Sentences with phrase «by sodium channel»

«The [pain] signal might get generated by sodium channel 1.7, but it does not get sent to the brain by 1.8,» Rowe says.

Not exact matches

In this case, over time, amino acids in three different sodium channels found in nerves and muscle changed, allowing select snakes to resist the numbness and paralysis typically brought on by the toxin.

In a major breakthrough several years ago, two research groups, the Zuker group at Columbia and the Bachmanov group at the Monell Center for Chemical Senses, each got around this problem by finding drugs that could temporarily block a certain type of sodium channel in mice's mouths.

The novel substance BIIB074 which was tested in this phase II study inhibits the sodium channel 1.7 state - dependent, meaning: The more active this sodium channel gets, the stronger it is blocked by BIIB074.

That suggests that this sodium channel could be a target for the development of drugs to prevent the pain caused by acid build - up — which happens in arthritis and other inflammatory disorders.

Blocking this sodium channel — e.g. by a local anesthetic — inhibits the pain.

In myotonic dystrophic patients, titration of MBNL protein by RNA containing expanded CUG repeats leads to expression of a fetal splicing form of the cardiac sodium channel, SCN5A, inappropriate to adult heart physiology, ultimately resulting in cardiac conduction delay and heart arrhythmias, which are two key features of myotonic dystrophy.

Researchers have known for decades that some microorganisms, such as single - celled green algae, have proteins that respond to light by opening a channel in the microbe's membranes, allowing the passage of electrically charged ions (such as calcium and sodium).

In effect, this sodium channel amplifies the pain signal so it can be «heard» by the brain, says King.

Nerves and other electrically - excitable cells communicate with one another by transmitting electrical signals, and sodium channels play a vital role in this process.

Using a technique called atomic force microscopy, Dilshan Balasuriya, led by Professor Mike Edwardson in Cambridge's Department of Pharmacology, imaged individual 3 trimers and confirmed that the complete 3 - subunit trimers cross-linked up to three sodium channel α - subunits.

Hund's team identified a phosphorylation site (Serine 571) on the voltage-gated sodium channel targeted by CaM kinase II that serves as a switch for inappropriate «late» sodium influx.

According to a research team led by Thomas Hund, the key may reside in voltage-gated sodium channels, nanoscopic pores that control the flow of sodium ions across the heart cell membrane.

Its additional sodium channels now malfunction, and the axon tries to compensate by creating even more channels.

Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem cells, stromal cells, haematopoietic stem cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters

Methodology / principal findings: Population genetic structure was assessed through microsatellite analysis, and the impact of insecticide pressure by genotyping two target - site mutations, Vgsc - 1014F of the voltage-gated sodium channel target of pyrethroid and DDT insecticides, and Ace1 - 119S of the acetylcholinesterase gene, target of carbamate and organophosphate insecticides.

The primary process by which mammals detect NaCl, common table salt, is well understood, and occurs via a sodium receptor known as ENaC (epithelial sodium channel).

After this induction period, miniature excitatory postsynaptic AMPA - R currents (mEPSCs) were recorded from DA neurons, which could be isolated by blocking inhibitory GABA - Rs and voltage gated sodium channels.

ëinhibitory effect of metal ions, alone or combined, on sodium channels (research indicate that body's radical quenchers like glutathione, L - cysteine and EDTA can prevent or reverse such inhibition by «friendly» metals like zinc, copper, iron and cobalt, but not that caused by heavy «metals like lead and mercury), possible inhibition of sodium channel activity by dopamine, and others.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.

It acts by binding to specific receptors and allowing sodium (Na +) or calcium (Ca +) to move into brain cells through channels.