Help with Neuromuscular Junction Physiology - Anatomy
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What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
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T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
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Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
At the neuromuscular junction, receptors respond to neurotransmitters to facilitate the depolarization of muscle cell membranes. This is the first step in that muscle cell's ultimate contraction. Which types of receptors would be most likely found on the muscle cell, directly interacting with the neurotransmitter at the neuromuscular junction?
At the neuromuscular junction, receptors respond to neurotransmitters to facilitate the depolarization of muscle cell membranes. This is the first step in that muscle cell's ultimate contraction. Which types of receptors would be most likely found on the muscle cell, directly interacting with the neurotransmitter at the neuromuscular junction?
Tap to see back →
Nicotinic ligand-gated channels interact with the acetylcholine released by neurons at the neuromuscular junction. By binding to the neurotransmitter, these channels change shape and allow ions to enter into the muscle cell membrane, thus depolarizing it and driving an ultimate contraction.
Voltage-gated sodium and calcium channels play an important role in propagating the membrane depolarization, but do not interact with the neurotransmitter at the neuromuscular junction. Muscarinic receptors are also stimulated by acetylcholine, but are most commonly found in the parasympathetic nervous system, and do not play a significant role in muscle contraction.
Nicotinic ligand-gated channels interact with the acetylcholine released by neurons at the neuromuscular junction. By binding to the neurotransmitter, these channels change shape and allow ions to enter into the muscle cell membrane, thus depolarizing it and driving an ultimate contraction.
Voltage-gated sodium and calcium channels play an important role in propagating the membrane depolarization, but do not interact with the neurotransmitter at the neuromuscular junction. Muscarinic receptors are also stimulated by acetylcholine, but are most commonly found in the parasympathetic nervous system, and do not play a significant role in muscle contraction.
Clostridium tetani is a microorganism that causes constant muscle contraction, and results in the characteristic risus sardonicus, or lockjaw. The toxin produced by this organism acts on inhibitory neurons that downregulate the activity of excitatory neurons directly involved in the neuromuscular junction.
The release of which neurotransmitters are most likely to be inhibited during Clostridium tetani infection?
I. Glycine
II. Glutamate
III. GABA
Clostridium tetani is a microorganism that causes constant muscle contraction, and results in the characteristic risus sardonicus, or lockjaw. The toxin produced by this organism acts on inhibitory neurons that downregulate the activity of excitatory neurons directly involved in the neuromuscular junction.
The release of which neurotransmitters are most likely to be inhibited during Clostridium tetani infection?
I. Glycine
II. Glutamate
III. GABA
Tap to see back →
Glycine and GABA are the main inhibitory neurotransmitters. Thus, they would be used by inhibitory neurons that work to downregulate the excitatory neurons at the neuromuscular junction. Inhibiting the release of these inhibitory signals would result in an involuntary, excitatory response, such as lockjaw.
It is important to note that neurons involved directly in the neuromuscular junction are ALWAYS excitatory. They can be turned off, via the inhibitory neurons discussed in the question above; however, if a neuron is directly part of the neuromuscular junction, it is excitatory.
Glycine and GABA are the main inhibitory neurotransmitters. Thus, they would be used by inhibitory neurons that work to downregulate the excitatory neurons at the neuromuscular junction. Inhibiting the release of these inhibitory signals would result in an involuntary, excitatory response, such as lockjaw.
It is important to note that neurons involved directly in the neuromuscular junction are ALWAYS excitatory. They can be turned off, via the inhibitory neurons discussed in the question above; however, if a neuron is directly part of the neuromuscular junction, it is excitatory.
An experimental drug is given to a patient. The drug is known to inhibit the activity of acetylcholinesterase. What effect would most likely be observed in the patient as a result of this drug?
An experimental drug is given to a patient. The drug is known to inhibit the activity of acetylcholinesterase. What effect would most likely be observed in the patient as a result of this drug?
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Acetylcholinesterase is an enzyme that is responsible for breaking down excess acetylcholine in the neuromuscular junction. Acetylcholinesterase inhibitors will thus reduce the activity the enzyme that breaks down acetylcholine (ACh), effectively increasing acetylcholine concentrations in the neuromuscular junction. The result of this change will be an exaggeration of the effect of ACh on the postsynaptic muscle at the neuromuscular junction.
Importantly, inhibitors of this enzyme will not increase the amount of ACh produced by the neuron. Instead, it just prolongs the time of synaptic residence for already released ACh.
