lead to multiple adverse effects. Targeting regulators of channel activity may facilitate improved analgesic properties associated with channel block and afford a broader therapeutic window. Towards this end, we recently identified a short peptide, designated CBD3, derived from collapsin response mediator protein 2 (CRMP-2) that supp

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15

Saeki, Kensuke, Shun-ichi Yasuda, Masami Kato, Mayumi Kano, Yuki Domon, Naohisa Arakawa та Yutaka Kitano. "Analgesic effects of mirogabalin, a novel ligand for α2δ subunit of voltage-gated calcium channels, in experimental animal models of fibromyalgia". Naunyn-Schmiedeberg's Archives of Pharmacology 392, № 6 (15 лютого 2019): 723–28. http://dx.doi.org/10.1007/s00210-019-01628-z.

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16

Bailey, Cole S., Hans J. Moldenhauer, Su Mi Park, Sotirios Keros, and Andrea L. Meredith. "KCNMA1-linked channelopathy." Journal of General Physiology 151, no. 10 (August 19, 2019): 1173–89. http://dx.doi.org/10.1085/jgp.201912457.

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KCNMA1 encodes the pore-forming α subunit of the “Big K+” (BK) large conductance calcium and voltage-activated K+ channel. BK channels are widely distributed across tissues, including both excitable and nonexcitable cells. Expression levels are highest in brain and muscle, where BK channels are critical regulators of neuronal excitability and muscle contractility. A global deletion in mouse (KCNMA1−/−) is viable but exhibits pathophysiology in many organ systems. Yet despite the important roles in animal models, the consequences of dysfunctional BK channels in humans are not well characterized

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17

Yam, Mun Fei, Chu Shan Tan, Mariam Ahmad, and Shibao Ruan. "Vasorelaxant Action of the Chloroform Fraction of Orthosiphon stamineus via NO/cGMP Pathway, Potassium and Calcium Channels." American Journal of Chinese Medicine 44, no. 07 (January 2016): 1413–39. http://dx.doi.org/10.1142/s0192415x16500798.

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Orthosiphon stamineus Benth. (Lamiaceae) is an important plant in traditional folk medicine that is used to treat hypertension and kidney stones. In humans, this plant has been tested as an addition regiment for antihypertensive treatment. Among the treatments for hypertension, O. stamineus had been to have diuretic and vasorelaxant effects in animal models. There is still very little information regarding the vasorelaxant effect of O. stamineus. Therefore, the present study was designed to investigate the vasorelaxant activity and mechanism of action of the fractions of O. stamineus. The vaso

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18

Cohan, Stanley L., David J. Redmond, Mei Chen, Dahlia Wilson, and Philip Cyr. "Flunarizine Blocks Elevation of Free Cytosolic Calcium in Synaptosomes following Sustained Depolarization." Journal of Cerebral Blood Flow & Metabolism 13, no. 6 (November 1993): 947–54. http://dx.doi.org/10.1038/jcbfm.1993.118.

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Gerbil cerebral cortical synaptosomes loaded with the fluorescent calcium probe FURA-2 were used to study depolarization-induced presynaptic cytosolic free calcium concentration, as an in vitro model of cerebral ischemia. The depolarization-induced increase in intrasynaptosomal cytosolic free calcium concentration is not sodium-dependent or sodium channel-dependent and may be due to an influx of extrasynaptosomal calcium resulting from a cadmium- and omega-conotoxin-sensitive, nickel-, nifedipine-, and nimodipine-insensitive voltage-regulated channel. The depolarization-induced increase in int

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19

Zoerle, Tommaso, Don C. Ilodigwe, Hoyee Wan, Katarina Lakovic, Mohammed Sabri, Jinglu Ai, and R. Loch Macdonald. "Pharmacologic Reduction of Angiographic Vasospasm in Experimental Subarachnoid Hemorrhage: Systematic Review and Meta-Analysis." Journal of Cerebral Blood Flow & Metabolism 32, no. 9 (April 25, 2012): 1645–58. http://dx.doi.org/10.1038/jcbfm.2012.57.

