Answer:
Phenytoin and ethosuximide are drugs that slow the recovery of the sodium channel during the inactivated state.
That is to say, they prolong the inactivation state of the channel, thus generating that in this way the neuron remains in resting potential and the action potential causing the epileptic attack is not triggered.
On the other hand, these drugs, according to the bibliography of the book "Golan, 3rd Edition, Principles of Pharmacology" have a use-dependent affect capacity, this means that those sodium channels that have more activity will be more affected, in this way Not only is epileptic shock avoided, but if the same happens independently in any neuron, it will not be able to propagate the action potential to its neighboring neurons, therefore the surrounding neurons will not be stimulated and will not be fulfilled. with the sudden rapid discharges that are the most dangerous in some cases of severe epilepsy.
It is important to understand that these drugs affect the ion channels responsible for exciting neurons, that is why by inhibiting them, a constant rest of these neurons is promoted, and they are unable to generate abrupt discharges and dissemination of the electric charge. among them generating epileptic shocks.
The ions in neurons are in charge of indicating or modulating the different neuronal states, if they are inactive, open or closed, they will directly affect the membrane potential, that is, the positive or negative charge of the neuron's membrane.
Explanation:
In order to finish completing the question, these drugs are excreted through the p450 protein, that is why if this excretion system becomes saturated because another drug is consumed that is excreted in the same way, these antiepileptics will remain longer in use. blood and in the body, generating a greater effect and enhancing adverse effects on the central nervous system.
