Adenosine as a signal for ion channel arrest in anoxia-tolerant organisms

Leslie Thomas Buck

doi:10.1016/j.cbpc.2004.04.002

Adenosine as a signal for ion channel arrest in anoxia-tolerant organisms

Comparative Biochemistry and Physiology Part B Biochemistry and Molecular Biology ◽

10.1016/j.cbpc.2004.04.002 ◽

2004 ◽

Vol 139 (3) ◽

pp. 401-414 ◽

Cited By ~ 33

Author(s):

Leslie Thomas Buck

Keyword(s):

Ion Channel ◽

Channel Arrest

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Adaptations of vertebrate neurons to hypoxia and anoxia: maintaining critical Ca2+ concentrations.

Journal of Experimental Biology ◽

10.1242/jeb.201.8.1141 ◽

1998 ◽

Vol 201 (8) ◽

pp. 1141-1152 ◽

Cited By ~ 2

Author(s):

P E Bickler ◽

L T Buck

Keyword(s):

Ion Channel ◽

Action Potentials ◽

G Protein Coupled Receptors ◽

Channel Activity ◽

Down Regulation ◽

Inhibitory Neurotransmitters ◽

Channel Arrest ◽

Postsynaptic Receptors ◽

G Protein Coupled ◽

The Brain

Down-regulation of ion channel activity ('channel arrest'), which aids in preserving critical ion gradients in concert with greatly diminished energy production, is one important strategy by which anoxia-tolerant neurons adapt to O2 shortage. Channel arrest results in the elimination of action potentials and neurotransmission and also decreases the need for ion transport, which normally requires a large energy expenditure. Important targets of this down-regulation may be channels in which activity would otherwise result in the toxic increases in intracellular [Ca2+] characteristic of anoxia-sensitive mammalian neurons. In turtles, Na+ channels and the Ca2+-permeable ion channel of the N-methyl-d-aspartate (NMDA)-type glutamate receptor undergo down-regulation during anoxia. Inactivation of NMDA receptors during hypoxia occurs by a variety of mechanisms, including alterations in the phosphorylation state of ion channel subunits, Ca2+-dependent second messenger activation, changes in Ca2+-dependent polymerization/depolymerization of actin to postsynaptic receptors and activation of other G-protein-coupled receptors. Release of inhibitory neurotransmitters (e.g. gamma-aminobutyrate) and neuromodulators (e.g. adenosine) into the brain extracellular fluids may play an important role in the down-regulation of these and other types of ion channels.

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Myrsinane and related diterpenes from Euphorbia falcata with selective potassium ion channel activity

Planta Medica ◽

10.1055/s-0035-1565539 ◽

2015 ◽

Vol 81 (16) ◽

Author(s):

A Vasas ◽

P Orvos ◽

L Tálosi ◽

P Forgo ◽

G Pinke ◽

...

Keyword(s):

Ion Channel ◽

Potassium Ion ◽

Channel Activity ◽

Potassium Ion Channel

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Ion channel alterations and epilepsy in mice and man

Neuropediatrics ◽

10.1055/s-2005-867952 ◽

2005 ◽

Vol 36 (02) ◽

Author(s):

CM Becker ◽

J Brill ◽

K Becker

Keyword(s):

Ion Channel

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Ion Channel Remodelling in Atrial Fibrillation

European Cardiology Review ◽

10.15420/ecr.2011.7.2.97 ◽

2011 ◽

Vol 7 (2) ◽

pp. 97 ◽

Cited By ~ 6

Author(s):

Niels Voigt ◽

Dobromir Dobrev ◽

◽

Keyword(s):

Atrial Fibrillation ◽

Ion Channel ◽

Antiarrhythmic Drugs ◽

Current Knowledge ◽

Bleeding Complications ◽

Large Size ◽

Cardiovascular Morbidity And Mortality ◽

Number Of Patients ◽

Life Threatening ◽

Underlying Mechanisms

Atrial fibrillation (AF) is the most common arrhythmia and is associated with substantial cardiovascular morbidity and mortality, with stroke being the most critical complication. Present drugs used for the therapy of AF (antiarrhythmics and anticoagulants) have major limitations, including incomplete efficacy, risks of life-threatening proarrhythmic events and bleeding complications. Non-pharmacological ablation procedures are efficient and apparently safe, but the very large size of the patient population allows ablation treatment of only a small number of patients. These limitations largely result from limited knowledge about the underlying mechanisms of AF and there is a hope that a better understanding of the molecular basis of AF may lead to the discovery of safer and more effective therapeutic targets. This article reviews the current knowledge about AF-related ion-channel remodelling and discusses how these alterations might affect the efficacy of antiarrhythmic drugs.

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