<p>The monoamine hypothesis postulates that the deficit of certain neurotransmitters is responsible for depression, and even that certain neurotransmitters are linked to specific symptoms.</p>

<p>If suppose serotonin deficit causes depression and antidepressants like TCAs causes increase in serotonin by decreasing uptake, it concludes to me that the increase in transmission via serotonergic receptors on post synaptic membrane alleviates depression.</p>

<p>My question is that how do antidepressants like <a href="https://en.m.wikipedia.org/wiki/Atypical_antidepressant" rel="noreferrer">atypical antidepressants</a> more specifically <a href="https://en.m.wikipedia.org/wiki/Trazodone" rel="noreferrer">Trazodone</a> which acts as 5-HT<sub>2</sub> antagonist show their antidepressant action? And <a href="https://en.m.wikipedia.org/wiki/Tricyclic_antidepressant" rel="noreferrer">TCAs</a> also show such antagonism.</p>

<p>I believe the idea of increased serotonin to cause antidepressant action is not being satisfied here especially in this case of atypical antidepressant as the transmission is being blocked by serotonin receptor antagonistll.</p>

CC BY-SA 4.0
2019-01-20T18:27:56.057Z
Did you search for articles online? There must be hypotheses and reviews on how different types of antidepressants are thought to be working.
CopperKettle
CC BY-SA 4.0
2019-01-20T23:30:39.793Z
The wikipedia page you linked to lists 10 atypical antidepressants. Sampling a few of them I see they have different mechanisms of action. So doesn't it seem unlikely there's a single explanation for all of them?
Carey Gregory
<depression>
How do serotonin antagonist and reuptake inhibitors work as an antidepressant?
Sikander
# How do serotonin antagonist and reuptake inhibitors work as an antidepressant?

(Asked by: username_0 on 2019-01-20)

The monoamine hypothesis postulates that the deficit of certain neurotransmitters is responsible for depression, and even that certain neurotransmitters are linked to specific symptoms.

If suppose serotonin deficit causes depression and antidepressants like TCAs causes increase in serotonin by decreasing uptake, it concludes to me that the increase in transmission via serotonergic receptors on post synaptic membrane alleviates depression.

My question is that how do antidepressants like [atypical antidepressants](https://en.m.wikipedia.org/wiki/Atypical_antidepressant) more specifically [Trazodone](https://en.m.wikipedia.org/wiki/Trazodone) which acts as 5-HT2 antagonist show their antidepressant action? And [TCAs](https://en.m.wikipedia.org/wiki/Tricyclic_antidepressant) also show such antagonism.

I believe the idea of increased serotonin to cause antidepressant action is not being satisfied here especially in this case of atypical antidepressant as the transmission is being blocked by serotonin receptor antagonistll.

**Tags:** depression

> **Comments:**
> **username_1**: Did you search for articles online? There must be hypotheses and reviews on how different types of antidepressants are thought to be working.  
> **username_2**: The wikipedia page you linked to lists 10 atypical antidepressants. Sampling a few of them I see they have different mechanisms of action. So doesn't it seem unlikely there's a single explanation for all of them?  

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## 0 answers

