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Articoli di riviste sul tema "Sodium channels – Animal models"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 13 febbraio 2022

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1

Wood, John N., and Federico Iseppon. "Sodium channels." Brain and Neuroscience Advances 2 (January 2018): 239821281881068. http://dx.doi.org/10.1177/2398212818810684.

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In 2000, with the completion of the human genome project, nine related channels were found to comprise the complete voltage-gated sodium gene family and they were renamed NaV1.1–NaV1.9. This millennial event reflected the extraordinary impact of molecular genetics on our understanding of electrical signalling in the nervous system. In this review, studies of animal electricity from the time of Galvani to the present day are described. The seminal experiments and models of Hodgkin and Huxley coupled with the discovery of the structure of DNA, the genetic code and the application of molecular ge

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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

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Hargus, Nicholas J., Aradhya Nigam, Edward H. Bertram, and Manoj K. Patel. "Evidence for a role of Nav1.6 in facilitating increases in neuronal hyperexcitability during epileptogenesis." Journal of Neurophysiology 110, no. 5 (September 1, 2013): 1144–57. http://dx.doi.org/10.1152/jn.00383.2013.

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During epileptogenesis a series of molecular and cellular events occur, culminating in an increase in neuronal excitability, leading to seizure initiation. The entorhinal cortex has been implicated in the generation of epileptic seizures in both humans and animal models of temporal lobe epilepsy. This hyperexcitability is due, in part, to proexcitatory changes in ion channel activity. Sodium channels play an important role in controlling neuronal excitability, and alterations in their activity could facilitate seizure initiation. We sought to investigate whether medial entorhinal cortex (mEC)

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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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Svajdova, S., and M. Brozmanova. "Regulation of Cough by Voltage-Gated Sodium Channels in Airway Sensory Nerves." Acta Medica Martiniana 18, no. 3 (December 1, 2018): 5–16. http://dx.doi.org/10.2478/acm-2018-0012.

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Abstract Chronic cough is a significant clinical problem in many patients. Current cough suppressant therapies are largely ineffective and have many dangerous adverse effects. Therefore, the identification of novel therapeutic targets and strategies for chronic cough treatment may lead to development of novel effective antitussive therapies with fewer adverse effects. The experimental research in the area of airway sensory nerves suggests that there are two main vagal afferent nerve subtypes that can directly activate cough – extrapulmonary airway C-fibres and Aδ-fibres (described as cough rec

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Takahashi, Hakuo. "Upregulation of the Renin-Angiotensin-Aldosterone-Ouabain System in the Brain Is the Core Mechanism in the Genesis of All Types of Hypertension." International Journal of Hypertension 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/242786.

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Basic research using animal models points to a causal role of the central nervous system in essential hypertension; however, since clinical research is technically difficult to perform, this connection has not been confirmed in humans. Recently, renal nerve ablation in humans proved to continuously decrease blood pressure in resistant hypertension. Furthermore, when electrical stimulation was continuously applied to the carotid baroreceptor nerve of human adults, their blood pressure lowered. These findings promoted the concept that the central nervous system may actually be involved in the pa

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7

Tiwari, Swasti, Shahla Riazi, and Carolyn A. Ecelbarger. "Insulin's impact on renal sodium transport and blood pressure in health, obesity, and diabetes." American Journal of Physiology-Renal Physiology 293, no. 4 (October 2007): F974—F984. http://dx.doi.org/10.1152/ajprenal.00149.2007.

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Insulin has been shown to have antinatriuretic actions in humans and animal models. Moreover, endogenous hyperinsulinemia and insulin infusion have been correlated to increased blood pressure in some models. In this review, we present the current state of understanding with regard to the regulation of the major renal sodium transporters by insulin in the kidney. Several groups, using primarily cell culture, have demonstrated that insulin can directly increase activity of the epithelial sodium channel, the sodium-phosphate cotransporter, the sodium-hydrogen exchanger type III, and Na-K-ATPase.

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Liu, Zhonghua, Qi Zhu, Tianfu Cai, Ze Wu, Jing Li, Dan Li, Weiwen Ning, et al. "260. Hainantoxin-III Inhibits Voltage-Gated Sodium Channel Nav 1.7 and Extenuates Inflammatory Pain in Animal Models." Toxicon 60, no. 2 (August 2012): 229–30. http://dx.doi.org/10.1016/j.toxicon.2012.04.261.

