Synaptic Transmission

Question 1

Which of the following describes the correct sequence of events which occur at the neuromuscular
junction?
A. Action potential in the motor neuron; depolarization of the motor end plate; Ca2+ entry into the
presynaptic nerve terminal
B. Release of ACh; action potential in the motor neuron; action potential in the muscle
C. Release of ACh; action potential in the motor end plate; action potential in the muscle
D. Ca2+ entry into the motor end plate; action potential in the motor end plate; action potential in
the muscle
E. Ca2+ entry into the presynaptic terminal; release of ACh; depolarization of the motor end plate

Answer 1

Answer: E.
Explanation: Acetylcholine (ACh) is stored in vesicles and is released when an action potential in the
motor nerve opens Ca2+ channels in the presynaptic terminal permitting calcium entry into the
presynaptic terminal. ACh diffuses across the synaptic cleft and binds to its receptor – a non-specific
cation channel - on the motor end plate. Opening of these channels permits influx of Na+ and efflux of K
+
,
depolarizing the motor end plate. Local depolarizations in the motor-end plate – graded potentials
called End Plate Potentials (EPPs) - depolarize the membrane to threshold producing an action potential
in the muscle.

Question 2

Which of the following statements correctly characterizes the end-plate potential (EPP) of skeletal
muscle?
A. A decrease in the transmembrane potential that is propagated throughout the cell
B. A local decrease in the transmembrane potential that is associated with little or no increase in
Na+ conductance
C. A local decrease in the transmembrane potential that is caused by an increased permeability
to Na+ and K+
D. A local reversal of charge originating at the end-plate
E. A reversal of charge originating at the end-plate and propagated throughout the cell
F. A small depolarization resulting from spontaneous release of a quantal package of

Answer 2

Answer: C.
Explanation: An EPP is a local depolarization (graded potential) caused by an influx of sodium ions
through acetylcholine receptors on the motor end plate. These non-specific cation channels also allow
passage of potassium. However, the main flux is the movement of sodium. The depolarization is not
great enough to produce a reversal of membrane charge. Release of a single “packet” or quanta of ACh
results in a miniature end plate potential (MEPP), a very small EPP, insufficient to initiate a muscle AP.

Question 3

Anticholinesterases are a class of drug that inhibit the enzyme (acetylcholinesterase) that breaks
down acetylcholine after its release into the neuromuscular junction. What would happen in a skeletal
muscle motor unit in response to a train of motor nerve impulses if the muscle was exposed to an
anticholinesterase?
A. Acetylcholine concentration would be higher in motor endplate synapse compared to
normal.
B. Endplate potentials would be diminished compared to normal.
C. The motor neuron would need to be stimulated at a higher frequency than normal to produce
normal amounts of acetylcholine at the motor endplate.
D. The skeletal muscle fiber could not form action potentials.
E. Release of acetylcholine from the motor neuron would be lower than normal.

Answer 3

Answer: A.
Explanation: The concentration of acetylcholine in the synaptic cleft is determined by the amount of
acetylcholine released into the junction from the motor neuron and the amount broken down by
acetylcholinesterase. Anticholinesterases would block acetylcholine breakdown and, thus, increase the
concentration of acetylcholine in the junction.
The endplate potential is proportional to the number of nicotinic receptors occupied by acetylcholine
and would likely be increased in the presence of an anticholinesterases. This would make it more likely
that muscle action potentials could be formed. In the presence of anticholinesterases, less motor
neuron stimulation (and, thus, less acetylcholine release) would be needed to maintain normal
concentrations of acetylcholine in the vicinity of the motor endplate. Finally, anticholinesterases have no
effect on the release of acetylcholine from the motor neuron terminal; these enzymes affect
acetylcholine after it is released.
When used in the treatment of Myasthenia Gravis, such agents improve symptoms of weakness. By
blocking the degradation of ACh in the neuromuscular junction, levels at the muscle end plate remain
high and act to partially compensate for the deficiency of nicotinic ACh receptors on the motor end
plate characteristic of this disorder.

Question 4

At the motor end plate, ACh binding to its receptor (A) opens which channel and (B) causes which
response(s)?
Channels Response
A)Na+ channels, depolarization toward the Na+ equilibrium potential
B)K+ channels depolarization toward the K+ equilibrium potential
C)Ca2+ channels depolarization toward the Ca2+ equilibrium potential
D)Na+/ K+ channels depolarization to a value halfway between the Na+ and K+ equilibrium potentials
E)Na+/ K+channels hyperpolarization to a value halfway between the Na+ and K+
equilibrium potentials
A. A
B. B
C. C
D. D
E. E

Answer 4

Answer: D.
Explanation: Binding of acetylcholine (ACh) to its receptor - non-specific cation channels - on the motor
end plate opens these channels and allows passage of both Na+ and K+ ions. Na+ will flow into the cell
down its electrochemical gradient, and K+ will flow out of the cell down its electrochemical gradient. The
resulting membrane potential will be depolarized to a value that is approximately halfway between their
respective equilibrium potentials.