Neurotransmitters are signalling molecules released by exocytosis from vesicles in the pre-synaptic cell causing depolarisation, they diffuse across the synaptic cleft in response to an action potential. The neurotransmitter causes an electrical change in the post-synaptic cell.
The signals can be excitatory (open cation channels (e.g. Na+)) or inhibitory (open Cl- or K+channels). Excitatory signals bring the cell closer to threshold where as inhibitory signals cause the cell to move away from threshold value. When the cell reaches threshold an action potential is fired.
Transmission of a signal between two neurones can be improved if the neurotransmitter is repeatedly released from the presynaptic membrane, this is called long term potentiation (LTP). An example of this is the release of the neurotransmitter glutamate. The postsynaptic membrane holds two ligand-gated ion channels (iontrophic receptors): the AMPA receptor and the NMDA receptor. When glutamate diffuses across the synaptic cleft and binds to the AMPA receptor, the ion channel opens and allows the entry of sodium ions (Na+) into the postsynaptic cell. Entry of sodium ions causes the voltage to become less negative. This initiates an EPSP (excitatory post-synaptic potential) which in turn can trigger an action potential if the voltage reaches or exceeds the threshold (-55 mV). In contrast, glutamate initially has no effect on the NMDA receptor as a magnesium ion (Mg2+) attached to the receptor inhibits it from opening. But as glutamate is repeatedly released, further depolarisation of the postsynaptic membrane triggers the release of the magnesium ion from the receptor. This allows the entry of calcium ions (Ca2+) which then activates other molecules in the secondary messenger pathway.