Acetylcholinesterase is an enzyme that is responsible for breaking down excess acetylcholine in the neuromuscular junction. Acetylcholinesterase inhibitors will thus reduce the activity the enzyme that breaks down acetylcholine (ACh), effectively increasing acetylcholine concentrations in the neuromuscular junction. The result of this change will be an exaggeration of the effect of ACh on the postsynaptic muscle at the neuromuscular junction.
Importantly, inhibitors of this enzyme will not increase the amount of ACh produced by the neuron. Instead, it just prolongs the time of synaptic residence for already released ACh.
What neurotransmitter is used to signal muscle contraction at the neuromuscular junction?
What neurotransmitter is used to signal muscle contraction at the neuromuscular junction?
Tap to see back →
A neuron at the neuromuscular junction uses the neurotransmitter acetylcholine to signal the contraction of the muscle via action potential generation, which signals the release of calcium from the muscle sarcoplasmic reticulum.
A neuron at the neuromuscular junction uses the neurotransmitter acetylcholine to signal the contraction of the muscle via action potential generation, which signals the release of calcium from the muscle sarcoplasmic reticulum.
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
Tap to see back →
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
Tap to see back →
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
At the neuromuscular junction, receptors respond to neurotransmitters to facilitate the depolarization of muscle cell membranes. This is the first step in that muscle cell's ultimate contraction. Which types of receptors would be most likely found on the muscle cell, directly interacting with the neurotransmitter at the neuromuscular junction?
At the neuromuscular junction, receptors respond to neurotransmitters to facilitate the depolarization of muscle cell membranes. This is the first step in that muscle cell's ultimate contraction. Which types of receptors would be most likely found on the muscle cell, directly interacting with the neurotransmitter at the neuromuscular junction?
Tap to see back →
Nicotinic ligand-gated channels interact with the acetylcholine released by neurons at the neuromuscular junction. By binding to the neurotransmitter, these channels change shape and allow ions to enter into the muscle cell membrane, thus depolarizing it and driving an ultimate contraction.
Voltage-gated sodium and calcium channels play an important role in propagating the membrane depolarization, but do not interact with the neurotransmitter at the neuromuscular junction. Muscarinic receptors are also stimulated by acetylcholine, but are most commonly found in the parasympathetic nervous system, and do not play a significant role in muscle contraction.
Nicotinic ligand-gated channels interact with the acetylcholine released by neurons at the neuromuscular junction. By binding to the neurotransmitter, these channels change shape and allow ions to enter into the muscle cell membrane, thus depolarizing it and driving an ultimate contraction.
Voltage-gated sodium and calcium channels play an important role in propagating the membrane depolarization, but do not interact with the neurotransmitter at the neuromuscular junction. Muscarinic receptors are also stimulated by acetylcholine, but are most commonly found in the parasympathetic nervous system, and do not play a significant role in muscle contraction.
Clostridium tetani is a microorganism that causes constant muscle contraction, and results in the characteristic risus sardonicus, or lockjaw. The toxin produced by this organism acts on inhibitory neurons that downregulate the activity of excitatory neurons directly involved in the neuromuscular junction.
The release of which neurotransmitters are most likely to be inhibited during Clostridium tetani infection?
I. Glycine
II. Glutamate
III. GABA
Clostridium tetani is a microorganism that causes constant muscle contraction, and results in the characteristic risus sardonicus, or lockjaw. The toxin produced by this organism acts on inhibitory neurons that downregulate the activity of excitatory neurons directly involved in the neuromuscular junction.
The release of which neurotransmitters are most likely to be inhibited during Clostridium tetani infection?
I. Glycine
II. Glutamate
III. GABA
Tap to see back →
Glycine and GABA are the main inhibitory neurotransmitters. Thus, they would be used by inhibitory neurons that work to downregulate the excitatory neurons at the neuromuscular junction. Inhibiting the release of these inhibitory signals would result in an involuntary, excitatory response, such as lockjaw.
It is important to note that neurons involved directly in the neuromuscular junction are ALWAYS excitatory. They can be turned off, via the inhibitory neurons discussed in the question above; however, if a neuron is directly part of the neuromuscular junction, it is excitatory.
Glycine and GABA are the main inhibitory neurotransmitters. Thus, they would be used by inhibitory neurons that work to downregulate the excitatory neurons at the neuromuscular junction. Inhibiting the release of these inhibitory signals would result in an involuntary, excitatory response, such as lockjaw.
It is important to note that neurons involved directly in the neuromuscular junction are ALWAYS excitatory. They can be turned off, via the inhibitory neurons discussed in the question above; however, if a neuron is directly part of the neuromuscular junction, it is excitatory.