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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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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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Martinez-Lavin, Manuel. "Fibromyalgia: When Distress Becomes (Un)sympathetic Pain." Pain Research and Treatment 2012 (September 19, 2012): 1–6. http://dx.doi.org/10.1155/2012/981565.

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Fibromyalgia is a painful stress-related disorder. A key issue in fibromyalgia research is to investigate how distress could be converted into pain. The sympathetic nervous system is the main element of the stress response system. In animal models, physical trauma, infection, or distressing noise can induce abnormal connections between the sympathetic nervous system and the nociceptive system. Dorsal root ganglia sodium channels facilitate this type of sympathetic pain. Similar mechanisms may operate in fibromyalgia. Signs of sympathetic hyperactivity have been described in this condition. Gen

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Bigiani, Albertino. "Does ENaC Work as Sodium Taste Receptor in Humans?" Nutrients 12, no. 4 (April 24, 2020): 1195. http://dx.doi.org/10.3390/nu12041195.

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Taste reception is fundamental for the proper selection of food and beverages. Among the several chemicals recognized by the human taste system, sodium ions (Na+) are of particular relevance. Na+ represents the main extracellular cation and is a key factor in many physiological processes. Na+ elicits a specific sensation, called salty taste, and low-medium concentrations of table salt (NaCl, the common sodium-containing chemical we use to season foods) are perceived as pleasant and appetitive. How we detect this cation in foodstuffs is scarcely understood. In animal models, such as the mouse a

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Bankir, Lise, Daniel G. Bichet, and Nadine Bouby. "Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?" American Journal of Physiology-Renal Physiology 299, no. 5 (November 2010): F917—F928. http://dx.doi.org/10.1152/ajprenal.00413.2010.

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Excessive sodium reabsorption by the kidney has long been known to participate in the pathogenesis of some forms of hypertension. In the kidney, the final control of NaCl reabsorption takes place in the distal nephron through the amiloride-sensitive epithelial sodium channel (ENaC). Liddle's syndrome, an inherited form of hypertension due to gain-of-function mutations in the genes coding for ENaC subunits, has demonstrated the key role of this channel in the sodium balance. Although aldosterone is classically thought to be the main hormone regulating ENaC activity, several studies in animal mo

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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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Dewis, Mark L., Tam-Hao T. Phan, ZuoJun Ren, Xuanyu Meng, Meng Cui, Shobha Mummalaneni, Mee-Ra Rhyu, John A. DeSimone, and Vijay Lyall. "N-geranyl cyclopropyl-carboximide modulates salty and umami taste in humans and animal models." Journal of Neurophysiology 109, no. 4 (February 15, 2013): 1078–90. http://dx.doi.org/10.1152/jn.00124.2012.

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Effects of N-geranyl cyclopropylcarboxamide (NGCC) and four structurally related compounds ( N-cyclopropyl E2,Z6-nonadienamide, N-geranyl isobutanamide, N-geranyl 2-methylbutanamide, and allyl N-geranyl carbamate) were evaluated on the chorda tympani (CT) nerve response to NaCl and monosodium glutamate (MSG) in rats and wild-type (WT) and TRPV1 knockout (KO) mice and on human salty and umami taste intensity. NGCC enhanced the rat CT response to 100 mM NaCl + 5 μM benzamil (Bz; an epithelial Na+ channel blocker) between 1 and 2.5 μM and inhibited it above 5 μM. N-(3-methoxyphenyl)-4-chlorocinna

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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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Gomez-Sanchez, E. P., and C. E. Gomez-Sanchez. "Effect of central amiloride infusion on mineralocorticoid hypertension." American Journal of Physiology-Endocrinology and Metabolism 267, no. 5 (November 1, 1994): E754—E758. http://dx.doi.org/10.1152/ajpendo.1994.267.5.e754.

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There is strong evidence from different types of studies, including the discrete infusion of agonists and antagonists and ablation of specific brain areas or transmitter-type neurons, that mineralocorticoids, in excess, act in the brain to elevate blood pressure. Aldosterone enhances the entry of Na+ through amiloride-sensitive Na+ channels in some mineralocorticoid-sensitive transport epithelial cells. To define possible cellular mechanisms involved in central mineralocorticoid action, benzamil, an amiloride analogue with selective affinity for the Na+ channel, was continuously infused intrac

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Zhong, Beihua, Shuangtao Ma, and Donna H. Wang. "Ablation of TRPV1 Abolishes Salicylate-Induced Sympathetic Activity Suppression and Exacerbates Salicylate-Induced Renal Dysfunction in Diet-Induced Obesity." Cells 10, no. 5 (May 18, 2021): 1234. http://dx.doi.org/10.3390/cells10051234.