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Animal models have been developed to simulate angiographic vasospasm secondary to subarachnoid hemorrhage (SAH) and to test pharmacologic treatments. Our aim was to evaluate the effect of pharmacologic treatments that have been tested in humans and in preclinical studies to determine if animal models inform results reported in humans. A systematic review and meta-analysis of SAH studies was performed. We investigated predictors of translation from animals to humans with multivariate logistic regression. Pharmacologic reduction of vasospasm was effective in mice, rats, rabbits, dogs, nonhuman p

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Turley, Sarah L., Kerry E. Francis, Denise K. Lowe, and William D. Cahoon. "Emerging role of ivabradine for rate control in atrial fibrillation." Therapeutic Advances in Cardiovascular Disease 10, no. 6 (September 22, 2016): 348–52. http://dx.doi.org/10.1177/1753944716669658.

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Control of ventricular rate is recommended for patients with paroxysmal, persistent, or permanent atrial fibrillation (AF). Existing rate-control options, including beta-blockers, nondihydropyridine calcium channel blockers, and digoxin, are limited by adverse hemodynamic effects and their ability to attain target heart rate (HR). Ivabradine, a novel HR-controlling agent, decreases HR through deceleration of conduction through If (‘funny’) channels, and is approved for HR reduction in heart failure patients with ejection fraction less than 35% and elevated HR, despite optimal pharmacological t

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Riva, M. A. "Epigenetic Signatures of Early Life Adversities in Animal Models: A Role for Psychopathology Vulnerability." European Psychiatry 41, S1 (April 2017): S29. http://dx.doi.org/10.1016/j.eurpsy.2017.01.145.

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Stressful experiences early in life (ELS) represent one of the most relevant factors for the vulnerability to psychopathologies. Epigenetic changes, such as DNA methylation, have emerged as a major mechanism through which ELS can alter adult behaviour leading to persistent changes of gene regulation.We performed DNA methylation analyses in the hippocampus and prefrontal cortex of adult rats exposed to stress during gestation (PNS), a model that is associated with persistent behavioral alterations relevant for psychiatric disorders.Using an epigenome-wide analysis, an overlap of 893 differentia

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Hori, Takayuki, Motoshi Ouchi, Naoyuki Otani, Masakatsu Nohara, Asuka Morita, Yusuke Otsuka, Promsuk Jutabha, et al. "The uricosuric effects of dihydropyridine calcium channel blockers in vivo using urate under-excretion animal models." Journal of Pharmacological Sciences 136, no. 4 (April 2018): 196–202. http://dx.doi.org/10.1016/j.jphs.2017.11.011.

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23

Berridge, M. J. "Elementary and global aspects of calcium signalling." Journal of Experimental Biology 200, no. 2 (January 1, 1997): 315–19. http://dx.doi.org/10.1242/jeb.200.2.315.

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Calcium is a ubiquitous second messenger used to regulate a wide range of cellular processes. This role in signalling has to be conducted against the rigid homeostatic mechanisms that ensure that the resting level of Ca2+ is kept low (i.e. between 20 and 100 nmol l-1) in order to avoid the cytotoxic effects of a prolonged elevation of [Ca2+]. Cells have evolved a sophisticated signalling system based on the generation of brief pulses of Ca2+ which enables this ion to be used as a messenger, thus avoiding its toxic effects. Such Ca2+ spikes usually result from the coordinated release of Ca2+ fr

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Daly, Norelle L., Brid Callaghan, Richard J. Clark, Simon T. Nevin, David J. Adams та David J. Craik. "Structure and Activity of α-Conotoxin PeIA at Nicotinic Acetylcholine Receptor Subtypes and GABAB Receptor-coupled N-type Calcium Channels". Journal of Biological Chemistry 286, № 12 (20 січня 2011): 10233–37. http://dx.doi.org/10.1074/jbc.m110.196170.

