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What effect of the action potential if sodium channels are kept closed?
Wiki User
∙ 12y ago
The action potential will not generate if the sodium channels are kept closed.
This is because the sodium channels are responsible for the dramatic rising phase of membrane depolarization that occurs when the threshold of activation is reached. As a membrane potential gradually depolarizes (which can occur for a variety of reasons such as neurotransmitter stimulation, mechanical deformation of the membrane, etc), that membrane potential gradually comes closer to that threshold of activation. Once that threshold is reached, the voltage gated sodium channels open and allow for a dramatic influx of sodium ions into the cell. This results in a rapid depolarization which is seen as the rising phase of that upward spike noted in an action potential. Without the ability to open these sodium channels we may reach the threshold of activation, but the actual action potential will not occur.
Wiki User
∙ 12y ago
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What is the effect of lidocaine on eliciting an action potential?
Ether prevents the action potential, by opening potassium ion pores, which allows the escape of potassium from the neurons, which results in hyper-polarization of the neuron, thus preventing the action potential from occurring.
What is the effect of tetrodotoxin?
Tetrodotoxin blocks action potentials by binding with the voltage-gated, fast sodium (Na+) channels in neural membranes. This prevents the influx of sodium ions required to propagate an action potential.
What passes from the neuron to the muscle cells and what effect does it produce?
Acetylcholine (ACh) is the neurotransmitter that passes from neuron to muscle cells and it causes the Na/K channels to open allowing Na+ to flow into the cell triggering an action potential.
What effect did an ether have on action potential?
Ether blocked the impulse transmission.
What effect does hypocalcemia have on the cardiac action potential?
It can prolong the cardiac action potential. It can also have other effects, such as torsades de pointes,and it can mask digitalis toxicity.
Why does tetrodotoxin effect your muscles?
It blocks the sodium channels that are required to create action potential in the muscles to make them contract.
What is the effect of lidocaine on eliciting an action potential?
Ether prevents the action potential, by opening potassium ion pores, which allows the escape of potassium from the neurons, which results in hyper-polarization of the neuron, thus preventing the action potential from occurring.
What was the effect of curare on eliciting an action potential?
It creates an action potential
What is the effect of tetrodotoxin?
Tetrodotoxin blocks action potentials by binding with the voltage-gated, fast sodium (Na+) channels in neural membranes. This prevents the influx of sodium ions required to propagate an action potential.
What would be the effect on action potential conduction at a region of axon where the disease had its effect?
Depends on disease
What effect did an ether have on action potential?
Ether blocked the impulse transmission.
What passes from the neuron to the muscle cells and what effect does it produce?
Acetylcholine (ACh) is the neurotransmitter that passes from neuron to muscle cells and it causes the Na/K channels to open allowing Na+ to flow into the cell triggering an action potential.
What are the effect of electricity?
effects of electricity: current passes through closed circuit, from higher potential to lower potential,it produces heat
What the Effect of ouabain drug on a neuron ability to generate action potential?
what effect does the drug quabain have on neuron
What effect does hypocalcemia have on the cardiac action potential?
It can prolong the cardiac action potential. It can also have other effects, such as torsades de pointes,and it can mask digitalis toxicity.
How are the mechanisms of action of class I and class III antiarrhythmic drugs in treating ventricular arrhythmia differents?
Class I antiarrhythmic drugs work by inhibiting the sodium channel. Class IA agents work by inhibiting open voltage-dependent Na+ channels. This will slow phase 0 and increase the length of the effective refractory period. Its effect is dependent on frequency. The drugs dissociate slowly from closed channels so when the frequency of the action potential is high, the drug can prevent the the Na+ channel from contributing to the action potential as it is still there. One example of a class IA agent is the procainamide which is used to treat ventricular arrhythmias when administered intravenously. Class IB agents work by blocking closed voltage-dependent Na+ channels. It is often used to treat ventricular arrhythmia after an acute myocardial infarction. An acute myocardial infarction often leads to anoxia so many Na+ channels will be inactiated and closed. These Na+ channels are hence susceptible to class IB agents. An example of a class IB agent is the lidocaine. Class III antiarrhythmic drugs work by blockign the outward K+ currents. This leads to the action potential belong prolonged. The QT interval will increase the the effective refractory period will also increase. One example of class III antiarrhythmic drug is the amiodarone. It inhibits the K+ channel, the inactivated Na+ channel, and the beta adrenoceptors.
What is the relationship between the action potential and the synapse?
A synapse and an action potential have a flip-flopping cause and effect relationship, in that an action potential in a presynaptic neuron initiates a release of neurotransmitters across a synapse, which can then subsequently potentially trigger an action potential in the axon of the postsynaptic neuron, which would then cause release of neurotransmitters across a following synapse.