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Sodium salicylate (SA), a cyclooxygenase inhibitor, has been shown to increase insulin sensitivity and to suppress inflammation in obese patients and animal models. Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel expressed in afferent nerve fibers. Cyclooxygenase-derived prostaglandins are involved in the activation and sensitization of TRPV1. This study tested whether the metabolic and renal effects of SA were mediated by the TRPV1 channel. Wild-type (WT) and TRPV1−/− mice were fed a Western diet (WD) for 4 months and received SA infusion (120mg/kg/day) or ve

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Nickolaus, Peter, Birgit Jung, Juan Sabater, Samuel Constant, and Abhya Gupta. "Preclinical evaluation of the epithelial sodium channel inhibitor BI 1265162 for treatment of cystic fibrosis." ERJ Open Research 6, no. 4 (October 2020): 00429–2020. http://dx.doi.org/10.1183/23120541.00429-2020.

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BackgroundEpithelial sodium channel (ENaC) is an important regulator of airway surface liquid volume; ENaC is hyperactivated in cystic fibrosis (CF). ENaC inhibition is a potential therapeutic target for CF. Here, we report in vitro and in vivo results for BI 1265162, an inhaled ENaC inhibitor currently in Phase II clinical development, administered via the Respimat® Soft Mist™ inhaler.MethodsIn vitro inhibition of sodium ion (Na+) transport by BI 1265162 was tested in mouse renal collecting duct cells (M1) and human bronchial epithelial cells (NCI-H441); inhibition of water transport was meas

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Galli, A., L. J. DeFelice, B. J. Duke, K. R. Moore, and R. D. Blakely. "Sodium-dependent norepinephrine-induced currents in norepinephrine-transporter-transfected HEK-293 cells blocked by cocaine and antidepressants." Journal of Experimental Biology 198, no. 10 (October 1, 1995): 2197–212. http://dx.doi.org/10.1242/jeb.198.10.2197.

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Transport of norepinephrine (NE+) by cocaine- and antidepressant-sensitive transporters in presynaptic terminals is predicted to involve the cotransport of Na+ and Cl-, resulting in a net movement of charge per transport cycle. To explore the relationship between catecholamine transport and ion permeation through the NE transporter, we established a human norepinephrine transporter (hNET) cell line suitable for biochemical analysis and patch-clamp recording. Stable transfection of hNET cDNA into HEK-293 (human embryonic kidney) cells results in lines exhibiting (1) a high number of transporter

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Shi, Xuan-Zheng, John H. Winston, and Sushil K. Sarna. "Differential immune and genetic responses in rat models of Crohn's colitis and ulcerative colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 1 (January 2011): G41—G51. http://dx.doi.org/10.1152/ajpgi.00358.2010.

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Crohn's disease and ulcerative colitis are clinically, immunologically, and morphologically distinct forms of inflammatory bowel disease (IBD). However, smooth muscle function is impaired similarly in both diseases, resulting in diarrhea. We tested the hypothesis that differential cellular, genetic, and immunological mechanisms mediate smooth muscle dysfunction in two animal models believed to represent the two diseases. We used the rat models of trinitrobenzene sulfonic acid (TNBS)- and dextran sodium sulfate (DSS)-induced colonic inflammations, which closely mimic the clinical and morphologi

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González-Cano, Rafael, M. Carmen Ruiz-Cantero, Miriam Santos-Caballero, Carlos Gómez-Navas, Miguel Á. Tejada, and Francisco R. Nieto. "Tetrodotoxin, a Potential Drug for Neuropathic and Cancer Pain Relief?" Toxins 13, no. 7 (July 12, 2021): 483. http://dx.doi.org/10.3390/toxins13070483.