An experimental drug is given to a patient. The drug is known to inhibit the activity of acetylcholinesterase. What effect would most likely be observed in the patient as a result of this drug?
An experimental drug is given to a patient. The drug is known to inhibit the activity of acetylcholinesterase. What effect would most likely be observed in the patient as a result of this drug?
Tap to see back →
Acetylcholinesterase is an enzyme that is responsible for breaking down excess acetylcholine in the neuromuscular junction. Acetylcholinesterase inhibitors will thus reduce the activity the enzyme that breaks down acetylcholine (ACh), effectively increasing acetylcholine concentrations in the neuromuscular junction. The result of this change will be an exaggeration of the effect of ACh on the postsynaptic muscle at the neuromuscular junction.
Importantly, inhibitors of this enzyme will not increase the amount of ACh produced by the neuron. Instead, it just prolongs the time of synaptic residence for already released ACh.
Acetylcholinesterase is an enzyme that is responsible for breaking down excess acetylcholine in the neuromuscular junction. Acetylcholinesterase inhibitors will thus reduce the activity the enzyme that breaks down acetylcholine (ACh), effectively increasing acetylcholine concentrations in the neuromuscular junction. The result of this change will be an exaggeration of the effect of ACh on the postsynaptic muscle at the neuromuscular junction.
Importantly, inhibitors of this enzyme will not increase the amount of ACh produced by the neuron. Instead, it just prolongs the time of synaptic residence for already released ACh.
What neurotransmitter is used to signal muscle contraction at the neuromuscular junction?
What neurotransmitter is used to signal muscle contraction at the neuromuscular junction?
Tap to see back →
A neuron at the neuromuscular junction uses the neurotransmitter acetylcholine to signal the contraction of the muscle via action potential generation, which signals the release of calcium from the muscle sarcoplasmic reticulum.
A neuron at the neuromuscular junction uses the neurotransmitter acetylcholine to signal the contraction of the muscle via action potential generation, which signals the release of calcium from the muscle sarcoplasmic reticulum.
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
Tap to see back →
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
Tap to see back →
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
At the neuromuscular junction, receptors respond to neurotransmitters to facilitate the depolarization of muscle cell membranes. This is the first step in that muscle cell's ultimate contraction. Which types of receptors would be most likely found on the muscle cell, directly interacting with the neurotransmitter at the neuromuscular junction?
At the neuromuscular junction, receptors respond to neurotransmitters to facilitate the depolarization of muscle cell membranes. This is the first step in that muscle cell's ultimate contraction. Which types of receptors would be most likely found on the muscle cell, directly interacting with the neurotransmitter at the neuromuscular junction?
Tap to see back →
Nicotinic ligand-gated channels interact with the acetylcholine released by neurons at the neuromuscular junction. By binding to the neurotransmitter, these channels change shape and allow ions to enter into the muscle cell membrane, thus depolarizing it and driving an ultimate contraction.
Voltage-gated sodium and calcium channels play an important role in propagating the membrane depolarization, but do not interact with the neurotransmitter at the neuromuscular junction. Muscarinic receptors are also stimulated by acetylcholine, but are most commonly found in the parasympathetic nervous system, and do not play a significant role in muscle contraction.
Nicotinic ligand-gated channels interact with the acetylcholine released by neurons at the neuromuscular junction. By binding to the neurotransmitter, these channels change shape and allow ions to enter into the muscle cell membrane, thus depolarizing it and driving an ultimate contraction.
Voltage-gated sodium and calcium channels play an important role in propagating the membrane depolarization, but do not interact with the neurotransmitter at the neuromuscular junction. Muscarinic receptors are also stimulated by acetylcholine, but are most commonly found in the parasympathetic nervous system, and do not play a significant role in muscle contraction.
Clostridium tetani is a microorganism that causes constant muscle contraction, and results in the characteristic risus sardonicus, or lockjaw. The toxin produced by this organism acts on inhibitory neurons that downregulate the activity of excitatory neurons directly involved in the neuromuscular junction.
The release of which neurotransmitters are most likely to be inhibited during Clostridium tetani infection?
I. Glycine
II. Glutamate
III. GABA
Clostridium tetani is a microorganism that causes constant muscle contraction, and results in the characteristic risus sardonicus, or lockjaw. The toxin produced by this organism acts on inhibitory neurons that downregulate the activity of excitatory neurons directly involved in the neuromuscular junction.
The release of which neurotransmitters are most likely to be inhibited during Clostridium tetani infection?
