It creates an action potential
it is an alpha-toxin that binds to acetylcholine binding sites on the postsynaptic cell membrane, which prevents the acetylcholine from acting. Curare blocks synaptic transmission by preventing neural impulses to flow from neuron to neuron. It does allow the action potential to travel in the axon, it just doesn't pass it on to the dendrite.
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.
Archibald Ross McIntyre has written: 'The mechanism of the action of extract of the posterior lobe of the pituitary body on the secretion of urine in the unanaesthetized dog' -- subject(s): Physiological effect, Pituitary extract, Urination, Dogs, Physiology 'Curare' -- subject(s): Curare
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.
Curare is a plant-derived poison that blocks nicotinic acetylcholine receptors at the neuromuscular junction, leading to muscle relaxation and paralysis. This can result in impaired breathing and death if respiratory muscles are affected.
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.
They both decrease action potential duration, but TTX is the only one that decreases the maximum rate of depolarization.
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 blocks the nicotinic cholinergic receptors on the muscle that normally bind the acetylcholine released by the motor neuron.
It makes the muscle totally relax as it blocks the action potential in the nerves.