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Tetrodotoxin (TTX) is a potent neurotoxin found mainly in puffer fish and other marine and terrestrial animals. TTX blocks voltage-gated sodium channels (VGSCs) which are typically classified as TTX-sensitive or TTX-resistant channels. VGSCs play a key role in pain signaling and some TTX-sensitive VGSCs are highly expressed by adult primary sensory neurons. During pathological pain conditions, such as neuropathic pain, upregulation of some TTX-sensitive VGSCs, including the massive re-expression of the embryonic VGSC subtype NaV1.3 in adult primary sensory neurons, contribute to painful hypers

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Alborghetti, Marika, and Ferdinando Nicoletti. "Different Generations of Type-B Monoamine Oxidase Inhibitors in Parkinson’s Disease: From Bench to Bedside." Current Neuropharmacology 17, no. 9 (August 22, 2019): 861–73. http://dx.doi.org/10.2174/1570159x16666180830100754.

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Three inhibitors of type-B monoamine oxidase (MAOB), selegiline, rasagiline, and safinamide, are used for the treatment of Parkinson’s disease (PD). All three drugs improve motor signs of PD, and are effective in reducing motor fluctuations in patients undergoing long-term L-DOPA treatment. The effect of MAOB inhibitors on non-motor symptoms is not uniform and may not be class-related. Selegiline and rasagiline are irreversible inhibitors forming a covalent bond within the active site of MAOB. In contrast, safinamide is a reversible MAOB inhibitor, and also inhibits voltage- sensitive sodium c

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Clauss, Wolfgang G. "Epithelial transport and osmoregulation in annelids." Canadian Journal of Zoology 79, no. 2 (February 1, 2001): 192–203. http://dx.doi.org/10.1139/z00-200.

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Epithelial transport related to osmoregulation has so far not been extensively investigated in annelids. Compared with the large body of information about ion transport across crustacean or insect epithelia, only a few studies have been done with isolated preparations of annelids, using the body wall of marine polychaetes or Hirudinea. Nephridial function and general body homeostasis have received more attention, and have probably been best investigated in Hirudinea. With recent advances in the molecular physiology of epithelial transport systems in vertebrates, the cloning of various transpor

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Kawashiri, Takehiro, Keisuke Mine, Daisuke Kobayashi, Mizuki Inoue, Soichiro Ushio, Mayako Uchida, Nobuaki Egashira, and Takao Shimazoe. "Therapeutic Agents for Oxaliplatin-Induced Peripheral Neuropathy; Experimental and Clinical Evidence." International Journal of Molecular Sciences 22, no. 3 (January 30, 2021): 1393. http://dx.doi.org/10.3390/ijms22031393.

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Oxaliplatin is an essential drug in the chemotherapy of colorectal, gastric, and pancreatic cancers, but it frequently causes peripheral neuropathy as a dose-limiting factor. So far, animal models of oxaliplatin-induced peripheral neuropathy have been established. The mechanisms of development of neuropathy induced by oxaliplatin have been elucidated, and many drugs and agents have been proven to have neuroprotective effects in basic studies. In addition, some of these drugs have been validated in clinical studies for their inhibitory effects on neuropathy. In this review, we summarize the bas

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Voskobiynyk, Yuliya, Gopal Battu, Stephanie A. Felker, J. Nicholas Cochran, Megan P. Newton, Laura J. Lambert, Robert A. Kesterson, et al. "Aberrant regulation of a poison exon caused by a non-coding variant in a mouse model of Scn1a-associated epileptic encephalopathy." PLOS Genetics 17, no. 1 (January 7, 2021): e1009195. http://dx.doi.org/10.1371/journal.pgen.1009195.

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Dravet syndrome (DS) is a developmental and epileptic encephalopathy that results from mutations in the Nav1.1 sodium channel encoded by SCN1A. Most known DS-causing mutations are in coding regions of SCN1A, but we recently identified several disease-associated SCN1A mutations in intron 20 that are within or near to a cryptic and evolutionarily conserved “poison” exon, 20N, whose inclusion is predicted to lead to transcript degradation. However, it is not clear how these intron 20 variants alter SCN1A expression or DS pathophysiology in an organismal context, nor is it clear how exon 20N is re

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Park, David S., Akshay Shekhar, John Santucci, Gabriel Redel-Traub, Sergio Solinas, Shana Mintz, Xianming Lin, et al. "Ionic Mechanisms of Impulse Propagation Failure in the FHF2-Deficient Heart." Circulation Research 127, no. 12 (December 4, 2020): 1536–48. http://dx.doi.org/10.1161/circresaha.120.317349.

