Sodium channels, inactivation

Vassilev, P., Scheuer, T. and Catterall, W. A. Identification of an intracellular peptide segment involved in sodium channel inactivation. Science 241,1658-1661,1988. 

West, J. W Patton, D. E., Scheuer, T. et al. A cluser of hydrophobic amino acid residues required for fast sodium channel inactivation. Proc. Natl. Acad. Sci. U.S.A. 89, 10910-10914,1992. 

Type I Block SRF by enhancing sodium channel inactivation Phenytoin Carbamazepine Oxcarbazepine Lamotrigine Felbamate ... 

Kontis KJ, Goldin AL 1997 Sodium channel inactivation is altered by substitution of voltage sensor positive charges. J Gen Physiol 110 403-413 (erratum 1997 Gen Physiol 110 763)... 

Rohl CA, Boeckman FA, Baker C, Scheuer T, CatteraU WA, Klevit RE 1999 Solution structure of the sodium channel inactivation gate. Biochemistry 38 855-861... 

Mickus T, J ung H, Spruston N 1999 Properties of slow, cumulative sodium channel inactivation in rat hippocampal CAI pyramidal neurons. Biophys J 76 846-860... 

Development of the slow tail current during a depolarizing pulse was taken as a measure of the rate at which the sodium channels are modified. It had a fast and a slow phase, and the latter disappeared after removal of sodium channel inactivation with pronase. Based on these and other results, a kinetic scheme was developed (Figure 2). Tetramethrin modifies the sodium channel in both closed and open states, and the modified channel opens and is inactivated much more slowly than the normal channel (15). However, we have very recently shown that the apparent inactivation of the modified sodium channel is a result of depletion of sodium ions in the periaxonal space (20). Figure 2 incorporates the revised version of the kinetic scheme. 

The reason for using a special kind of subunits in this particular model is that, for example, such enzymes as pronase can eliminate sodium channel inactivation without affecting its conductance. Generally speaking, the gate itself might be performing the function of field sensor, but the portion of... 

Prolonged subthreshold stimuli can produce the phenomenon of accommodation. A long-duration cathodic pulse to mammalian axon that produces subthreshold depolarization will increase sodium inactivation, reducing the number of axons that can be recruited and so increasing the threshold. This is not a problem with brief pulses that are shorter than the time constant of sodium channel inactivation, but can be with more prolonged pulses. 

It is believed that a slow activation of the TRPV1 receptor also produces a slow depolarization and increases intracellular Ca into A8- and C-fibers. This slow rate of activation results in significant sodium channel inactivation and an analgesic effect, but less activation of the fibers (less burning and stinging sensation). The depolarization produced by capsaicin, however, is fast, showing sensory afferents always spike before their sodium channels become inactivated (before analgesia) [108]. Thus, the quantification of... 

Standker, L., Beress, L., Garateix, A., Christ, T, Ravens, U., Salceda, E., Soto, E., John, H, Eorssmann, W.-G., and Aneiros, A. (2006) A new toxin from the sea anemone Condylactis gigantea with effect on sodium channel inactivation. Toxicon, 48, 211-220. 

Pharmacologic analysis of sodium channel inactivation in a nerve fiber membrane. Neirofiziologiya 12, 317—331 (1980). 

There are three proposed major mechanisms of action of AEDs (1) sodium channel inactivation, (2) calcium channel blockade, and (3) interaction with GABA-A receptors/ channels. With sodium channel inactivation antiepileptic dmgs have the ability to extend the inactivation of sodium channels which reduces the frequency of the firing of the neurons, which is a feature of the seizures. Dmgs that are associated with this inactivation include phenytoin, carbamazepine and valproate. Calcium channel blockade (T-type) is related to the modulation of neuronal firing associated with absence of seizures and is associated with ethosuximide and zonisamide activity. L-type calcium channel blockade is reportedly associated... 

Conotoxins with the co-type 6-Cys/4-loop framework (C—C—CC—C—-C) are the most abundant group of peptides isolated from Conus venoms so far. This structural class encompasses at least four known pharmacological classes co-conotoxins that block voltage-sensitive calcium channels, 5-conotoxins that retard sodium channel inactivation, the sodium channel blocker conotoxin-GS, and two peptides recently found in C. marmoreus that affect both sodium and calcium currents. In addition, three co-type 6-Cys/4-Ioop peptides with still unknown targets have been found in C. textile (Cruz et al., 1992) and C. quercinus (Abogadie et al., 1990 Olivera et al., 1990). 

Fainzilber, M., Kofman, O., Zlotkin, E. and Gordon, D. 1994. A new neurotoxin receptor site on sodium channels is identified by a conotoxin that affects sodium channel inactivation in molluscs and acts as an antagonist in rat brain. J. Biol Chem. 269 2574-2580. 

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