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α-Conotoxins are peptides from cone snails that target the nicotinic acetylcholine receptor (nAChR). RgIA and Vc1.1 have analgesic activity in animal pain models. Both peptides target the α9α10 nAChR and inhibit N-type calcium channels via GABAB receptor activation, but the mechanism of action of analgesic activity is unknown. PeIA has previously been shown to inhibit the α9α10 and α3β2 nAChRs. In this study, we have determined the structure of PeIA and shown that it is also a potent inhibitor of N-type calcium channels via GABAB receptor activation. The characteristic α-conotoxin fold is pres

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Shepherd, Greene, and Wendy Klein-Schwartz. "High-Dose Insulin Therapy for Calcium-Channel Blocker Overdose." Annals of Pharmacotherapy 39, no. 5 (May 2005): 923–30. http://dx.doi.org/10.1345/aph.1e436.

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OBJECTIVE: To evaluate the evidence for using high-dose insulin therapy with supplemental dextrose and potassium in calcium-channel blocker (CCB) overdose. DATA SOURCES: Evidence of efficacy for high-dose insulin therapy with supplemental dextrose and potassium was sought by performing a search of MEDLINE and Toxline between 1966 and July 2004 using combinations of the terms calcium-channel blocker, overdose, poisoning, antidote, and insulin. Abstracts from the North American Congress of Clinical Toxicology for the years 1996–2003 were also reviewed. STUDY SELECTION AND DATA EXTRACTION: Identi

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Yan, Simin, Thomas C. Resta, and Nikki L. Jernigan. "Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling." Antioxidants 9, no. 10 (October 15, 2020): 999. http://dx.doi.org/10.3390/antiox9100999.

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Elevated resistance of pulmonary circulation after chronic hypoxia exposure leads to pulmonary hypertension. Contributing to this pathological process is enhanced pulmonary vasoconstriction through both calcium-dependent and calcium sensitization mechanisms. Reactive oxygen species (ROS), as a result of increased enzymatic production and/or decreased scavenging, participate in augmentation of pulmonary arterial constriction by potentiating calcium influx as well as activation of myofilament sensitization, therefore mediating the development of pulmonary hypertension. Here, we review the effect

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Behringer, Erik, and Md Hakim. "Functional Interaction among KCa and TRP Channels for Cardiovascular Physiology: Modern Perspectives on Aging and Chronic Disease." International Journal of Molecular Sciences 20, no. 6 (March 19, 2019): 1380. http://dx.doi.org/10.3390/ijms20061380.

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Effective delivery of oxygen and essential nutrients to vital organs and tissues throughout the body requires adequate blood flow supplied through resistance vessels. The intimate relationship between intracellular calcium ([Ca2+]i) and regulation of membrane potential (Vm) is indispensable for maintaining blood flow regulation. In particular, Ca2+-activated K+ (KCa) channels were ascertained as transducers of elevated [Ca2+]i signals into hyperpolarization of Vm as a pathway for decreasing vascular resistance, thereby enhancing blood flow. Recent evidence also supports the reverse role for KC

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Bett, Glenna C. L. "Hormones and sex differences: changes in cardiac electrophysiology with pregnancy." Clinical Science 130, no. 10 (April 1, 2016): 747–59. http://dx.doi.org/10.1042/cs20150710.

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Disruption of cardiac electrical activity resulting in palpitations and syncope is often an early symptom of pregnancy. Pregnancy is a time of dramatic and dynamic physiological and hormonal changes during which numerous demands are placed on the heart. These changes result in electrical remodelling which can be detected as changes in the electrocardiogram (ECG). This gestational remodelling is a very under-researched area. There are no systematic large studies powered to determine changes in the ECG from pre-pregnancy, through gestation, and into the postpartum period. The large variability b

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Fritz, Elsa, Pamela Izaurieta, Alexandra Weiss, Franco R. Mir, Patricio Rojas, David Gonzalez, Fabiola Rojas, Robert H. Brown, Rodolfo Madrid, and Brigitte van Zundert. "Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability." Journal of Neurophysiology 109, no. 11 (June 1, 2013): 2803–14. http://dx.doi.org/10.1152/jn.00500.2012.