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Rationale: FHFs (fibroblast growth factor homologous factors) are key regulators of sodium channel (Na V ) inactivation. Mutations in these critical proteins have been implicated in human diseases including Brugada syndrome, idiopathic ventricular arrhythmias, and epileptic encephalopathy. The underlying ionic mechanisms by which reduced Na v availability in Fhf2 knockout ( Fhf2 KO ) mice predisposes to abnormal excitability at the tissue level are not well defined. Objective: Using animal models and theoretical multicellular linear strands, we examined how FHF2 orchestrates the interdependenc

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Schultz, Jacob G., Stine Andersen, Asger Andersen, Jens Erik Nielsen-Kudsk, and Jan M. Nielsen. "Evaluation of cardiac electrophysiological properties in an experimental model of right ventricular hypertrophy and failure." Cardiology in the Young 26, no. 3 (April 14, 2015): 451–58. http://dx.doi.org/10.1017/s1047951115000402.

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AbstractBackgroundMalignant arrhythmias are a major cause of sudden cardiac death in adults with congenital heart disease. We developed a model to serially investigate electrophysiological properties in an animal model of right ventricular hypertrophy and failure.MethodWe created models of compensated (cHF; n=11) and decompensated (dHF; n=11) right ventricular failure in Wistar rats by pulmonary trunk banding. Healthy controls underwent sham operation (Control; n=13). Surface electrocardiography was recorded from extremities, and inducibility of ventricular tachycardia was evaluated in vivo by

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Kögler, Gesine, Sandra Sensken, Judith A. Airey, Thorsten Trapp, Markus Müschen, Niklas Feldhahn, Stefanie Liedtke, et al. "A New Human Somatic Stem Cell from Placental Cord Blood with Intrinsic Pluripotent Differentiation Potential." Journal of Experimental Medicine 200, no. 2 (July 19, 2004): 123–35. http://dx.doi.org/10.1084/jem.20040440.

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Here a new, intrinsically pluripotent, CD45-negative population from human cord blood, termed unrestricted somatic stem cells (USSCs) is described. This rare population grows adherently and can be expanded to 1015 cells without losing pluripotency. In vitro USSCs showed homogeneous differentiation into osteoblasts, chondroblasts, adipocytes, and hematopoietic and neural cells including astrocytes and neurons that express neurofilament, sodium channel protein, and various neurotransmitter phenotypes. Stereotactic implantation of USSCs into intact adult rat brain revealed that human Tau-positive

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Gáll, Zsolt, Krisztina Kelemen, István Mihály, Pál Salamon, Ildikó Miklóssy, Brigitta Zsigmond, and Melinda Kolcsár. "Role of Lacosamide in Preventing Pentylenetetrazole Kindling-Induced Alterations in the Expression of the Gamma-2 Subunit of the GABAA Receptor in Rats." Current Molecular Pharmacology 13, no. 3 (July 9, 2020): 251–60. http://dx.doi.org/10.2174/1874467213666200102095023.

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Background: Epilepsy remains challenging to treat still no etiologic treatment has been identified, however, some antiepileptic drugs (AEDs) are able to modify the pathogenesis of the disease. Lacosamide (LCM) has been shown to possess complex anticonvulsant and neuroprotective actions, being an enhancer of the slow inactivation of voltage-gated sodium channels, and it has the potential to prevent epileptogenesis. Recent evidence has shown that LCM indirectly improves the function of GABAA receptors. Receptors at most GABAergic synapses involve the gamma-2 subunit, which contributes to both ph

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Kaufmann, Dan, Emily A. Bates, Boris Yagen, Meir Bialer, Gerald H. Saunders, Karen Wilcox, H. Steve White, and KC Brennan. "sec-Butylpropylacetamide (SPD) has antimigraine properties." Cephalalgia 36, no. 10 (July 19, 2016): 924–35. http://dx.doi.org/10.1177/0333102415612773.

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Background Though migraine is disabling and affects 12%–15% of the population, there are few drugs that have been developed specifically for migraine prevention. Valproic acid (VPA) is a broad-spectrum antiepileptic drug (AED) that is also used for migraine prophylaxis, but its clinical use is limited by its side effect profile. sec-Butylpropylacetamide (SPD) is a novel VPA derivative, designed to be more potent and tolerable than VPA, that has shown efficacy in animal seizure and pain models. Methods We evaluated SPD’s antimigraine potential in the cortical spreading depression (CSD) and nitr

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Krylova, Irina B., Albina F. Safonova, and Natalia R. Evdokimova. "Correction of hypoxic state by metabolic precursors of endogenous activator of mitochondrial ATP-dependent K+channels." Reviews on Clinical Pharmacology and Drug Therapy 16, no. 3 (December 15, 2018): 25–31. http://dx.doi.org/10.17816/rcf16325-31.

