Figure 1.

The hypothesis of modulation of monoaminergic transmitters in the pathophysiology of depression. (a) Normal neurotransmission in the monoamine system and (b) Potential disruptions of precursors, enzymes, storage and release of monoamines, monoamine receptors, and exocytosis, leading to a deficiency in neurotransmission. Solid arrows show the course of monoamine synthesis, transportation of monoamine neurotransmitters in the synaptic vesicles, and the release of neurotransmitters into the synaptic cleft. Dashed arrows show the reuptake of monoamine neurotransmitters from the synaptic cleft into the presynaptic neuron for recycling or to be broken down by monoamine oxidase