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Amyotrophic lateral sclerosis (ALS) is a devastating paralytic disorder caused by dysfunction and degeneration of motoneurons starting in adulthood. Recent studies using cell or animal models document that astrocytes expressing disease-causing mutations of human superoxide dismutase 1 (hSOD1) contribute to the pathogenesis of ALS by releasing a neurotoxic factor(s). Neither the mechanism by which this neurotoxic factor induces motoneuron death nor its cellular site of action has been elucidated. Here we show that acute exposure of primary wild-type spinal cord cultures to conditioned medium de

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Góra, Małgorzata, Anna Czopek, Anna Rapacz, Anna Dziubina, Monika Głuch-Lutwin, Barbara Mordyl, and Jolanta Obniska. "Synthesis, Anticonvulsant and Antinociceptive Activity of New Hybrid Compounds: Derivatives of 3-(3-Methylthiophen-2-yl)-pyrrolidine-2,5-dione." International Journal of Molecular Sciences 21, no. 16 (August 11, 2020): 5750. http://dx.doi.org/10.3390/ijms21165750.

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The present study aimed to design and synthesize a new series of hybrid compounds with pyrrolidine-2,5-dione and thiophene rings in the structure as potential anticonvulsant and antinociceptive agents. For this purpose, we obtained a series of new compounds and evaluated their anticonvulsant activity in animal models of epilepsy (maximal electroshock (MES), psychomotor (6 Hz), and subcutaneous pentylenetetrazole (scPTZ) seizure tests). To determine the mechanism of action of the most active anticonvulsant compounds (3, 4, 6, 9), their influence on the voltage-gated sodium and calcium channels

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Khaleel, Anas, Mei-Shin Wu, Henry Sung-Ching Wong, Yu-Wen Hsu, Yii-Her Chou, and Hsiang-Yin Chen. "A Single Nucleotide Polymorphism (rs4236480) inTRPV5Calcium Channel Gene Is Associated with Stone Multiplicity in Calcium Nephrolithiasis Patients." Mediators of Inflammation 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/375427.

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Nephrolithiasis is characterized by calcification of stones in the kidneys from an unknown cause. Animal models demonstrated the functional roles of the transient receptor potential vanilloid member 5 (TRPV5) gene in calcium renal reabsorption and hypercalciuria. Therefore,TRPV5was suggested to be involved in calcium homeostasis. However, whether genetic polymorphisms ofTRPV5are associated with kidney stone multiplicity or recurrence is unclear. In this study, 365 Taiwanese kidney-stone patients were recruited. Both biochemical data and DNA samples were collected. Genotyping was performed by a

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Burmeister, David, Tamer AbouShwareb, Ralph D'Agostino, Karl-Erik Andersson, and George J. Christ. "Impact of partial urethral obstruction on bladder function: time-dependent changes and functional correlates of altered expression of Ca2+ signaling regulators." American Journal of Physiology-Renal Physiology 302, no. 12 (June 15, 2012): F1517—F1528. http://dx.doi.org/10.1152/ajprenal.00016.2012.