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Aim. The antihypoxic properties of uridine and uridine-5'-monophosphate (UMP), which are the metabolic precursors of the natural activator of mitochondrial ATP-dependent K+ channels (mitoKATP channels) uridine diphosphat were investigated on the models of hypoxic hypoxia with hypercapnia (HHH), hemic hypoxia and local circulatory hypoxia. Methods. HHH was created in males and females white mice weighing 28-30 g. The animals were placed one by one in hermetically closed container and the duration of their life was determined. The antihypoxic activity of the substances was compared with th

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Downs, Charles A., David Trac, Elizabeth M. Brewer, Lou Ann Brown, and My N. Helms. "Chronic Alcohol Ingestion Changes the Landscape of the Alveolar Epithelium." BioMed Research International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/470217.

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Similar to effects of alcohol on the heart, liver, and brain, the effects of ethanol (EtOH) on lung injury are preventable. Unlike other vital organ systems, however, the lethal effects of alcohol on the lung are underappreciated, perhaps because there are no signs of overt pulmonary disorder until a secondary insult, such as a bacterial infection or injury, occurs in the lung. This paper provides overview of the complex changes in the alveolar environment known to occur following both chronic and acute alcohol exposures. Contemporary animal and cell culture models for alcohol-induced lung dys

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Jurj, Ancuta, Ciprian Tomuleasa, Tiberiu T. Tat, Ioana Berindan Neagoe, Stefan V. Vesa, and Daniela C. Ionescu. "Antiproliferative and Apoptotic Effects of Lidocaine on Human Hepatocarcinoma Cells. A preliminary study." Journal of Gastrointestinal and Liver Diseases 26, no. 1 (March 1, 2017): 45–50. http://dx.doi.org/10.15403/jgld.2014.1121.261.juj.

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Background & Aims: It is now well documented that certain anesthetic techniques may influence long term outcome in cancer patients undergoing surgery. More recently, local anesthetics proved certain antiproliferative effects in cancer cells. In our study, we aimed to investigate if lidocaine has antiproliferative effects in human hepatocarcinoma cells and to identify possible mechanisms of these effects.Methods. We investigated the inhibitory effect of different concentrations of lidocaine on the proliferation of cultured HepG2 human hepatocarcinoma cells and LX2 normal liver fibroblasts.

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Keita, Hawa, Claire Lepouse, Danielle Henzel, Jean-Marie Desmonts, and Jean Mantz. "Riluzole Blocks Dopamine Release Evoked by N-methyl-D-aspartate, Kainate, and Veratridine in the Rat Striatum." Anesthesiology 87, no. 5 (November 1, 1997): 1164–71. http://dx.doi.org/10.1097/00000542-199711000-00021.

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Background Dopamine (DA) is released in large amounts during cerebral ischemia and may exacerbate tissue damage. Riluzole (54274 RP) is a recently developed agent that depresses glutamate neurotransmission in the central nervous system (CNS) and that may protect against ischemic injury in some animal models. Because glutamate stimulates the release of DA in the striatum, the authors hypothesized that riluzole could antagonize DA release in this structure. Methods Assay for DA release consisted of superfusing 3H-DA preloaded synaptosomes with artificial cerebrospinal fluid (1 ml/min, 37 degrees

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Wang, Qing, Sophie Clement, Giulio Gabbiani, Jean-Daniel Horisberger, Michel Burnier, Bernard C. Rossier, and Edith Hummler. "Chronic hyperaldosteronism in a transgenic mouse model fails to induce cardiac remodeling and fibrosis under a normal-salt diet." American Journal of Physiology-Renal Physiology 286, no. 6 (June 2004): F1178—F1184. http://dx.doi.org/10.1152/ajprenal.00386.2003.

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Primary aldosteronism causes severe hypertension in humans (Conn's syndrome) with cardiac hypertrophy, characterized by a fibrosis more severe than the one observed in patients with essential hypertension. This suggests that aldosterone by itself may have specific and direct effects on cardiac remodeling through the activation of the cardiac mineralocorticoid receptor. Experimental evidence obtained in studying uninephrectomized rats treated with aldosterone or deoxycorticosterone (DOC) together with salt loading has led to similar conclusions. To examine the direct consequences of chronically

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Lemme, Marta, Ingke Braren, Maksymilian Prondzynski, Bülent Aksehirlioglu, Bärbel M. Ulmer, Mirja L. Schulze, Djemail Ismaili, et al. "Chronic intermittent tachypacing by an optogenetic approach induces arrhythmia vulnerability in human engineered heart tissue." Cardiovascular Research 116, no. 8 (October 9, 2019): 1487–99. http://dx.doi.org/10.1093/cvr/cvz245.

