Synapse Biochemistry - Biochemistry
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The release of which ion triggers release of neurotransmitters at the axon terminal of a presynaptic cell?
The release of which ion triggers release of neurotransmitters at the axon terminal of a presynaptic cell?
The release of calcium ions at the axon terminal is responsible for the exocytosis of vesicles carrying neurotransmitters.
The release of calcium ions at the axon terminal is responsible for the exocytosis of vesicles carrying neurotransmitters.
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Acetylcholine transferase is an enzyme involved in the synthesis of acetylcholine. Which of the following molecules are involved in this reaction?
I. Choline
II. Acetyl-CoA
III. Acetic acid
Acetylcholine transferase is an enzyme involved in the synthesis of acetylcholine. Which of the following molecules are involved in this reaction?
I. Choline
II. Acetyl-CoA
III. Acetic acid
When an action potential reaches the synapse, choline enters the neuron. Once inside, the choline molecule binds to acetyl-CoA and forms acetylcholine, which is then packaged into vesicles. Upon calcium influx, the acetylcholine vesicles fuse with the synaptic membrane and release acetylcholine into the synaptic cleft. The acetylcholine molecules can now bind to receptors on the postsynaptic membrane and initiate an action potential in the postsynaptic neuron.
When an action potential reaches the synapse, choline enters the neuron. Once inside, the choline molecule binds to acetyl-CoA and forms acetylcholine, which is then packaged into vesicles. Upon calcium influx, the acetylcholine vesicles fuse with the synaptic membrane and release acetylcholine into the synaptic cleft. The acetylcholine molecules can now bind to receptors on the postsynaptic membrane and initiate an action potential in the postsynaptic neuron.
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Myasthenia gravis is an autoimmune disease that decreases muscle contraction. Circulating antibodies bind to acetylcholine receptors and prevent acetylcholine from binding to the receptors. Which of the following could alleviate the symptoms of Myasthenia gravis?
Myasthenia gravis is an autoimmune disease that decreases muscle contraction. Circulating antibodies bind to acetylcholine receptors and prevent acetylcholine from binding to the receptors. Which of the following could alleviate the symptoms of Myasthenia gravis?
Acetylcholine is a neurotransmitter found in neuromuscular junctions. Release of acetylcholine into the synaptic cleft allows acetylcholine to bind to its receptors on the muscle membrane. Once bound, acetylcholine activates a signaling cascade that eventually leads to muscle contraction. Circulating antibodies in Myasthenia gravis patients prevent this interaction between acetylcholine and its receptor, thus decreasing muscle contraction. One way to treat this disease is by administering drugs that increase the half-life of each acetylcholine molecule. The most common way to do this is by administering an acetylcholinesterase inhibitor. Acetylcholinesterase is an enzyme that breaks down acetylcholine molecules in the synaptic cleft; decreasing or inhibiting this enzyme will lead to increased acetylcholine concentration. This increased concentration will compete with the antibodies and facilitate muscle contraction. Decreasing calcium influx in the presynaptic neuron will decrease the release of acetylcholine into the synaptic cleft. This will make Myasthenia gravis symptoms worse.
Acetylcholine is a neurotransmitter found in neuromuscular junctions. Release of acetylcholine into the synaptic cleft allows acetylcholine to bind to its receptors on the muscle membrane. Once bound, acetylcholine activates a signaling cascade that eventually leads to muscle contraction. Circulating antibodies in Myasthenia gravis patients prevent this interaction between acetylcholine and its receptor, thus decreasing muscle contraction. One way to treat this disease is by administering drugs that increase the half-life of each acetylcholine molecule. The most common way to do this is by administering an acetylcholinesterase inhibitor. Acetylcholinesterase is an enzyme that breaks down acetylcholine molecules in the synaptic cleft; decreasing or inhibiting this enzyme will lead to increased acetylcholine concentration. This increased concentration will compete with the antibodies and facilitate muscle contraction. Decreasing calcium influx in the presynaptic neuron will decrease the release of acetylcholine into the synaptic cleft. This will make Myasthenia gravis symptoms worse.
