Biochemistry › Synapse Biochemistry
Norepinephrine can be removed from the synaptic cleft via __________.
norepinephrine transporter proteins (NETs)
tryptophan hydroxylase
amino acid decarboxylase
vanillylmandelic acid (VMA)
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.
What serves as the original substrate for serotonin synthesis?
Tryptophan
Tyrosine
Dopamine
Epinephrine
Tryptophan is the original substrate for serotonin synthesis. All other answers are involved in the catecholamine synthesis pathway.
Which of the following is used to degrade catecholamines and serotonin?
Catechol-O-methyltransferase (COMT)
Phenylethanolamine N-methyltransferase (PNMT)
Dopamine beta-hydroxylase
L-aromatic amino acid decarboxylase
Of the options, only COMT is involved with catecholamine and serotonin breakdown. The rest are enzymes in the catecholamine synthesis pathway.
How is acetylcholine removed from the synaptic space after acting on its receptors in the postsynaptic membrane?
Acetylcholinesterase breaks down the acetylcholine and returns it to the presynaptic neuron
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
Acetylcholine is absorbed through its receptor on 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.
Which neurotransmitter makes up the majority of neurotransmitters released by chromaffin cells in response to stress?
Epinephrine
Norepinephrine
Dopamine
Glutamate
Chromaffin cells release both epinephrine and norepinephrine, but 80% of the neurotransmitters released is epinephrine.
All of the following are released from storage vesicles upon nerve firing except __________.
Dihydroxyphenylalanine (DOPA)
Dopamine
Epinephrine
Norepinephrine
Dihydroxyphenylalanine (DOPA) is the precursor for dopamine. Of the options, only dopamine, epinephrine, and norepinephrine are released upon nerve firing.
Which of the following neurotransmitters do chromaffin cells release?
Epinephrine
Dopamine
Serotonin
Glutamate
Chromaffin cells are located in the adrenal gland, and release epinephrine and norepinephrin.
The absolute refractory period during depolarization is the result of which of these?
Inactivation of the voltage-gated sodium channels
Inactivation of the voltage-gated potassium channels
Closing of the voltage-gated sodium channels
Closing of the voltage-gated potassium channels
Inactivation of both the voltage-gated sodium and voltage-gated potassium 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.
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 calcium channels
Voltage-gated sodium channels
Ligand-gated calcium channels
Voltage-gated potassium channels
Ligand-gated sodium 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.
Parkinson disease therapy is difficult because of all the following reasons except:
L-DOPA is converted to dopamine in the brain
Dopamine does not cross blood brain barrier
L-DOPA is subject to degradation
L-DOPA can be degraded by two difference enzymes
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.