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Abstract Aims Chronic tachypacing is commonly used in animals to induce cardiac dysfunction and to study mechanisms of heart failure and arrhythmogenesis. Human induced pluripotent stem cells (hiPSC) may replace animal models to overcome species differences and ethical problems. Here, 3D engineered heart tissue (EHT) was used to investigate the effect of chronic tachypacing on hiPSC-cardiomyocytes (hiPSC-CMs). Methods and results To avoid cell toxicity by electrical pacing, we developed an optogenetic approach. EHTs were transduced with lentivirus expressing channelrhodopsin-2 (H134R) and stim

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Butler, Stephen. "Buprenorphine—Clinically useful but often misunderstood." Scandinavian Journal of Pain 4, no. 3 (July 1, 2013): 148–52. http://dx.doi.org/10.1016/j.sjpain.2013.05.004.

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AbstractBackgroundThere are a number of false myths about buprenorphine based on unconfirmed animal data, even from isolated animal organs, and early clinical research. These myths came into textbooks on pharmacology and pain about 30 years ago and have been difficult to eradicate. Animal models of pain and pain relief are notoriously unreliable as predictors of human clinical effects. The fact is that in clinical practice there is NO bell-shaped dose-response curve, there is NO plateau on the dose-response curve, and there is NO antagonist effect from buprenorphine on other mu-opioid agonists

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Zennaro, Maria-Christina, Amanda Jane Rickard, and Sheerazed Boulkroun. "Genetics in endocrinology: Genetics of mineralocorticoid excess: an update for clinicians." European Journal of Endocrinology 169, no. 1 (July 2013): R15—R25. http://dx.doi.org/10.1530/eje-12-0813.

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Abstract (sommario):

Aldosterone plays a major role in the regulation of sodium and potassium homeostasis and blood pressure. More recently, aldosterone has emerged as a key hormone mediating end organ damage. In extreme cases, dysregulated aldosterone production leads to primary aldosteronism (PA), the most common form of secondary hypertension. However, even within the physiological range, high levels of aldosterone are associated with an increased risk of developing hypertension over time. PA represents the most common and curable form of hypertension, with a prevalence that increases with the severity of hyper

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Billen, Bert, Frank Bosmans, and Jan Tytgat. "Animal Peptides Targeting Voltage-Activated Sodium Channels." Current Pharmaceutical Design 14, no. 24 (August 1, 2008): 2492–502. http://dx.doi.org/10.2174/138161208785777423.

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Ozawa, T., Y. Nagakura, Y. Ohkura, S. Kakimoto, H. Suzaka, T. Kiso, T. Watabiki, et al. "F639 A NOVEL STATE-DEPENDENT SODIUM CHANNEL INHIBITOR 3-METHOXY-N-{2-[4-(2-PHENYLETHYL)PIPERIDIN-1-YL]ETHYL}- PYRIDINE-4-CARBOXAMIDE (AS1512706-00) EXERTS ANALGESIC EFFECTS IN A BROAD RANGE OF CHRONIC PAIN ANIMAL MODELS." European Journal of Pain Supplements 5, S1 (September 2011): 180. http://dx.doi.org/10.1016/s1754-3207(11)70619-8.

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Liebeskind, Benjamin J., David M. Hillis, and Harold H. Zakon. "Independent acquisition of sodium selectivity in bacterial and animal sodium channels." Current Biology 23, no. 21 (November 2013): R948—R949. http://dx.doi.org/10.1016/j.cub.2013.09.025.

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Deuchar, Graeme A., Danielle McLean, Patrick W. F. Hadoke, David G. Brownstein, David J. Webb, John J. Mullins, Karen Chapman, Jonathan R. Seckl та Yuri V. Kotelevtsev. "11β-Hydroxysteroid Dehydrogenase Type 2 Deficiency Accelerates Atherogenesis and Causes Proinflammatory Changes in the Endothelium in Apoe−/− Mice". Endocrinology 152, № 1 (1 січня 2011): 236–46. http://dx.doi.org/10.1210/en.2010-0925.