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__________ muscle contains electrical synapses and __________ muscle contains chemical synapses.
__________ muscle contains electrical synapses and __________ muscle contains chemical synapses.
There are two types of synapses: electrical and chemical. Electrical synapses have gap junctions between adjacent cells and are usually found between cardiac muscle cells. Chemical synapses are more abundant and utilize neurotransmitters (such as acetylcholine) to transmit signals between adjacent cells. They are typically found in neuromuscular junctions of skeletal muscle cells.
There are two types of synapses: electrical and chemical. Electrical synapses have gap junctions between adjacent cells and are usually found between cardiac muscle cells. Chemical synapses are more abundant and utilize neurotransmitters (such as acetylcholine) to transmit signals between adjacent cells. They are typically found in neuromuscular junctions of skeletal muscle cells.
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Which of the following neurotransmitters is not a catecholamine?
Which of the following neurotransmitters is not a catecholamine?
Out of all the neurotransmitters listed, the only one that isn't a catecholamine is serotonin. This neurotransmitter is initially derived from the amino acid tryptophan, whereas the catecholamines are derived from the amino acid tyrosine.
Dopamine, norepinephrine, and epinephrine are all catecholamine neurotransmitters. In fact, in the metabolic pathway that produces these compounds, dopamine is an intermediate that can be converted into norepinephrine, which can subsequently be converted into epinephrine.
Out of all the neurotransmitters listed, the only one that isn't a catecholamine is serotonin. This neurotransmitter is initially derived from the amino acid tryptophan, whereas the catecholamines are derived from the amino acid tyrosine.
Dopamine, norepinephrine, and epinephrine are all catecholamine neurotransmitters. In fact, in the metabolic pathway that produces these compounds, dopamine is an intermediate that can be converted into norepinephrine, which can subsequently be converted into epinephrine.
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What category of neurotransmitters are synthesized in the endoplasmic reticulum, and are typically packaged in dense-core vesicles when examined via electron microscopy?
What category of neurotransmitters are synthesized in the endoplasmic reticulum, and are typically packaged in dense-core vesicles when examined via electron microscopy?
Transferases are not neurotransmitters and can be omitted from selection. Catecholamines and small-molecule transmitters are overlapping categories and are typically packed in small, clear core vesicles. Gasotransmitters are membrane permeable and do not require vesicles for release. Neuropeptides are unique in that they are large and are synthesized at the ER, and are packed in large, dense vesicles, and thus this is the correct answer.
Transferases are not neurotransmitters and can be omitted from selection. Catecholamines and small-molecule transmitters are overlapping categories and are typically packed in small, clear core vesicles. Gasotransmitters are membrane permeable and do not require vesicles for release. Neuropeptides are unique in that they are large and are synthesized at the ER, and are packed in large, dense vesicles, and thus this is the correct answer.
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Mutations in ion channels can often cause defects in synaptic transmission since propagation of an electrical signal is crucial to proper transmission at the synaptic cleft. You examine mutant mice and identify that the step in synaptic transmission that is defective is at the vesicle release step; that is, the presynaptic cell undergoes a massive depolarization, vesicles in the presynaptic cell dock at the membrane, but the vesicles do not fuse and therefore neurotransmitter is not released into the cleft. Which ion channel is most likely mutated in these animals?
Mutations in ion channels can often cause defects in synaptic transmission since propagation of an electrical signal is crucial to proper transmission at the synaptic cleft. You examine mutant mice and identify that the step in synaptic transmission that is defective is at the vesicle release step; that is, the presynaptic cell undergoes a massive depolarization, vesicles in the presynaptic cell dock at the membrane, but the vesicles do not fuse and therefore neurotransmitter is not released into the cleft. Which ion channel is most likely mutated in these animals?
An influx of calcium at the presynaptic terminal is absolutely required to activate fusion of vesicles with the membrane, and therefore release of their contents into the presynaptic cleft. Given that the specific deficit in these mutants is at the final stage of fusion, we know that the action potential propagated (so it's likely not sodium or potassium) and the presynaptic membrane is not responding to the voltage change to permit an influx of calcium. Therefore, voltage-gated calcium channels are the likely cause of this deficit.
