Voltage dependent blockade

Moczydlowski E, Hall S, Garber SS, Strichartz GS, Miller C (1984) Voltage-dependent blockade of muscle Na + chaimels by guanidininm toxins. J Gen Physiol 84 687-704... 

The (+)-anatoxin-a analogs (/ )- or (5)-iV-methylanatoxinol, both possess the ability to block the ion channel [the voltage-dependence of their characteristics differ in a way which is the topic of another report (34). As is often the case, the blocked state induced by (/ )-7Y-methylanatoxinol and the closed state differed significantly in duration, such that the blocked state was associated with short closed periods within groups of openings called bursts (Figure 4). The number of short closed periods per burst increased with the concentration of the drug because the likelihood of channel blockade increased relative to the likelihood of channel closure. 

Several mechanisms have been suggested for the action of valproic acid, including blockade of voltage-dependent Na+ channel, potentiation of y-aminobutryric acid... 

Four main mechanisms of action underlie the beneficial pharmaceutical effect of AED (1) blockade of the voltage-dependent sodium channels (2) increased GABAergic inhibition of neurotransmission (3) blockade of glutaminergic transmission (4) blockade of type T calcium channels. AEDs are thus classed according to their known predominant effect ... 

It is phenyltriazine compound, chemically unrelated to existing antiepileptic drugs. It acts primarily via a dose dependent blockade of voltage sensitive sodium channels in their slow inactivated state, thus stabilizing the presynaptic neuronal membrane inhibiting release of excitatory neurotransmitters mainly glutamate. 

Sodium channel blockers including local anesthetic, anticonvulsant and antiarrhythmic drugs exhibit voltage- and frequency-dependent blockade which makes them useful drugs for blocking hyperexcitable neurons... 

The pharmacological activity of decahydroquinoline ci5-195A and analogs in neuromuscular preparations appears to involve noncompetitive blockade both of nicotinic receptor-channels and of voltage-dependent sodium and potassium channels (see reviews in Refs. 3 and 5). Recently, both cis- and rra/i5-decahydroquinolines were shown to block ion flux through nicotinic receptor channels in pheochromocytoma cells and to enhance the rate of desensitization of such nicotinic channels (64,82). 

Local anesthetics prevent the voltage-dependent increase in sodium ion conductance and thus block the initiation and propagation of action potentials. This occurs via two mechanisms. Firstly, non-specific activity on the membrane surface causes the membrane to swell, physically preventing sodium ions getting through the membrane pores. Secondly, blockade of sodium channels occurs. 

Seizure Type Anticonvulsant Agent Blockade of Voltage/ Dependent Na+ Channels Potentiation cf GABAergic Mechanisms Blockade of Thalamic T-type Ca Channels Blockade of Glutamatergic Mechanisms... 

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