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In animal models of partial urethral obstruction (PUO), altered smooth muscle function/contractility may be linked to changes in molecules that regulate calcium signaling/sensitization. PUO was created in male rats, and urodynamic studies were conducted 2 and 6 wk post-PUO. Cystometric recordings were analyzed for the presence or absence of nonvoiding contractions [i.e., detrusor overactivity (DO)]. RT-PCR and Western blots were performed on a subpopulation of rats to study the relationship between the expression of RhoA, L-type Ca2+ channels, Rho kinase-1, Rho kinase-2, inositol 1,4,5-trispho

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Cáceres-Chávez, Verónica Alejandra, Ricardo Hernández-Martínez, Jesús Pérez-Ortega, Marco Arieli Herrera-Valdez, Jose J. Aceves, Elvira Galarraga, and José Bargas. "Acute dopamine receptor blockade in substantia nigra pars reticulata: a possible model for drug-induced Parkinsonism." Journal of Neurophysiology 120, no. 6 (December 1, 2018): 2922–38. http://dx.doi.org/10.1152/jn.00579.2018.

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Dopamine (DA) depletion modifies the firing pattern of neurons in the substantia nigra pars reticulata (SNr), shifting their mostly tonic firing toward irregularity and bursting, traits of pathological firing underlying rigidity and postural instability in Parkinson’s disease (PD) patients and animal models of Parkinsonism (PS). Drug-induced Parkinsonism (DIP) represents 20–40% of clinical cases of PS, becoming a problem for differential diagnosis, and is still not well studied with physiological tools. It may co-occur with tardive dyskinesia. Here we use in vitro slice preparations including

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Laher, Ismail, and John H. Zhang. "Protein Kinase C and Cerebral Vasospasm." Journal of Cerebral Blood Flow & Metabolism 21, no. 8 (August 2001): 887–906. http://dx.doi.org/10.1097/00004647-200108000-00001.

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Twenty-five years after the discovery of protein kinase C (PKC), the physiologic function of PKC, and especially its role in pathologic conditions, remains a subject of great interest with 30,000 studies published on these aspects. In the cerebral circulation, PKC plays a role in the regulation of myogenic tone by sensitization of myofilaments to calcium. Protein kinase C phosphorylates various ion channels including augmenting voltage-dependent Ca2+ channels and inhibiting K+ channels, which both lead to vessel contraction. These actions of PKC amplify vascular reactivity to different agonist

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Martac, Ljiljana. "Fractal dimension and neurotoxicity in rats intoxicated by aluminium." Veterinarski glasnik 69, no. 1-2 (2015): 21–29. http://dx.doi.org/10.2298/vetgl1502021m.

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We used animal model of neurotoxicity in rats, which provided the possibility of studying biological pathophysiological phenomena in vivo and afterwards in vitro conditions. The analysis of electrocortical brain activity using mathematical methods can describe the changes induced by aluminum intoxication in rat as an animal model. In physiological and pathophysiological conditions, on experimental models, mechanisms related to changes in behavior, plasticity and accumulation of aluminum in nervous tissue of the rat brain were observed. Animal models of rats used in the experiments described ch

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Shi, Yun, Yong Wang, and Huafeng Wei. "Dantrolene : From Malignant Hyperthermia to Alzheimer’s Disease." CNS & Neurological Disorders - Drug Targets 18, no. 9 (January 15, 2020): 668–76. http://dx.doi.org/10.2174/1871527317666180619162649.

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Dantrolene, a ryanodine receptor antagonist, is primarily known as the only clinically acceptable and effective treatment for Malignant Hyperthermia (MH). Inhibition of Ryanodine Receptor (RyR) by dantrolene decreases the abnormal calcium release from the Sarcoplasmic Reticulum (SR) or Endoplasmic Reticulum (ER), where RyR is located. Recently, emerging researches on dissociated cells, brains slices, live animal models and patients have demonstrated that altered RyR expression and function can also play a vital role in the pathogenesis of Alzheimer’s Disease (AD). Therefore, dantrolene is now

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Cussac, Laure-Anne, Guillaume Cardouat, Nichiren Tiruchellvam Pillai, Marilyne Campagnac, Paul Robillard, Anaïs Montillaud, Christelle Guibert, et al. "TRPV4 channel mediates adventitial fibroblast activation and adventitial remodeling in pulmonary hypertension." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L135—L146. http://dx.doi.org/10.1152/ajplung.00084.2019.

