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.
It doesn't, it causes the opposite: a depolarisation block, which is why is used as a muscle relaxant in some circumstances. It may be that your recording electrodes were near a cell where curare had not yet diffused to. Or it may be related to disinhibition from blocking interneurons that express nicotinic accetylcholine receptors.
Curare is an example of a non-depolarizing muscle relaxant that blocks the nicotinic acetylcholine receptor (nAChR), one of the two types of acetylcholine (ACh) receptors. The main toxin of curare, d-tubocurarine, occupies the same position on the receptor as ACh with an equal or greater affinity, and elicits no response, making it a competitive antagonist.
Curare blocks nicotinic acetylcholine receptors so that when acetylcholine is released into the synaptic cleft it cannot induce the opening of sodium channels (as its binding to receptors is prevented) in the post-synaptic membrane, thus the membrane cannot be depolarised.
Curare binds to and competitively inhibits nicotinic acetylcholine receptors, thus preventing acetylcholine from binding to and activating those same receptors. In doing so, it prevents the excitatory signal from being formed, and prevents (or reduces) the probability of an action potential being formed.
Curare binds to and inhibits (blocks) nicotinic acetylcholine receptors. By doing this, it prevents acetylcholine from binding to and activating those same receptors. This prevents the excitatory "signal" from forming, and prevents the action potential from forming.
It doesn't generate an action potential. It blocks the receptors sites on the skeletal muscle, so the muscle doesn't react. An action potential occurs, but it is generated by something else.
It blocks the receptors for acetylcholine, so the nerve cells cannot receive the signal to generate an action potential.
Depends on disease
what effect does the drug quabain have on neuron
It is possible for chemicals to affect the body's motor nerve receptors, thereby making movement impossible.
An inhibitory effect would curtail the intentions of the person planning an action.
A gene that takes time to come into effect such as puberty hormones and greying hair.
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.
Depends on disease
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
Ether blocked the impulse transmission.
what effect does the drug quabain have on neuron
It can prolong the cardiac action potential. It can also have other effects, such as torsades de pointes,and it can mask digitalis toxicity.
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 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.
They both decrease action potential duration, but TTX is the only one that decreases the maximum rate of depolarization.
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.