1. A presynaptic membrane in the distal part of the axon
2. This presynaptic membrane also contains Na⁺, K⁺ and Ca²⁺ ion channels.
3. Vesicles in the presynaptic cell that contains the (neuro) transmitter.
4. Neuro-transmitter. In the motor endplate, the neuro-transmitter is always acetylcholine (ACh)
5. A postsynaptic membrane of the muscle cell. These are typically folded (guess why?)
6. Receptor operated channels (=ROC) located in the postsynaptic membrane.

1.
A nerve action potential propagates down the axon towards the pre-synaptic membrane.

2.
The action potential, in the last part of the axon, opens the Ca²⁺ channels.

3.
Because of the concentration gradient (more calcium outside and less calcium inside), calcium ions will flow into the cell.

4.
This intracellular calcium will induce one of the vesicles to move towards the pre-synaptic membrane.

5.
Once at the pre-synaptic membrane, the vesicles will fuse with the membrane and release its content (acetylcholine) into the synaptic cleft. This process is called exocytosis.

6.
The transmitter molecules (Acetycholine = ACh) will diffuse through the synaptic cleft and some will reach the post-synaptic membrane.

7.
These acetylcholine molecules will then couple to the specific receptors (ACh-receptors) located in the post-synaptic membrane.

8.
The ACh-receptors are linked to ion channels (receptor operated channels = ROC).

9.
The coupling of acetylcholine to the ACh-receptor will open that particular channel.

10.
As more and more transmitters attach to the receptors, more and more channels will open.

11.
Opening of the channels will cause a flow of Na⁺ ions into the post-synaptic cell (=influx).

12.
These positive ions will cause a depolarization around that membrane.

13.
This potential is called a generator potential.

14.
When the generator potential reaches threshold, an action potential is generated.

15.
The action potential, once initiated, will propagate along the muscle membrane all around the cell, and into the transversal tubuli.

16.
This will start the process of contractions in the sarcomeres (see next page).

1.
In the synaptic cleft, between the pre- and post-synaptic cleft, there is an enzyme, called acetylcholinesterase (= AChE)

2.
This acetylcholinesterase breaks down the acetylcholine.

3.
This breaking-down is a necessary step to stop the ACh from coupling continuously to the ACh-receptors.

4.
Without this enzyme, the post-synaptic membrane would be constantly depolarized which will no longer induce new action potentials.

1.
It is important to realize that the breaking-down of the transmitter takes place in the synaptic cleft. This is actually extracellular space (= outside the cell).

2.
This makes it easy to influence this mechanism by poisons or drugs.

3.
For example, curare is a well-known poison that competes with acetylcholine (ACh) to occupy the receptor-operated channels.

4.
But, in contrast to ACh, curare does not open the channels and therefore does not induce a generator potential.

5.
As curare does not induce a generator potential, it does not induce action potentials and therefore there will be no contractions. Effectively, curare induces paralysis!.

6.
Curare was used by the South American Indians to kill their preys (and humans too!). The question now is why does curare kill a mammalian organism (like humans)?

7.
At this point, students will often say that curare also blocks the heart.

8.
But the heart is not a skeletal muscle, does not have motor-end plates, so curare cannot block these non-existing ACh-receptors.

9.
But the respiration in the body is performed by the muscles of the chest. And these are skeletal muscles.

10.
So, curare paralyses the muscles of the respiration and therefore the unlucky prey is killed by suffocation!!

11.
Nowadays, the pharmaceutical industry has developed curera-mimetica (mimetica = works like curare).

12.
With these drugs, one can temporarily block all skeletal muscle activity. This is useful for example during surgery.

13.
But then of course, one must also make sure that the respiration is not stopped. As the respiratory muscles are paralyzed, respiration is taken over by a mechanical ventilator.

14.
Probably, even more important, is to make the patient unconscious.

15.
Because, if the patient during surgery is not unconscious, he is effectively paralysed, and cannot scream, move or talk!

16.
This is the stuff of nightmares!

1.
Receptor-operated channels are 'operated' by the transmitter (=ACh) coupling to the receptor.

2.
Voltage-operated channels are 'operated' by voltage (this is the voltage across the membrane; which, at rest, it negative inside and positive outside).

1.
The generator potential does not propagate and is therefore a local phenomenon (whereas the action potentials can and do propagate).

2.
A generator potential is graded; it is small when only a few transmitters are coupled to their receptors and becomes larger when a lot of transmitters are attached (so, not restricted by the famous All-or-None law!).

3.
Therefore, if the generator potential does not reach the threshold, then there will be no action potential.

4.
The generator potential also does not have a refractory period whereas the action potential does.

1.
In a previous page, we saw the structure and function of a chemical synapse; the connection between two nerve cells.

2.
In this page, we have introduced another type of chemical synapse, the motor end-plate, which connects a nerve cell to a skeletal muscle cell.

3.
There are several important differences between these two structures that we need to discuss here.

4.
The major structural difference is that the post-synaptic membrane in the motor end-plate is folded (why?) which is usually not the case in a synapse.

5.
Crucial differences between synapse and motor end-plate:
a. Transmitters
b. 1:1
c. Generator potential vs. IPSP or EPSP

6.
In a motor end plate, the transmitter is always acetylcholine (= ACh). In the synapse, it can be any of numerous (neuro-) transmitters (ACh, adrenaline, DOPA, etc).

7.
The transmitters in the motor end-plate always create a generator potential that depolarizes the membrane towards threshold.

8.
In the chemical synapse, depending on the type of transmitter, either depolarizing (=EPSP) or hyperpolarizing (IPSP) currents are generated (see Link: Chemical Synapse)

9.
Finally, in the motor end plate, induction of a generator potential always reaches threshold (and therefore initiates an action potential in the muscle cell). Therefore, transmission of an action potential to a skeletal muscle cell is always successful. The ratio is therefore 1:1.

10.
As discussed (Chemical Synapse), this is not the case in the synapse where a ratio of pre- to post-synaptic action potentials is typically 1:10.

1.
By folding the membrane at that location, the surface area of that part of the membrane is increased.

2.
A larger surface area means that more ROC’s can be located on this membrane.

3.
Therefore, when ACh diffuses from the pre-synaptic membrane into the synaptic cleft, this transmitter can couple to more available ROC’s.

4.
This in turn will create a larger Na⁺ influx and therefore a larger generator potential.

5.
This will make sure that an action potential is always created in the muscle cell.

6.
In short, the folding makes this type of synapse more sensitive!