When the action potential reaches the pre-synaptic terminal, it is converted from an electrical signal into
a chemical signal.
‣ First, the action potential causes Ca2+ entry into the presynaptic terminal. This promotes that vesicles
loaded with neurotransmitters (proteins) fuse with the presynaptic membrane.
‣ This causes neurotransmitters to be released into the synaptic cleft. There, they diffuse and eventually
bind to receptors (proteins), that swim in the membrane of the post-synaptic cell.
‣ There are several different types of receptors in the post-synaptic membrane of neurons in the CNS.
Each receptor can bind a particular neurotransmitter. For example, the AMPA and NMDA receptors are
glutamate receptors, binding the neurotransmitter glutamate.
‣ Binding the neurotransmitter can cause a specific action of the receptor. For example, some receptors
can form channels that allow electrically charged molecules (ions) to enter the post-synaptic terminal.
Now the chemical signal has been converted back into an electrical signal.
‣ This influx of electrically charged molecules can cause a depolarisation of the post-synaptic neuron,
which can then lead to the neuron firing an action potential. Some neurotransmitters can have the
opposite outcome, they are inhibitory, not excitatory.
‣ Some receptors do not lead to changes in charge when neurotransmitters bind to them, but they
influence biochemical processes in the neuron, which can change the structure or functioning of the
neuron.
‣ Released neurotransmitters are removed from the synapse by enzymatic degradation or reuptake into
the presynaptic terminal.
‣ Some psychopharmacological drugs influence these processes. SSRIs (selective serotonin reuptake
inhibitors) for example artificially increase the amount of the neurotransmitter serotonin in the synapse,
which is used as antidepressant treatment.