It causes the vesicles (which are in the axon terminal) to move to the cell membrane at the end of the axon terminal, where they merge with the cell membrane, releasing their load of neurotransmitters into the synaptic cleft (gap), where they quickly diffuse to receptors in the post-synaptic
neuron's dendrites, initiating a graded potential which moves down the dendrites, along the soma,
to the axon hillock where it can cause an action potential in that second
neuron.
The calcium ion is responsible for causing the presynaptic vesicle to fuse to the axon membrane in a process called exocytosis. When an action potential reaches the presynaptic terminal, calcium ions enter the terminal and trigger the fusion of the vesicle with the axon membrane, releasing neurotransmitters into the synaptic cleft.
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.
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.
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.
It creates an action potential
The calcium ion is responsible for causing the presynaptic vesicle to fuse to the axon membrane in a process called exocytosis. When an action potential reaches the presynaptic terminal, calcium ions enter the terminal and trigger the fusion of the vesicle with the axon membrane, releasing neurotransmitters into the synaptic cleft.
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.
When the action potential arrives, synaptic vesicles containing neurotransmitters are released by a process called exocytosis. This involves the fusion of the vesicle membrane with the presynaptic membrane, leading to the release of neurotransmitters into the synaptic cleft.
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 sodium channels that are required to create action potential in the muscles to make them contract.
It makes the muscle totally relax as it blocks the action potential in the nerves.
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.
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.