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Serotogenic Axons; downregulation

somedud

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So I know 5 HT downregulation is a result of MDMA use, I also know axon degeneration is another one.

Now SSRIs are also shown to cause downregulation.

I'm currently asking the beat method for repair, Ive read SSRIs "rewire" sections of the brain critical for thinking and emotions, aswell areas that are most susceptible for MDMA induced damage.

Now, after MDMA recovery occurs, so I'm wondering if low-moderate dose SSRI would halt these "small" serotogenic axons from sprigging further or stunt recovery in any way? Or would it do the opposite.

And how long does it take for SSRIs to cause downregulation?

I'm curious because I feel I need SSRIs for my minor depression, but Mia lynanxiety and problems seeing things from other point of view, basically frontal lobe "damage" or trauma as I like to call it.


Someone mind shedding some light on those questions, thanks.
 
You don't have frontal lobe damage, as evidenced by the fact that you're typing and thinking. Frontal lobe damage is very severe. I also note a lack of any sort of CT or MRI scans both pre- and post-MDMA usage, so consider that notion discarded on the basis it's pure speculation. Axon degeneration doesn't happen unless you take seriously irresponsible doses (multiple grams at once) or go hyperthermic, and the brain recovers fairly quickly from minor damage.

Anxiety and inability to be empathetic with everyone are normal (especially if you live in a high-stress lifestyle as is common in most of the US, or perhaps you're guilty about hiding your drug usage from others). "Minor depression" doesn't even warrant pharmaceuticals.

Global levels of 5-HT fall after chronic MDMA usage because it depletes stored serotonin (suprise). The downregulation caused by SSRIs is a different issue, and is due to autoreceptors being activated by the increased levels of serotonin. The important thing to note is that neither are permanent. (unless you take huge, unreasonable bolus doses)

A fall in 5-HT levels is present for perhaps a week after a dose of MDMA wears off. The downregulation from SSRI usage starts (drug dependent) either a few days to a month into continuous-dosing treatment and abates after you stop taking the drug.

Both are cured (and symptoms greatly reduce) by abstaining from drugs that mess with serotonin levels (psychedelics, MAOIs, SSRIs/SNRIs, MDxx and other releasing agents) and time. The length of time to fully "recover" may vary from a month or two to several years depending on duration of drug usage, dosage, and the drug itself (SSRIs, esp. those with long half-lives seem to cause longer periods of withdrawal). Excercise is also a major factor in recovery, the more you do the better you will feel (to a certain point). Even 15 minutes of jogging a day will help.

No drug is responsible for "rewiring your brain" - there is no instant panacea for post-MDMA depression. Sorry. Don't think of new axonal growth as actually meaning anything, either. Growing more brain cells doesn't neccesarily mean they will be connected in the right manner to do anything.
 
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Percieved deficits in cognition are not evidence of frontal lobe damage.

Severe, crippling cognitive impairment, loss of activity, and radical personality changes are. And they're not easily noticed if you go and cook your frontal lobe.

Get a MRI and talk to your doctor(s) if you think you have frontal lobe damage. Don't complain on an internet forum.
 
Now SSRIs are also shown to cause downregulation.

sekio,

I thought acute SSRI dosing caused widespread 5-HT release "downregulation" relatively quickly through action at inhibitory somatodendritic 5-HT1a receptors, especially in the midbrain. Desensitization of these receptors with sustained SSRI use results in the resumption of baseline or higher 5-HT release.

Also, high dose MDMA appears to result in internalization of the serotonin transporter differently than SSRI's in time and spatially along the cell.
 
I thought it was the other way around - SSRIs initially elevate peripheral serotonin levels and the body takes a few days to adapt by decreasing release (5-HT1a autoreceptors do play a part). Perhaps it is species-, drug-, dose- or person-specific.

High dose MDMA damage is definitely of a different character than long-term SSRI treatment. There are more factors than just SERT to worry about if you are ingesting multiple grams of MDMA in a sitting.
 
acetyl carnitine arginate can help regenerate the axons i think (i saw it in ED harm reduction supplements)
 
I thought it was the other way around - SSRIs initially elevate peripheral serotonin levels and the body takes a few days to adapt by decreasing release (5-HT1a autoreceptors do play a part). Perhaps it is species-, drug-, dose- or person-specific.

High dose MDMA damage is definitely of a different character than long-term SSRI treatment. There are more factors than just SERT to worry about if you are ingesting multiple grams of MDMA in a sitting.

Thanks for your reply sekio. After some frantic literature searching, I believe you are right, though the situation remains pretty unclear. In any case, I must have been thinking of something like Buspar specifically.

A quote from Time course of the effects of the serotonin-selective reuptake inhibitor sertraline on central and peripheral serotonin neurochemistry in the rhesus monkey

SER (sertraline) rapidly and substantially increases cCSF levels of 5-HT in primates, the extent of elevation is relatively constant during prolonged administration, and values return to baseline shortly after discontinuation. The results suggest that response latency for SSRIs in depression is not due to gradually increasing brain extracellular fluid 5-HT levels and tend not to support theories that posit SSRI response latency as being due to autoreceptor desensitization, transporter downregulation, or drug accumulation.
 
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