[1][2] These chemicals can be accumulated by a neuron or secretory cell, are then packaged in secretory / synaptic vesicles, and then released with other neurotransmitters when an action potential provides the necessary stimulus for release.
[3] The concept of a false transmitter is credited to Irwin Kopin of the National Institute of Neurological Disorders and Stroke who determined that the drug tyramine increased blood pressure by being loaded and then released from secretory vesicles of the adrenal chromaffin cells.
Tyramine can also be converted into octopamine by dopamine β-hydroxylase (DBH) which itself acts as a false transmitter by displacing noredrenaline from its vesicle but not activating the postsynaptic α-adrenergic receptor.
By extension, drugs that affect the uptake affinity of neurotransmitter transporters directly affect the efficacy of these substitute neurotransmitters, as shown by the interference that selective serotonin reuptake inhibitors have on serotonergic psychedelic drugs.
A family of fluorescent false neurotransmitters have been developed by Dalibor Sames and David Sulzer at Columbia University that act as analogs for dopamine and other monoamines and enable an optical means for video analysis of neurotransmitter uptake and release.