Hello
Few days ago I read that scientists have finally figured why antidepressants take weeks to start showing their effects. According to the study SSRI’s increase the synaptic density and many more things which I didnt understand. I am curious to know what this study tells because I was a SSRI user for 2 years and am excited to know what this study tells.
[https://www.psychiatrist.com/news/why-antidepressants-may-take-weeks-to-show-benefits/](https://www.psychiatrist.com/news/why-antidepressants-may-take-weeks-to-show-benefits/)
[https://scitechdaily.com/brain-plasticity-ssris-breakthrough-on-how-antidepressants-work-why-they-take-weeks-to-kick-in/](https://scitechdaily.com/brain-plasticity-ssris-breakthrough-on-how-antidepressants-work-why-they-take-weeks-to-kick-in/)
Peer reviewed study – [https://www.nature.com/articles/s41380-023-02285-8](https://www.nature.com/articles/s41380-023-02285-8)
Thank you
In: 12
As the name suggests SSRIs inhibit the uptake of Serotonin back into the neurons. However, this direct effect actually ISN’T what causes the clinically significant effects of these drugs. That is caused by epigenetic factors in the nucleus of our cells which modify our gene expression to change the number of receptors expressed on each cells. These genetic changes take some time which is why SSRIs don’t work immediately like most other drugs thst affect neurotransmitters.
Neuroscientist here.
Short answer is that we do not know. Furthermore, we don’t really know how SSRIs work. We know what they do, but how that translates into relief from depression we don’t really know. Mostly because we don’t really know much about pathophysiology of depression.
There is a lot of interest in rapid-acting antidepressants, with drugs like ketamine, MDMA (ecstasy) and, potentially, psilocybin (active ingredient in magic mushrooms) being in various stages of research/usage. Ketamine (esketamine specifically) was approved for treatment-resistant depression in 2019.
All these drugs, from psychedelics to SSRIs affect neurotransmitters, but the truth of how these changes actually translate into clinical effect still remains unknown.
Think of your neurons like tiny bubbles. They don’t actually touch, and they communicate with each other by sending different kinds of even tinier bubbles to the next bubble in line. When they finish telling the next bubble what’s going on, they go back to their home bubble.
These tinier bubbles are called neurotransmitters, and most antidepressants make it so that after the message has been delivered some of the neurotransmitters don’t return home. In the case of SSRIs, the flavor is serotonin.
We don’t know if depression gets better in some cases because there’s more tiny serotonin bubbles floating between the big neuron bubbles and that does something, or if the big bubbles have to make MORE serotonin bubbles and so having more total does something, or if something COMPLETELY different is happening because of all that.
Depression is almost certainly more than one thing, but we don’t understand the brain well enough to be and to tell why things like that happen, in the same way that you can have two people that have a fever but have completely different illnesses. In that same way, just because we can treat one person’s fever with a particular medicine doesn’t always mean it will work for the other person! We just don’t know how to tell what’s causing the ‘fever’ when we’re talking about brain stuff yet.
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