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Example Questions
Example Question #1 : Synapse Biochemistry
The release of which ion triggers release of neurotransmitters at the axon terminal of a presynaptic cell?
Chloride
Calcium
Potassium
Sodium
Cobalt
Calcium
The release of calcium ions at the axon terminal is responsible for the exocytosis of vesicles carrying neurotransmitters.
Example Question #86 : Biochemical Signaling
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
I and II
II and III
I, II, and III
I and III
I and II
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.
Example Question #1 : Synapse Biochemistry
__________ muscle contains electrical synapses and __________ muscle contains chemical synapses.
Skeletal . . . cardiac
Skeletal . . . skeletal
Cardiac . . . cardiac
Cardiac . . . skeletal
Cardiac . . . skeletal
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.
Example Question #4 : Synapse Biochemistry
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?
Increasing acetylcholine half-life
Decreasing the activity of acetylcholinesterase
Decreasing calcium influx in presynaptic neuron
More than one of these are correct
More than one of these are correct
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.
Example Question #1 : Synapse Biochemistry
Which of the following neurotransmitters is not a catecholamine?
Norepinephrine
Dopamine
Serotonin
Epinephrine
All of these are catecholamines
Serotonin
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.
Example Question #2 : Synapse Biochemistry
What category of neurotransmitters are synthesized in the endoplasmic reticulum, and are typically packaged in dense-core vesicles when examined via electron microscopy?
Catecholamines
Small molecule neurotransmitters
Transferases
Gasotransmitters
Neuropeptides
Neuropeptides
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.
Example Question #5 : Synapse Biochemistry
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?
Voltage-gated sodium channels
Voltage-gated calcium channels
Ligand-gated calcium channels
Voltage-gated potassium channels
Ligand-gated sodium channels
Voltage-gated calcium channels
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.
Example Question #6 : Synapse Biochemistry
Which of the following is false about endocrine cells and nerve cells?
Neurotransmitter receptors have a relatively low affinity for their ligand, compared to hormone receptors.
Endocrine signaling is relatively slow compared to synaptic signaling.
Neurotransmitters are locally concentrated; hormones are diffused.
The electrical impulses of nerve cells travel at speeds of up to
Neurotransmitters are delivered through the bloodstream, whereas hormones are found primarily in the synaptic cleft.
Neurotransmitters are delivered through the bloodstream, whereas hormones are found primarily in the synaptic cleft.
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.
Example Question #7 : Synapse Biochemistry
The absolute refractory period during depolarization is the result of which of these?
Closing of the voltage-gated sodium channels
Inactivation of the voltage-gated sodium channels
Inactivation of both the voltage-gated sodium and voltage-gated potassium channels
Closing of the voltage-gated potassium channels
Inactivation of the voltage-gated potassium channels
Inactivation of the voltage-gated sodium channels
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.
Example Question #1 : Synapse Biochemistry
How is acetylcholine removed from the synaptic space after acting on its receptors in the postsynaptic membrane?
Choline acetyltransferase moves acetylcholine from the synaptic space back into the presynaptic neuron
Acetylcholine is taken up into the presynaptic neuron by reuptake channels
Acetylcholine's effect simply wears off and it is not necessary to remove it from the synapse
Acetylcholinesterase breaks down the acetylcholine and returns it to the presynaptic neuron
Acetylcholine is absorbed through its receptor on the postsynaptic membrane
Acetylcholinesterase breaks down the acetylcholine and returns it to the presynaptic neuron
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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