'Typically' chemical synaptic transmission takes place when an influx of calcium ions during a presynaptic nerve impulse triggers exocytosis of neurotransmitter substance from synaptic vesicles. The neurotransmitter diffuses across the synaptic cleft and occupies receptors embedded in the subsynaptic membrane. This interaction (directly or via a second messenger) operates characteristic ion channels and produces an increase in the postsynaptic membrane permeability to particular ions. Depending on the ionic species to which the postsynaptic membrane becomes more permeable, the physiological response will be an excitatory or an inhibitory postsynaptic potential. The action of neurotransmitters may be terminated either by enzymic inactivation or by cellular uptake mechanisms. Over the last decade it has become clear that a neurotransmitter substance may exert a number of different actions on a single postsynaptic neurone. These may involve opening or closure of either voltage-independent or voltage-dependent ion channels. It is also possible that in some instances transmitters may act on neuronal biochemical systems to modify the physiology of postsynaptic cells without directly altering their electrical characteristics. Analysis of the postsynaptic actions of neurotransmitter substances has become further complicated by the increasing body of evidence which indicates that more than one transmitter substance (one of which may be a peptide) can be released from a single presynaptic neurone. The significance of such dual transmitter systems has yet to be fully elucidated. The efficacy of transmission across many synapses may be modified by either presynaptic or postsynaptic mechanisms; both transmitter release and postsynaptic responsiveness may depend on the recent history of a single synapse, on synaptic inputs from other neurones or on circulating neuroactive substances.