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.
Ouabain blocks the Na+/K+ ATPase pump, preventing it from properly maintaining the Na+ and K+ gradients across the cell membrane. This disrupts the resting membrane potential and impairs the neuron's ability to generate action potentials.
The disease may disrupt the normal flow of ions necessary for generating and propagating action potentials, leading to decreased conduction velocity or even blockage of action potentials in that region of the axon. This could result in impaired communication between neurons and affect the overall function of the nervous system in that area.
No, neurotransmitters can be either stimulatory or inhibitory. Stimulatory neurotransmitters excite the receiving neuron and increase the likelihood of an action potential, while inhibitory neurotransmitters decrease the likelihood of an action potential. Both types are essential for maintaining a balance in neural signaling within the brain and nervous system.
binds to specific receptors on the postsynaptic cell membrane, leading to changes in the cell's membrane potential. This can either excite or inhibit the postsynaptic neuron, influencing the likelihood of an action potential being generated. Ultimately, the effect of the neurotransmitter can influence the communication between neurons in the nervous system.
Yes, an action is typically the stimulus that triggers a response in a system or organism. In the context of cause and effect, the action is what instigates the reaction or outcome.
It creates 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.
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.