I. Glycine
II. Glutamate
III. GABA
Tap to see back →
Glycine and GABA are the main inhibitory neurotransmitters. Thus, they would be used by inhibitory neurons that work to downregulate the excitatory neurons at the neuromuscular junction. Inhibiting the release of these inhibitory signals would result in an involuntary, excitatory response, such as lockjaw.
It is important to note that neurons involved directly in the neuromuscular junction are ALWAYS excitatory. They can be turned off, via the inhibitory neurons discussed in the question above; however, if a neuron is directly part of the neuromuscular junction, it is excitatory.
Glycine and GABA are the main inhibitory neurotransmitters. Thus, they would be used by inhibitory neurons that work to downregulate the excitatory neurons at the neuromuscular junction. Inhibiting the release of these inhibitory signals would result in an involuntary, excitatory response, such as lockjaw.
It is important to note that neurons involved directly in the neuromuscular junction are ALWAYS excitatory. They can be turned off, via the inhibitory neurons discussed in the question above; however, if a neuron is directly part of the neuromuscular junction, it is excitatory.
An experimental drug is given to a patient. The drug is known to inhibit the activity of acetylcholinesterase. What effect would most likely be observed in the patient as a result of this drug?
An experimental drug is given to a patient. The drug is known to inhibit the activity of acetylcholinesterase. What effect would most likely be observed in the patient as a result of this drug?
Tap to see back →
Acetylcholinesterase is an enzyme that is responsible for breaking down excess acetylcholine in the neuromuscular junction. Acetylcholinesterase inhibitors will thus reduce the activity the enzyme that breaks down acetylcholine (ACh), effectively increasing acetylcholine concentrations in the neuromuscular junction. The result of this change will be an exaggeration of the effect of ACh on the postsynaptic muscle at the neuromuscular junction.
Importantly, inhibitors of this enzyme will not increase the amount of ACh produced by the neuron. Instead, it just prolongs the time of synaptic residence for already released ACh.
Acetylcholinesterase is an enzyme that is responsible for breaking down excess acetylcholine in the neuromuscular junction. Acetylcholinesterase inhibitors will thus reduce the activity the enzyme that breaks down acetylcholine (ACh), effectively increasing acetylcholine concentrations in the neuromuscular junction. The result of this change will be an exaggeration of the effect of ACh on the postsynaptic muscle at the neuromuscular junction.
Importantly, inhibitors of this enzyme will not increase the amount of ACh produced by the neuron. Instead, it just prolongs the time of synaptic residence for already released ACh.
What neurotransmitter is used to signal muscle contraction at the neuromuscular junction?
What neurotransmitter is used to signal muscle contraction at the neuromuscular junction?
Tap to see back →
A neuron at the neuromuscular junction uses the neurotransmitter acetylcholine to signal the contraction of the muscle via action potential generation, which signals the release of calcium from the muscle sarcoplasmic reticulum.
A neuron at the neuromuscular junction uses the neurotransmitter acetylcholine to signal the contraction of the muscle via action potential generation, which signals the release of calcium from the muscle sarcoplasmic reticulum.
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
What part of the muscle cell allows an action potential to spread uniformly throughout the cell?
Tap to see back →
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
T-tubules are small tunnels in the membrane of a muscle cell that allow an action potential to spread evenly. This allows for the whole muscle cell to contract smoothly and in unison.
A neuromuscular junction is the synaptic interface between a neuron and a muscle cell. When an action potential reached the junction, it causes depolarization of the sarcolemma (muscle cell membrane). This depolarization spreads to the T-tubules, which house proteins that directly interface with the sarcoplasmic reticulum. When depolarization of the T-tubules stimulates the sarcoplasmic reticulum, it releases calcium into the cytoplasm. The calcium bind to troponin to initiate the contraction of the sarcomere.
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
A scientist is studying a type of cell and discovers that this cell uses kinesin to transport secretory vesicles down long cytoplasmic extensions. Upon further study, the vesicles are found to contain the substance acetylcholine. What is the most likely classification of this cell?
Tap to see back →
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.
Acetylcholine is transported in vesicles, via the protein kinesin, in excitatory motor neurons. Muscle cells typically do not transport secretory vesicles, as they are not active secretors of most proteins. Neurons, in contrast, function to release neurotransmitters from secretory vesicles at synapses.
This logic leaves us with either type of neuron specified in the question. The best answer is motor neuron, as acetylcholine is the primary excitatory neurotransmitter at the neuromuscular junction. Had the question specified that the vesicle was filled with GABA or glycine, inhibitory neuron would have been the better answer.