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Pulmonary arterial adventitial fibroblasts (PAF), the most abundant cellular constituent of adventitia, act as a key regulator of pulmonary vascular wall structure and function from the outside-in. Previous studies indicate that transient receptor potential vanilloid 4 (TRPV4) channel plays an important role in the development of pulmonary hypertension (PH), but no attention has been given so far to its role in adventitial remodeling. In this study, we thus investigated TRPV4 implication in PAF activation occurring in PH. First, we isolated and cultured PAF from rat adventitial intrapulmonary

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Kim, Galina A., Tamara S. Gan’shina, Elena V. Kurza, Ilya N. Kurdyumov, Denis V. Maslennikov, and Ruben S. Mirzoian. "New cerebrovascular agent with hypotensive activity." Research Results in Pharmacology 5, no. 2 (June 27, 2019): 71–77. http://dx.doi.org/10.3897/rrpharmacology.5.35392.

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Introduction: In cerebrovascular disorders, special attention is paid to a hypertensive cerebrovascular crisis, which combines a vascular injury of the brain and hypertension. The paper studies the cerebrovascular properties of the calcium channel blocker of S-Amlodipine nicotinate antihypertensive agent. Materials and methods: Tests were performed on 96 nonlinear male rats, measuring local blood flow in the cerebral cortex in 36 awake animals, using a laser Doppler flowmeter. Cerebral circulation was recorded in the animals when modeling ischemic and hemorrhagic brain injuries. Results and di

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Yoder, Bradley K., Sharon Mulroy, Hannah Eustace, Catherine Boucher, and Richard Sandford. "Molecular pathogenesis of autosomal dominant polycystic kidney disease." Expert Reviews in Molecular Medicine 8, no. 2 (January 17, 2006): 1–22. http://dx.doi.org/10.1017/s1462399406010362.

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Autosomal dominant polycystic kidney disease (ADPKD) is one of the commonest inherited human disorders yet remains relatively unknown to the wider medical, scientific and public audience. ADPKD is characterised by the development of bilateral enlarged kidneys containing multiple fluid-filled cysts and is a leading cause of end-stage renal failure (ESRF). ADPKD is caused by mutations in two genes: PKD1 and PKD2. The protein products of the PKD genes, polycystin-1 and polycystin-2, form a calcium-regulated, calcium-permeable ion channel. The polycystin complex is implicated in regulation of the

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Khan, Mohd Muazzam, Badruddeen, Mohd Mujahid, Juber Akhtar, Mohammad Irfan Khan, and Usama Ahmad. "An Overview of Stroke: Mechanism, In vivo Experimental Models Thereof, and Neuroprotective Agents." Current Protein & Peptide Science 21, no. 9 (December 11, 2020): 860–77. http://dx.doi.org/10.2174/1389203721666200617133903.

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Background: Stroke is one of the causes of death and disability globally. Brain attack is because of the acute presentation of stroke, which highlights the requirement for decisive action to treat it. Objective: The mechanism and in-vivo experimental models of stroke with various neuroprotective agents are highlighted in this review. Method: The damaging mechanisms may proceed by rapid, nonspecific cell lysis (necrosis) or by the active form of cell death (apoptosis or necroptosis), depending upon the duration and severity and of the ischemic insult. Results: Identification of injury mediators

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Bauer, Claudia S., Wahida Rahman, Alexandra Tran-Van-Minh, Rafael Lujan, Anthony H. Dickenson та Annette C. Dolphin. "The anti-allodynic α2δ ligand pregabalin inhibits the trafficking of the calcium channel α2δ-1 subunit to presynaptic terminals in vivo". Biochemical Society Transactions 38, № 2 (22 березня 2010): 525–28. http://dx.doi.org/10.1042/bst0380525.

