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.
Increasing the voltage in a nerve can lead to an increased rate of nerve firing, resulting in more frequent action potentials. This can affect the overall excitability and sensitivity of the nerve. As voltage increases, the threshold for eliciting an action potential decreases, making the nerve more likely to fire in response to stimuli.
Ether can enhance the excitability of nerve cell membranes, leading to a decrease in the threshold for action potential generation. This can result in an increase in the frequency and amplitude of action potentials.
Ether causes potassium ion pores to open, allowing potassium ions to leave the neuron, hyper-polarizing the neuron so it is unable to fire an action potential.
Hypocalcemia can lead to a prolongation of the cardiac action potential due to reduced calcium influx. This can result in an increased risk of arrhythmias, as well as potential impairment of cardiac muscle contractility.
No, neurotransmitters that depress the resting potential are called inhibitory neurotransmitters. Excitatory neurotransmitters have the opposite effect, causing depolarization and increasing the likelihood of an action potential.
It creates an action potential
They both decrease action potential duration, but TTX is the only one that decreases the maximum rate of depolarization.
Increasing the voltage in a nerve can lead to an increased rate of nerve firing, resulting in more frequent action potentials. This can affect the overall excitability and sensitivity of the nerve. As voltage increases, the threshold for eliciting an action potential decreases, making the nerve more likely to fire in response to stimuli.
No, they are two different substances. Lidocaine was given the -caine ending only due to the anesthetic effect it shares with cocaine. However, sometimes cocaine is adulterated with lidocaine to increase the perceived potency of the product (due to lidocaine's numbing effects).
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.
Ether can enhance the excitability of nerve cell membranes, leading to a decrease in the threshold for action potential generation. This can result in an increase in the frequency and amplitude of action potentials.
Not even close--in fact, one usage of Lidocaine is to combat heart arrhythmia, which is a potential side-effect of Phen-Fen (Phentermine-Fenfluramine). Lidocaine is primarily an anesthetic, used in sunburn treatments. The use as an anti-arrhythmia treatment is much less common. Phen-Fen is (a pair of drugs used in concert as) an appetite suppressant. It was found to potentially cause damage to heart valves, however, and its use was discontinued in the U.S. in 1995.
Hypocalcemia can lead to a prolongation of the cardiac action potential due to reduced calcium influx. This can result in an increased risk of arrhythmias, as well as potential impairment of cardiac muscle contractility.
Ether causes potassium ion pores to open, allowing potassium ions to leave the neuron, hyper-polarizing the neuron so it is unable to fire an action potential.
It makes the muscle totally relax as it blocks the action potential in the nerves.
It blocks the sodium channels that are required to create action potential in the muscles to make them contract.
A negative effect is any result of an action which is perceived to be detrimental. This means its a subjective opinion. What might be negative to you may be positive to someone else.