An influx of calcium at the presynaptic terminal is absolutely required to activate fusion of vesicles with the membrane, and therefore release of their contents into the presynaptic cleft. Given that the specific deficit in these mutants is at the final stage of fusion, we know that the action potential propagated (so it's likely not sodium or potassium) and the presynaptic membrane is not responding to the voltage change to permit an influx of calcium. Therefore, voltage-gated calcium channels are the likely cause of this deficit.
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Which of the following is false about endocrine cells and nerve cells?
Which of the following is false about endocrine cells and nerve cells?
Neurotransmitters are found in the synaptic cleft; hormones travel through the bloodstream. Endocrine signaling is much slower than synaptic signaling, but hormone receptors have a much higher affinity for their ligand, than neurotransmitter receptors do. The highest speed of nerve cell electrical impulses is somewhere around 
. Neurotransmitters are localized around the synaptic cleft; hormones are dispersed in the blood.
Neurotransmitters are found in the synaptic cleft; hormones travel through the bloodstream. Endocrine signaling is much slower than synaptic signaling, but hormone receptors have a much higher affinity for their ligand, than neurotransmitter receptors do. The highest speed of nerve cell electrical impulses is somewhere around
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The absolute refractory period during depolarization is the result of which of these?
The absolute refractory period during depolarization is the result of which of these?
The absolute refractory period during depolarization is the period in which it is impossible for another depolarization to occur. The reason that another depolarization can not occur is that the voltage-gated sodium channels are inactivated. This renders them unable to function, and also unable to receive any signal to activate again. If the channels were closed rather than inactivated, they could still receive electrical input to open again.
The absolute refractory period during depolarization is the period in which it is impossible for another depolarization to occur. The reason that another depolarization can not occur is that the voltage-gated sodium channels are inactivated. This renders them unable to function, and also unable to receive any signal to activate again. If the channels were closed rather than inactivated, they could still receive electrical input to open again.
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How is acetylcholine removed from the synaptic space after acting on its receptors in the postsynaptic membrane?
How is acetylcholine removed from the synaptic space after acting on its receptors in the postsynaptic membrane?
After acetylcholine is excised from the presynaptic neuron to act on its receptors in the postsynaptic neuron, it is removed from the synaptic space by the enzyme, acetylcholinesterase. Acetylcholinesterase breaks it down into acetate and choline which can then be removed.
After acetylcholine is excised from the presynaptic neuron to act on its receptors in the postsynaptic neuron, it is removed from the synaptic space by the enzyme, acetylcholinesterase. Acetylcholinesterase breaks it down into acetate and choline which can then be removed.
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Which of the following would not be able to flow through a gap junction?
Which of the following would not be able to flow through a gap junction?
Gap junctions serve as connections between cells for communication. Molecules that are polar and small enough to fit through gap junctions will be able to move between the communicating cells. Ions, sugars, amino acids, and nucleotides are all small enough to move through. However, proteins will generally be too large to fit through the small (roughly 20 angstroms wide) gap junctions.
Gap junctions serve as connections between cells for communication. Molecules that are polar and small enough to fit through gap junctions will be able to move between the communicating cells. Ions, sugars, amino acids, and nucleotides are all small enough to move through. However, proteins will generally be too large to fit through the small (roughly 20 angstroms wide) gap junctions.
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What is the rate-limiting enzyme in catecholamine synthesis?
What is the rate-limiting enzyme in catecholamine synthesis?
Tyrosine hydroxylase is the rate-limiting enzyme for catecholamine synthesis. It catalyzes the conversion of tyrosine to dihydroxy-phenylalanine (DOPA). Tryptophan hydroxylase is the rate-limiting step for serotonin synthesis. Dopamine beta-hydroxylase converts dopamine to norepinephrine. Amino acid decarboxylase converted DOPA to dopamine.
