When an action potential reaches the end of the axon it reaches the gap between itself and the next nerve cell. This gap is the synapse. Although the gap is only a few thousandths of a millimetre in width the action potential cannot cross it. A fresh action potential must be started in the next nerve cell. As the action potential reaches the presynaptic membrane it opens channels which allow calcium ions (Ca⁺⁺) through the presynaptic membrane into the cytoplasm. Within the cytoplasm there are numerous tiny vesicles containing neurotransmitter substances. There are two main types called acetylcholine and noradrenalin. Those which release acetylcholine are referred to as cholinergic neurons, whilst those releasing noradrenalin are called andrenergic neurons.

When the Ca⁺⁺ ions flood into the presynaptic ending they cause vesicles to adhere to the presynaptic membrane and open up to release the neurotransmitter contained within. The neurotransmitter diffuses across the synaptic gap and attaches to receptor molecules on the post synaptic membrane. These receptor molecules are attached to ion channel proteins and when the neurotransmitter attaches, the ion channel is opened up. The receptor also has the enzymic function of reducing the transmitter substance to its component parts. Thus the channel opens only briefly while the transmitter is undamaged. Na⁺ move through these channels into the post synaptic ending and cause an excitatory potential, much like an action potential, but not able to propagate itself. If enough excitatory potentials occur within a short time span sodium channels in the adjacent axon membrane will alter their permeability to Na⁺ and these will flood into the axon causing depolarisation. This action potential will then propagate itself along the nerve cell. The neurotransmitter component parts will diffuse back into the presynaptic nerve ending and be reconstituted as neurotransmitter and placed in vesicles to be used when further action potentials arrive at the presynaptic membrane. the Ca⁺⁺ ions within the presynaptic ending will be pumped out of the axon to prevent continued release of neurotransmitter. It appears that the neurotransmitter is released in a set amount for each action potential which arrives at the synapse.

Inhibition of synapses

The ability of an excitatory potential to be caused in the post synaptic membrane can be severely reduced if Chloride ions(Cl^-) are allowed to enter the post synaptic cytoplasm. There are chloride channels at many synapses and these respond to a different neurotransmitter. When an inhibitory nerve ending releases this transmitter into the synapse the chloride channels open and the post synaptic membrane becomes hyperpolarised and if the sodium channels are opened by the normal transmitter being released from the excitatory nerve ending the influx of sodium ions will be unable to cause an action potential to develop. The ability to switch synapses off in this way allows the system to prevent a circuit from becoming active and therefore suppress a particular action.

Drug effects

There are about 50 known transmitter substances, many of which perform specialised functions with the circuitry of the brain. Many drugs can mimic the effects of these specialised transmitters and therefore can alter the activity of different circuits within the brain. This altered sensitivity of the synapses can lead to unusual effects or sensations within the brain. Due to the alteration of the receptor concentrations which result from an attempt by the system to reestablish normal function in the presence of high concentrations of ‘neurotransmitter’, the activity rate of the synapses can be drastically reduced under normal circumstances when the drug is absent from the brain. It becomes necessary for the drug to be present for the synapses to react in a normal fashion and the person becomes addicted to the presence of the drug. Nicotine for example mimics acetylcholine.

Neuromuscular synapse

This is essentially the same as a nerve to nerve synapse except that here the nerve is forming a synapse with skeletal muscle. The presynaptic membrane receives the nerve impulse and this causes the release of neurotransmitter from vesicles into the synaptic gap which opens pores on the post synaptic membranes of the muscle tissue. The action potential which develops travels over the adjacent muscle membranes (sarcolemma) causing Calcium ions to enter the contractile sarcomeres of the muscle tissue. The action potential in the post synaptic membrane has only a limited ability to propagate and dies out after a short distance has been travelled. This prevents the whole of the muscle from gradually contracting when only a single impulse has been received.