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MOAIs
inhibit enzyme responsible for intraneuronal breakdown of 5-HT, NE, and DA
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TCAs
- 5-HT/SRI/NRI
- "dirty receptors":
- a1-adrenergic
- histamine-1
- muscarinic anticholinergic
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Bupropion
norepinephrine/dopamine reuptake inhibitor
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Venlafaxine/desvenlafaxine/duloxetine
- 5-HT and NE reuptake inhibitors
- weak inhibitors of DA reuptake
- Duloxetine has balanced SRI and NRI activities and higher affinity for the reuptake sites
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Nefazodone
- 5-HT antagonists/reuptake inhibitors
- 5-HT activity not as great as SSRIs, but portently block 5-HT2a receptors, which allows more 5-HT to interact at postsynaptic 5-HT1a sites
-
Trazodone
- 5-HT antagonists/reuptake inhibitors
- 5-HT activity not as great as SSRIs, but portently block 5-HT2a receptors, which allows more 5-HT to interact at postsynaptic 5-HT1a sites
- Also blocks histaminergic and a-adrenergic receptors (nefazodone is weak)
-
Mirtazapine
- noradrenergic and specific serotonergic
- blocks presynaptic a2 receptors, both autoreceptors on noradrenergic neurons and heteroreceptors on serotonergic neurons => increase NE and 5-HT synaptic concenrations
- Blocks various postsynaptic serotonergic receptors and histamine-1 receptors
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