Tyrosine hydroxylase is the rate-limiting enzyme for catecholamine synthesis. It catalyzes the conversion of tyrosine to dihydroxy-phenylalanine (DOPA). Tryptophan hydroxylase is the rate-limiting step for serotonin synthesis. Dopamine beta-hydroxylase converts dopamine to norepinephrine. Amino acid decarboxylase converted DOPA to dopamine.
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Which of the following neurotransmitters do chromaffin cells release?
Which of the following neurotransmitters do chromaffin cells release?
Chromaffin cells are located in the adrenal gland, and release epinephrine and norepinephrin.
Chromaffin cells are located in the adrenal gland, and release epinephrine and norepinephrin.
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Which neurotransmitter makes up the majority of neurotransmitters released by chromaffin cells in response to stress?
Which neurotransmitter makes up the majority of neurotransmitters released by chromaffin cells in response to stress?
Chromaffin cells release both epinephrine and norepinephrine, but 80% of the neurotransmitters released is epinephrine.
Chromaffin cells release both epinephrine and norepinephrine, but 80% of the neurotransmitters released is epinephrine.
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Which neurotransmitter is synthesized in a storage vesicle?
Which neurotransmitter is synthesized in a storage vesicle?
Of the options given, only norepinephrine is synthesized in storage vesicles. The rest are synthesized in cytoplasm.
Of the options given, only norepinephrine is synthesized in storage vesicles. The rest are synthesized in cytoplasm.
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All of the following are released from storage vesicles upon nerve firing except __________.
All of the following are released from storage vesicles upon nerve firing except __________.
Dihydroxyphenylalanine (DOPA) is the precursor for dopamine. Of the options, only dopamine, epinephrine, and norepinephrine are released upon nerve firing.
Dihydroxyphenylalanine (DOPA) is the precursor for dopamine. Of the options, only dopamine, epinephrine, and norepinephrine are released upon nerve firing.
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If a cell contains tyrosine hydroxylase and L-aromatic amino acid decarboxylase, it is capable of releasing what catecholamine?
If a cell contains tyrosine hydroxylase and L-aromatic amino acid decarboxylase, it is capable of releasing what catecholamine?
Tyrosine hydroxylase is the rate-limiting enzyme for all catecholamine synthesis reactions. L-aromatic amino acid decarboxylase is needed to catalyze the step from DOPA to dopamine. Norepinephrine synthesis requires dopamine beta-hydroxylase and epinephrine synthesis requires dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase (PNMT) in addition to the other enzymes mentioned.
Tyrosine hydroxylase is the rate-limiting enzyme for all catecholamine synthesis reactions. L-aromatic amino acid decarboxylase is needed to catalyze the step from DOPA to dopamine. Norepinephrine synthesis requires dopamine beta-hydroxylase and epinephrine synthesis requires dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase (PNMT) in addition to the other enzymes mentioned.
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Norepinephrine can be removed from the synaptic cleft via __________.
Norepinephrine can be removed from the synaptic cleft via __________.
NETs are used to remove norepinephrine from the synaptic cleft. Tryptophan hydroxylase and amino acid decarboxylase are part of the serotonin synthesis pathway. VMA is a breakdown product of norepinephrine.
NETs are used to remove norepinephrine from the synaptic cleft. Tryptophan hydroxylase and amino acid decarboxylase are part of the serotonin synthesis pathway. VMA is a breakdown product of norepinephrine.
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Parkinson disease therapy is difficult because of all the following reasons except:
Parkinson disease therapy is difficult because of all the following reasons except:
Parkinson disease is associated with decreased dopamine concentration. It is commonly treated with L-DOPA, which can cross the blood brain barrier and be converted to dopamine.
Parkinson disease is associated with decreased dopamine concentration. It is commonly treated with L-DOPA, which can cross the blood brain barrier and be converted to dopamine.
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What serves as the original substrate for serotonin synthesis?
What serves as the original substrate for serotonin synthesis?
Tryptophan is the original substrate for serotonin synthesis. All other answers are involved in the catecholamine synthesis pathway.
Tryptophan is the original substrate for serotonin synthesis. All other answers are involved in the catecholamine synthesis pathway.
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