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Abstract Mineralocorticoid receptor (MR) activation is proinflammatory and proatherogenic. Antagonism of MR improves survival in humans with congestive heart failure caused by atherosclerotic disease. In animal models, activation of MR exacerbates atherosclerosis. The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) prevents inappropriate activation of the MR by inactivating glucocorticoids in mineralocorticoid-target tissues. To determine whether glucocorticoid-mediated activation of MR increases atheromatous plaque formation, we generated Apoe−/−/11β-HSD2−/− double-knockout (E/b2) m

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Bosmans, Frank, Mirela Milescu, and Kenton J. Swartz. "Palmitoylation Affects the Interaction of Animal Toxins with Sodium Channels." Biophysical Journal 100, no. 3 (February 2011): 422a. http://dx.doi.org/10.1016/j.bpj.2010.12.2497.

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Liebeskind, Benjamin J., David M. Hillis, and Harold H. Zakon. "Phylogeny Unites Animal Sodium Leak Channels with Fungal Calcium Channels in an Ancient, Voltage-Insensitive Clade." Molecular Biology and Evolution 29, no. 12 (July 19, 2012): 3613–16. http://dx.doi.org/10.1093/molbev/mss182.

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Bagnéris, Claire, Claire E. Naylor, Emily C. McCusker, and B. A. Wallace. "Structural model of the open–closed–inactivated cycle of prokaryotic voltage-gated sodium channels." Journal of General Physiology 145, no. 1 (December 15, 2014): 5–16. http://dx.doi.org/10.1085/jgp.201411242.

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Abstract (sommario):

In excitable cells, the initiation of the action potential results from the opening of voltage-gated sodium channels. These channels undergo a series of conformational changes between open, closed, and inactivated states. Many models have been proposed for the structural transitions that result in these different functional states. Here, we compare the crystal structures of prokaryotic sodium channels captured in the different conformational forms and use them as the basis for examining molecular models for the activation, slow inactivation, and recovery processes. We compare structural simila

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Rehberg, Benno, Yong-Hong Xiao, and Daniel S. Duch. "Central Nervous System Sodium Channels Are Significantly Suppressed at Clinical Concentrations of Volatile Anesthetics." Anesthesiology 84, no. 5 (May 1, 1996): 1223–33. http://dx.doi.org/10.1097/00000542-199605000-00025.

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Abstract (sommario):

Background Although voltage-dependent sodium channels have been proposed as possible molecular sites of anesthetic action, they generally are considered too insensitive to be likely molecular targets. However, most previous molecular studies have used peripheral sodium channels as models. To examine the interactions of volatile anesthetics with mammalian central nervous system voltage-gated sodium channels, rat brain IIA sodium channels were expressed in a stably transfected Chinese hamster ovary cell line, and their modification by volatile anesthetics was examined. Methods Sodium currents we

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Smith, Natalie E., and Ben Corry. "Mutant bacterial sodium channels as models for local anesthetic block of eukaryotic proteins." Channels 10, no. 3 (March 18, 2016): 225–37. http://dx.doi.org/10.1080/19336950.2016.1148224.

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URBAN, BERND W., CHRISTIAN FRENKEL, DANIEL S. DUCH, and AUDREY B. KAUFF. "Molecular Models of Anesthetic Action on Sodium Channels, Including Those from Human Brain." Annals of the New York Academy of Sciences 625, no. 1 Molecular and (June 1991): 327–43. http://dx.doi.org/10.1111/j.1749-6632.1991.tb33861.x.

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Otsuki, Makoto, Mitsuyoshi Yamamoto, and Taizo Yamaguchi. "Animal Models of Chronic Pancreatitis." Gastroenterology Research and Practice 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/403295.

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Abstract (sommario):

Animal models for CP in rats can be classified into 2 groups: one is noninvasive or nonsurgical models and the other is invasive or surgical models. Pancreatic injury induced by repetitive injections of supramaximal stimulatory dose of caerulein (Cn) or by intraductal infusion of sodium taurocholate (NaTc) recovered within 14 days, whereas that caused by repetitive injection of arginine or by intraductal infusion of oleic acid was persistent. However, the destroyed acinar tissues were replaced by fatty tissues without fibrosis. Transient stasis of pancreatic fluid flow by 0.01% agarose and min

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