The Importance of sodium and calcium channels on a neuron
Phenytoin (sodium channel blocker) and ethosuximide (calcium channel blocker) are anti-seizure drugs that stop seizures from happening. These drugs work by inhibiting electrical impulses (action potentials) from occurring. Explain the importance of sodium and calcium channels on a neuron and and the reasons why action potentials do not occur when these channels are inhibited. Be sure to include the phases of an action potential, the channels involved, and the importance of an action potential.
Solution
The Importance of sodium and calcium channels on a neuron
Neurons are essential in our body to perform communication with each other cells. They usually consist of a cell body, dendrites, and an axon. These cells are especially interesting because they communicate with chemical signals (neurotransmitters) as well as electrical signals (action potentials). In order for neurons to be triggered, they must be depolarized to their threshold (-50mV), from their resting potential (-70mV) to initiate an action potential. Depending on the neurotransmitter or drug being used, a neuron’s membrane potential can either be depolarizing (becomes more positive and less negative and moves towards threshold with excitatory neurotransmitters), or hyperpolarizing (becomes less positive, and more negative, with inhibitory neurotransmitters). Excitatory neurotransmitters allow for ligand gated sodium channels to open, and cause an influx of Na+ which makes the cell more positive and towards the threshold. Inhibitory neurotransmitters allow for ligand gated chloride channels to open, and cause an influx of Cl- that make the cell more negative and move from threshold. When an action potential occurs, it causes voltage gated calcium channels to open, and calcium enters the axon terminal. The calcium causes synaptic vesicles to release neurotransmitters by exocytosis, and diffuse across the synaptic cleft towards the synaptic membrane where they can bind with specific receptors depending on the neurotransmitter.
Phenytoin and ethosuximide can inhibit electrical impulses from occurring because they block sodium channels and calcium channels. These two drugs work in different ways to stop seizures, but still overall prevent action potentials from happening. Phenytoin blocks sodium channels, which is usually opened by excitatory neurotransmitters. In this instance the neuron that receives the excitatory neurotransmitter would normally open the ligand gated sodium channel, and allow for the influx of Na+. This would normally cause the cell to become more positive, depolarize and continue to release neurotransmitters and signal more neurons. With Phenytoin, the sodium channel is blocked, and the cell cannot become more positive and hit threshold. If the cell membrane never reaches threshold, an action potential cannot occur, and more neurotransmitters will not be released. Ethosuximide blocks calcium channels, which is usually stimulated and opened by an action potential. Calcium channels when opened normally release calcium that allow for synaptic vesicles to release their neurotransmitter contents to diffuse across the synaptic cleft and bind to the postsynaptic membrane. When ethosuximide blocks the calcium channels from opening, the synaptic vesicles are unable to release their neurotransmitter contents. If the neurotransmitter never reaches the synaptic cleft, it cannot stimulate the next neuron to release an action potential and continue the neuron activity.
References:
Silverthorn, D. U. (2013). Human physiology. Harlow: Pearson Education.
