Selective Serotonin Re-uptake Inhibitors (SSRI)
Serotonin Norepinephrine Re-uptake Inhibitors (SNRI)
Tricyclic Anti-depressants (TCA)
Serotonin Modulators (5-HT modulators)
Tetracyclic and unicyclic Anti-depressants.
Monoamine Oxidase Inhibitors (MAOI)
They all result in the increase in the concentration of limbic monoamines (Serotonin, Norepinephrine and Dopamine)
It could anything from 14-21 days or it could be even longer. The reason for this slow onset of action is due to the already low concentrations of the monoamines in the limbic system that has to firstly be restored to normal levels, this could take a long time.
The efficacy of these medications are similar.
SSRI’s have less side effects than TAD’s. TAD’s also has a higher affinity to cause anti-cholinergic effects, although SSRI’s has a higher chance of causing Serotonin Syndrome.
SSRI’s are safer than TAD’s as they have less side effects.
Mirtazepine blocks the inhibitory Alpha2 receptors which then has an advance in the Norepinephrine and Serotonin release from presynaptic nerves.
Venlafaxine is an SNRI, thus it blocks the re-uptake of 5-HT as well as NE, although it be more potent for 5-HT. This then causes an increase in presynaptic 5-HT and NE.
Agomelatine is a Melatonin derivative, thus it has and agonistic effect on the Melatonin (MT) 1 and 2 receptors as well as an antagonistic effect on the 5-HT2C receptors. This agonism causes a regulation of the patient’s circadian rhythm which helps the patient sleep better and then reduce the symptoms of depression.