The detailed structure of a synapse and of a neuromuscular junction. Candidates should be able to explain • unidirectionality • temporal and spatial summation • inhibition. The sequence of events involved in transmission across a cholinergic synapse and across a neuromuscular junction. When provided with information, candidates should be able to predict and explain the effects of specific drugs on a synapse. Recall of the names and mode of action of individual drugs will not be required.

At a synapse a signal is passed from one neurone to another, or between a neurone and an effector (neuromuscular junction), by chemical signals.

The chemicals used are called neurotransmitters and they are created by smooth endoplasmic reticulum using energy made by mitochondria. Golgi apparatus packages these neurotransmitters up into vesicles.

When an action potential reaches the end (/knob) of the first neurone (/presynaptic neurone) it sets off a sequence of events:

• The increase in positivity causes voltage gated calcium ion channels to open
• Calcium ions bind vesicles to the membrane of the knob, which causes the neurotransmitters within them to be released into the cleft
• The neurotransmitters bind to receptors on the postsynaptic neurone

There are different neurotransmitters which complement different receptors, in the diagram above there are sodium ion channel receptors, which would bind to the neurotransmitter acetylcholine (known as a cholinergic synapse) and cause the following effects:

• The sodium ion channels open causing (positive) sodium to move in (down a concentration gradient)
• The positivity in the cell is increased, making an action potential more likely to start (excitation)

However, if there were chloride ion channels which bonded to the neurotransmitter GABA then:

• The chloride ion channels open causing (negative) chlorine to move in
• The positivity in the cell is decreased making an action potential less likely to start (inhibition)

Excitatory synapse

Inhibitory synapse

After the neurotransmitter has effected the receptor it can be broken down into different components, at which travel back into the presynaptic knob. Here they are joined back together using ATP produced by mitochondria.

Because receptors are only on the postsynaptic membrane, and neurotransmitters are only released from the presynaptic neurone, signals can only move one way (unidirectionality) entering a neurone at the dendrites and leaving a neurone at the axon terminals.

Synapses allow signals to go through multiple neurones in order to create multiple responses to a stimuli by letting a presynaptic neurone release neurotransmitters to multiple postsynaptic neurones.

There are also synapses where multiple presynaptic neurones meet a single postsynaptic neurone. The advantage of this is that if they are both sending neurotransmitters, the effect is stronger. So for example if one presynaptic neurone sends acetlyecholine accross it will make the postsynaptic neurone let in some Na+ and become more positive, but it may not reach the threshold to create a new action potential; however if another presynaptic neurone were to send neurotransmitters accross too this would make the postsynaptic neurone let in even more Na+ and become even more positive, enough to cause a new action potential. This is called spatial summation.

Temporal summation would be if there was only one presynaptic neurone sending neurotransmitters, but the first time there were not enough to let in enough Na+ to start an action potential, however there are multiple action potentials coming down it so it conitnues to send neurotransmitters and in the end there are enough to let in enough Na+ to start an action potential.

Drugs can effect signals at synapses in several ways:

• Mimic neurotransmitters
• Inhibit enzymes that break neurotransmitters
• Inhibit the release of neurotransmitters
• Block receptors