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channelopathies/kalium
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Autoimmune Voltage-Gated Potassium Channelopathy Presenting With Catecholamine Excess.
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BACKGROUND
Autoimmune voltage-gated potassium channelopathies have been associated with a range of neurological presenting symptoms, including central, peripheral, and autonomic dysfunction.
UNASSIGNED
We describe a 12-year-old boy who presented with nine months of pain, anxiety, and 30-pound weight
In Vivo Analysis of Potassium Channelopathies: Loose Patch Recording of Purkinje Cell Firing in Living, Awake Zebrafish.
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Zebrafish is a lower vertebrate model organism that facilitates integrative analysis of the in vivo effects of potassium and other ion channel mutations at the molecular, cellular, developmental, circuit, systems, and behavioral levels of analysis. Here, we describe a method for extracellular, loose
Acquired neuromyotonia: a new autoantibody-mediated neuronal potassium channelopathy.
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Neuromyotonia (Isaacs syndrome) is a rare and heterogenous syndrome of continuous motor unit activity of peripheral nerve origin that manifests as various combinations of muscle stiffness, cramps, twitching, weakness, and delayed muscle relaxation. Although neuromyotonia may accompany an assortment
A new type of ATP-sensitive potassium channelopathy : Cantú syndrome.
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Multiple mutations in Kir6.x and SURx genes have implicated ATP-sensitive potassium (KATP) channels and, as a result, have led to diverse diseases, ranging from diabetes and hyperinsulinism to cardiac arrhythmias and cardiovascular disease. These diseases are referred to as KATP channelopathies.
Pharmacogenetics of KCNQ channel activation in 2 potassium channelopathy mouse models of epilepsy.
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Antiseizure drugs are the leading therapeutic choice for treatment of epilepsy, but their efficacy is limited by pharmacoresistance and the occurrence of unwanted side effects. Here, we examined the therapeutic efficacy of KCNQ channel activation by retigabine in preventing seizures and neurocardiac
Channelopathies of inwardly rectifying potassium channels.
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Mutations in genes encoding ion channels have increasingly been identified to cause disease conditions collectively termed channelopathies. Recognizing the molecular basis of an ion channel disease has provided new opportunities for screening, early diagnosis, and therapy of such conditions. This
Peripheral channelopathies as targets for potassium channel openers.
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Potassium channel openers (KCOs) are important tools that are often used to gain a greater understanding of K(+) channels. Agents that can induce or maintain the opening of K(+) channels also offer a therapeutic approach to controlling of cell excitability and offer a means of producing stability in
Neurological potassium channelopathies.
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Potassium channel dysfunction has been implicated in a variety of genetic and acquired neurological disorders that are collectively referred to as the potassium channelopathies. These include acquired neuromyotonia, episodic ataxia type-1, hereditary deafness syndromes, benign familial neonatal
Inward-rectifying potassium channelopathies: new insights into disorders of sodium and potassium homeostasis.
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Inward-rectifying potassium (Kir) channels allow more inward than outward potassium flux when channels are open in mammalian cells. At physiological resting membrane potentials, however, they predominantly mediate outward potassium flux and play important roles in regulating the resting membrane
[Potassium channelopathies and Morvan's syndromes].
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Interest in Morvan's disease or syndrome has grown, owing to its close links with various potassium channelopathies. Potassium is crucial for gating mechanisms (channel opening and closing), and especially for repolarization. Defective potassium regulation can lead to neuronal hyperexcitability.
Minireview: potassium channels and aldosterone dysregulation: is primary aldosteronism a potassium channelopathy?
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Primary aldosteronism is the most common form of secondary hypertension and has significant cardiovascular consequences. Aldosterone-producing adenomas (APAs) are responsible for half the cases of primary aldosteronism, and about half have mutations of the G protein-activated inward rectifying
[From Morvan's disease to potassium channelopathies].
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The term Morvan's disease, first coined in 1890, is still in use, although the generic term neuromyotonia--which is not exempt from criticism--has largely superseded it. Symptoms and signs are variable, ranging from benign painful fasciculations, pseudomyotonic cases, rigid forms, cases in which
Isaacs' syndrome as a potassium channelopathy of the nerve.
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Isaacs' syndrome (acquired neuromyotonia) is an antibody-mediated potassium channel disorder (channelopathy). The target channel proteins of the antigens are voltage-gated potassium channels (VGKCs), especially dendrotoxin-sensitive fast potassium channels. The suppression of voltage-gated outward
Voltage-gated potassium channelopathy: an expanding spectrum of clinical phenotypes.
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Autoimmune voltage-gated potassium channelopathies represent a wide and expanding spectrum of neurological conditions. We present a case demonstrating the phenotypic heterogeneity of antivoltage-gated potassium channels (VGKC)-associated disorders. Such cases may easily be dismissed as functional
Molecular mechanisms of cardiac voltage-gated potassium channelopathies.
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Potassium channels form highly K+ ion-selective pores in the plasma membrane of excitable cells. Voltage-gated potassium (Kv) channels open in response to membrane depolarization to allow rapid diffusion of K+ ions out of the cell, thus repolarizing the cell to restore a negative resting membrane
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