BCH 316: Neurochemistry….
Practice question B
1. The stimulation of post-synaptic neurons does not occur all the time. Justify.
For the stimulation of a post-synaptic neuron to occur, a neurotransmitter must first be
released from the pre-synaptic axon terminal
into the synaptic cleft. These neurotransmitters then bind onto a receptor on
the post-synaptic contact site, often a spine on the dendrite or the main soma.
Hence, the post-synaptic neuron is stimulated. Stimulation does not occur all
The time due to resting periods/ refractory periods with which repolarization of the
neuron occurs and the action potential dies down. There are also
other factors like EPSP and IPSP which may excite or inhibit the ability
of the neuron, respectively to reach the threshold potential, affecting stimulation rates.
2. What happens when an inhibitory neurotransmitter binds to a receptor?
When an inhibitory neurotransmitter binds to a receptor, it triggers
The opening of ligand-gated ion channels which allows the diffusion of ions into the
membrane. Specifically, it triggers the opening of negatively charged ion channels such as
that of chloride ions, allowing said ions to diffuse down its concentration gradient into the
membrane. When this happens, it leads to the decrease in voltage of the main cell body
compared to its environment. This is the inhibitory post-synaptic potential and could even
cause hyper polarization of the cell.
This process inhibits the neurons ability to reach its threshold potential.
3. Why would GABA be taken up by the nerve terminal during synaptic transmission?
The main reason why GABA is taken up by the nerve terminal is to be
repackaged into seminar vesicles by VIAAT and to be released by the
depolarization once more. This prevents the prolonged exposure of the
post-synaptic contact site to inhibitory signals.
4. Highlight 3 significances of serotogenic neurons
They are essential for mood regulation and emotional wellbeing
They modulate pain perception by altering the transmission of pain signals
They are also involved in the maintenance of gastrointestinal function.
5. Illustrate the pathway involved in the synthesis of epinephrine (with the
inclusion of enzymes, coenzymes and cofactors)
L-tyrosine + Tetrahydrobiopterin(BH4) + O2 -------> L-3,4-dihydroxyphenylalanine
(DOPA) + Dihydrobiopterin(BH4) + H2O.
Enzyme: Tyrosine hydroxylase. Cofactor: Fe2+. Coenzyme: Tetrahydrobiopterin(BH4).
This is the rate limitimg step
L-3,4-dihydroxyphenylalanine -------> Dopamine + CO2.
Enzyme: Aromatic L-aminoacid decarboxylase/ DOPA decarboxylase
Coenzyme: Pyridoxal phosphate (Vitamin b6).
Dopamine + Ascorbate + O2 -------> Norepinephrine + Dihydroascorbate + H2O.
Enzyme: Dopamine-β-hydroxylase. Cofactor: Cu2+. Coenzyme: Ascorbate(vitamin C).
Norepinephrine + S-adenosyl methionine -------> Epinephrine + S-adenosyl
homocysteine.
Enzyme: Phenylethanolamine N-methyl transferase. Coenzyme: S-adenosyl methionine.
6. Explain the relationship between monoamine oxidase and;
I. Serotonin
II. Dopamine
……….
I. Monoamine oxidase is an enzyme that breaks down monoamines, including serotonin
(5-hydroxytryptamine) in an effort to regulate serotonin. There are two main types of
Monoamine oxidase with MAO-A being the type used on serotonin. Low levels of
Monoamine oxidase equates to increased levels of serotonin corresponding to increase in
mood and appetite but an extremely elevated level of this could cause pathological
problems. On the other hand, high levels of this enzyme has been linked to neurological
Conditions like depression and anxiety.
II. Monoamine oxidase breaks down hormones/neurotransmitters like dopamine for its
regulation as well. The type specifically used for Dopamine is MAO-B. Inhibition on
monoamine oxidase could produce therapeutic effects and produce an impact on the
drives of consciousness such as reward sense and motivation. Neurological disorders
linked to change in the concentration of MAO-B include Parkinson’s disease,e.t.c.
7. Highlight the events occurring in the axon right from resting state to depolarization
until the neuron is ready to fire again.
During the resting state, the axon has all its channels closed including the voltage-gated
Na+ channels and Voltage-gated potassium ion channels. The inside of the neuron is
Negatively charged and the neuron is in a state of rest. Then a stimulus occurs, causing
the Ligand-gated sodium ion channel to open flooding the neuron with sodium ions and
reducing its negative charge(depolarization). As the sodium ions spread aroumd the
cell,It eventually reaches the potential threshold (around 55 mV[varies depending on the
membrane]) and causes the voltage-gated sodium ion channels at the axon to open
decreasing its negative charge even more. This charge could take it as high as +40mV
relative to its external environment. This is the action potential and the signal travels
down the axon to start the release of neurotransmitters into the synaptic cleft. Back at the
axon, the voltage-gated K+ ion Channel opens as the sodium ion channel enters a state of
inactivation. The potassium channel diffuses its ions into the outside of the membrane
reducing the cell’s positive charge.A Sodium/Potassium pump then activates taking 3
sodium ions out of the cell and 2 potassium ions into the cell gradually reducing the cells
charge in a repolarisation phase. The cell then enters a state of hyperpolarisation which is
a state where the current charge is lower than the resting charge(say about -70mV). It
eventually stabilizes and enters the resting phase.
8. Mention the importance of Ca2+ ions in synaptic transmissions
Calcium ions are responsible for causing the synaptic vesicles in the pre-synaptic axon
terminal to move to the membrane and fuse together. This allows the neurotransmitters
in said vesicles to be grouped allowing for their effective release when the vesicles fuse
with the membrane and expel the neurotransmitters via exocytosis.
9. Upon completion of the action potential, what possible events are effected on the
Neurotransmitters stored in the synaptic vesicles
The synaptic vesicles all move to the membrane and fuse together with all the
neurotransmitters inside. Then they fuse with the membrane directly facing the synaptic
cleft and expel the neurotransmitters through exocytosis. These neurotransmitters travel
through the 20-40nm gap and reach the receptors of the next neuron they were meant
signal. This stimulus triggers the opening of channels and the diffusion of ions in that
neuron.
10. Differentiate between agonists and antagonists, what is the third pharmacological
agent called, state its function
Agonists can copy the characteristics of neurotransmitters and bind with the receptor
leading to a physiological response. While Antagonists block receptors activation by
blocking neurotransmitters from binding to the receptors.
The third pharmacological agent is called allosteric modulators and their function is to
bind to sites other than the active sites on the receptors, called the allosteric site which
influences the receptors reaction to its natural neurotransmitter. It indirectly affects the
neurotransmitter.