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Neuropathic pain is caused by lesion or dysfunction of the peripheral sensory nervous system. Up-regulation of the voltage-gated Ca2+ channel subunit α2δ-1 in DRG (dorsal root ganglion) neurons and the spinal cord correlates with the onset of neuropathic pain symptoms such as allodynia in several animal models of neuropathic pain. The clinically important anti-allodynic drugs gabapentin and pregabalin are α2δ-1 ligands, but how these drugs alleviate neuropathic pain is poorly understood. In the present paper, we review recent advances in our understanding of their molecular mechanisms.

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Fan, Youjia, Gaici Xue, Qianbo Chen, Ye Lu, Rong Dong, and Hongbin Yuan. "CY-09 Inhibits NLRP3 Inflammasome Activation to Relieve Pain via TRPA1." Computational and Mathematical Methods in Medicine 2021 (August 14, 2021): 1–10. http://dx.doi.org/10.1155/2021/9806690.

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Peripheral tissue damage leads to inflammatory pain, and inflammatory cytokine releasing is the key factor for inducing the sensitization of nociceptors. As a calcium ion channel, TRPA1 plays an important role in pain and inflammation, thus becoming a new type of anti-inflammatory and analgesic target. However, there is no consensus on the role of this channel in mechanical hyperalgesia caused by inflammation. Here, we aim to explore the role and underlying mechanism of the inflammasome inhibitor CY-09 in two classic inflammatory pain models. We evaluated pain behavior on animal models, cytoki

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Ma, Di, Liangshu Feng, Fang Deng, and Jia-Chun Feng. "Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6891645.

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Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in

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Felberg, Robert A., W. Scott Burgin, and James C. Grotta. "Neuroprotection and the Ischemic Cascade." CNS Spectrums 5, no. 3 (March 2000): 52–58. http://dx.doi.org/10.1017/s1092852900012967.

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AbstractBrain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the “ischemic cascade”) that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted.Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clini

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Simard, J. Marc, S. Kyoon Woo, Gary T. Schwartzbauer, and Volodymyr Gerzanich. "Sulfonylurea Receptor 1 in Central Nervous System Injury: A Focused Review." Journal of Cerebral Blood Flow & Metabolism 32, no. 9 (June 20, 2012): 1699–717. http://dx.doi.org/10.1038/jcbfm.2012.91.

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The sulfonylurea receptor 1 (Sur1)-regulated NCCa-ATP channel is a nonselective cation channel that is regulated by intracellular calcium and adenosine triphosphate. The channel is not constitutively expressed, but is transcriptionally upregulated de novo in all cells of the neurovascular unit, in many forms of central nervous system (CNS) injury, including cerebral ischemia, traumatic brain injury (TBI), spinal cord injury (SCI), and subarachnoid hemorrhage (SAH). The channel is linked to microvascular dysfunction that manifests as edema formation and delayed secondary hemorrhage. Also implic

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Chen, Guangping, Yuan Yang, Otto Fröhlich, Janet D. Klein, and Jeff M. Sands. "Suppression subtractive hybridization analysis of low-protein diet- and vitamin D-induced gene expression from rat kidney inner medullary base." Physiological Genomics 41, no. 3 (May 2010): 203–11. http://dx.doi.org/10.1152/physiolgenomics.00129.2009.

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Protein restriction and hypercalcemia result in a urinary concentrating defect in rats and humans. Previous tubular perfusion studies show that there is an increased active urea transport activity in the initial inner medullary (IM) collecting duct in low-protein diet (LPD) and vitamin D (Vit D) animal models. To investigate the possible mechanisms that cause the urinary concentrating defect and to clone the new active urea transporter, we employed a modified two-tester suppression subtractive hybridization (ttSSH) approach and examined gene expression induced by LPD and Vit D in kidney IM bas

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Bocchi, Leonardo, Monia Savi, Valeria Naponelli, Rocchina Vilella, Gianluca Sgarbi, Alessandra Baracca, Giancarlo Solaini, Saverio Bettuzzi, Federica Rizzi, and Donatella Stilli. "Long-Term Oral Administration of Theaphenon-E Improves Cardiomyocyte Mechanics and Calcium Dynamics by Affecting Phospholamban Phosphorylation and ATP Production." Cellular Physiology and Biochemistry 47, no. 3 (2018): 1230–43. http://dx.doi.org/10.1159/000490219.

