By Novartis Foundation
Fresh development has resulted in a greater knowing of the molecular constitution of sodium channels, how they paintings and the mechanisms that limit their expression to specific mobile forms.
This booklet explains how those channels are modulated in numerous pathological states to allow the improvement of healing innovations according to sodium channel recovery.
The authors current the most up-tp-date examine on sodium channels and neuronal functionality.
- Brings jointly either the elemental biology and biophysics with targeted attention of the clinical functions in persistent soreness and epilepsy.
- Includes assurance of channelopathies, sodium channel gene expression, the modulation of sodium channels, and molecular mechanisms of gating and drug block of sodium channels.
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Additional info for Sodium Channels and Neuronal Hyperexcitability
Sample text
Nature 403:321^325 Hirschberg B, Rovner A, Lieberman M, Patlak J 1995 Transfer of twelve charges is needed to open skeletal muscle Na+ channels. J Gen Physiol 106:1053^1068 Hodgkin AL, Huxley AF 1952 Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo. J Physiol 116:176^195 Horn R 2000 A new twist in the saga of charge movement in voltage-dependent ion channels. Neuron 25:511^514 Horn R, Ding S, Gruber HJ 2000 Immobilizing the moving parts of voltage-gated ion channels.
It is a real ¢shing expedition. They have to get reasonably close to cross-link. Some people have recently been using bifunctional cysteine reagents to see if they can ¢nd cross-linking. Even in that case, if you were able to cross-link an a subunit 32 DISCUSSION with a b subunit, you wouldn’t know it unless there were an e¡ect. The chances of there being an e¡ect are pretty small. Isom: I will show in my paper (Isom 2002, this volume) that if you knock out b1 or b2 you do see functional e¡ects.
If you are trying to do any standard ¢tting, therefore, you have multiple minima to play with and it is not possible to arrive at unique ¢ts. We did ¢nally ¢t the data quite nicely in the paper by Keynes & Elinder (1998a). There was a great deal of argument earlier about the currents in the slowly rising phase, because Stimers et al (1987) had claimed that it was an artefact due to incomplete compensation for the Schwann cell series resistance in setting up the voltage clamp. However, this certainly did not apply to the observations of Keynes et al (1990), made with very careful adjustment of the feedback, or to the results of Keynes & Elinder (1998a).