Concept explainers
hen an action potential arrives at the nerve terminal of a neuromuscular junction, which of the following statements best describes the events that occur?
Depolarisation of the nerve terminal causes the release of ACh which activates nicotinic receptors on the skeletal muscle membrane to cause Ca2+ entry and muscle contraction. |
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Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which activates voltage-gated Na+ channels at the end-plate. |
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Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which binds to muscarinic receptors at the end plate. |
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Depolarisation of the nerve terminal opens voltage-gated Ca2+ channels, Ca2+ entry brings vesicles containing ACh to the membrane which form fusion pores causing the release of ACh which binds to ligand gated cation channels at the end-plate. |
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- Order the steps of the neuromuscular junction transmission using the following images. Then, usethe to describe what is happening in the step. Neuromuscular Junction Transmission - Contraction 1. Action potential travels from motor neuron cell body along the myelinated axon to neuromuscular junction. 2. Acetylcholine (ACh) is released from axon (neuron), crosses synapse (space between axon and sarcolemma).ACh binds to ACh receptors (channel) in sarcolemma. 3.ACh channels open. Ions (like sodium, Na+) flow into sarcolemma.Action potential spreads in sarcolemma and into transverse tubules. 4. Action potential causes the release of calcium (Ca2+) from sarcoplasmic reticulum into sarcoplasm 5.Ca2+ goes to the troponin, which moves the tropomyosin away from actin 6. Myosin head breaks down ATP, causing the sliding filament mechanism to shorten sarcomereMuscle contractsarrow_forwardPlease answer question 39arrow_forwardWhen curare, a neuromuscular poison, is dropped onto an isolated muscle-nerve preparation in a laboratory, the muscle does not contract when the nerve is stimulated, even though neurotransmitter is released from the nerve cell. Why does this happen? How might this action of curare be lethal to an individual who has been poisoned?arrow_forward
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- Neuromuscular Junction: -Activation of nicotinic ACh receptors in the motor end plate results in both Na+ influx into and K+ efflux from the muscle fiber - An action potential in a motor neuron always produces a graded depolarization in the motor endplate and an action potential in the sarcolemma. -Acetylcholine released from the motor presynaptic terminal binds to voltage-gated ACh receptors in the motor endplate. -all of the above -a and b are rightarrow_forwardWhat happens when the muscular action potential spreads through transverse (T) tubules of the sarcolemma? The action potential in T tubules triggers the release of acetylcholine from the axon terminals of the motor neuron. The action potential in T tubules triggers closing of sodium channels and opening of potassium channels, which enables myosin cross bridges to form. The action potential in T tubules opens voltage-sensitive calcium channels in the T tubules, allowing calcium to flow into the sarcoplasm. The action potential in T tubules causes a shape change in voltage-sensitive proteins that pull open calcium channels in the sarcoplasmic reticulum.arrow_forwardPut in order the steps of activation, excitation and contraction of skeletal muscle.arrow_forward
- What type of action potential conduction is found on the surface of skeletal muscle cell? continuous conduction saltatory conduction the most common cause of muscle cramps is low potassium. True :/ falsearrow_forwardplace in correct order 1. ACH binds to receptors on the postsynaptic membrane 2. AP travels along the sarcolemma and T tubules 3. Ca++ ion bind to troponin 4. Ca++ ions diffuse into the sarcoplasm 5. voltage-gated Ca++ ion channels in the sarcoplasmic reticulum openarrow_forwardInterruption of spindle discharge from a muscle causes contraction of the muscle to become jerky and irregular due to :-a- increased activity of reverberating circuits causing fluctuation of the motor discharge to the muscleb- increased activity of inhibitory interneurons causing oscillating inhibition of the α-motor neurons of the musclec- irregular discharge of excitatory inputs to the α-motor neurons of the muscle d- post-tetanic potentiation of the α-motor neurons of the musclearrow_forward
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