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Background/Aims: Dietary polyphenols from green tea have been shown to possess cardio-protective activities in different experimental models of heart diseases and age-related ventricular dysfunction. The present study was aimed at evaluating whether long term in vivo administration of green tea extracts (GTE), can exert positive effects on the normal heart, with focus on the underlying mechanisms. Methods: The study population consisted of 20 male adult Wistar rats. Ten animals were given 40 mL/day tap water solution of GTE (concentration 0.3%) for 4 weeks (GTE group). The same volume of water

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Abram, Michał, Marcin Jakubiec, Anna Rapacz, Szczepan Mogilski, Gniewomir Latacz, Rafał M. Kamiński, and Krzysztof Kamiński. "The Search for New Anticonvulsants in a Group of (2,5-Dioxopyrrolidin-1-yl)(phenyl)Acetamides with Hybrid Structure—Synthesis and In Vivo/In Vitro Studies." International Journal of Molecular Sciences 21, no. 22 (November 20, 2020): 8780. http://dx.doi.org/10.3390/ijms21228780.

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Epilepsy belongs to the most common and debilitating neurological disorders with multifactorial pathophysiology and a high level of drug resistance. Therefore, with the aim of searching for new, more effective, and/or safer therapeutics, we discovered a focused series of original hybrid pyrrolidine-2,5-dione derivatives with potent anticonvulsant properties. We applied an optimized coupling reaction yielding several hybrid compounds that showed broad-spectrum activity in widely accepted animal seizure models, namely, the maximal electroshock (MES) test and the psychomotor 6 Hz (32 mA) seizure

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Swaminathan, Akila, Uma Maheswari Balaguru, Reji Manjunathan, Srinivasan Bhuvaneswari, Dharanibalan Kasiviswanathan, Bandi Sirishakalyani, Prasunpriya Nayak, and Suvro Chatterjee. "Live Imaging and Analysis of Vasoactive Properties of Drugs Using an in-ovo Chicken Embryo Model: Replacing and Reducing Animal Testing." Microscopy and Microanalysis 25, no. 4 (May 10, 2019): 961–70. http://dx.doi.org/10.1017/s1431927619000588.

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AbstractVasodilation occurs as a result of the relaxation of the smooth muscle cells present in the walls of blood vessels. Various suitable models are available for the analysis of the vasoactive properties of drugs with therapeutic applications. But all these models have limitations, such as ethical issues and high cost. The purpose of this study is to develop an alternative model for studying the vasoactive properties of drugs using an in-ovo chicken embryo model. In the preliminary experiment, we used a well-known vasoconstrictor (adrenaline) and a vasodilator (spermine NoNoate) in the chi

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Henry, Clémence O., Emilie Dalloneau, Maria-Teresa Pérez-Berezo, Cristina Plata, Yongzheng Wu, Antoine Guillon, Eric Morello, et al. "In vitro and in vivo evidence for an inflammatory role of the calcium channel TRPV4 in lung epithelium: Potential involvement in cystic fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 3 (September 1, 2016): L664—L675. http://dx.doi.org/10.1152/ajplung.00442.2015.

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Cystic fibrosis (CF) is an inherited disease associated with chronic severe lung inflammation, leading to premature death. To develop innovative anti-inflammatory treatments, we need to characterize new cellular and molecular components contributing to the mechanisms of lung inflammation. Here, we focused on the potential role of “transient receptor potential vanilloid-4” (TRPV4), a nonselective calcium channel. We used both in vitro and in vivo approaches to demonstrate that TRPV4 expressed in airway epithelial cells triggers the secretion of major proinflammatory mediators such as chemokines

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