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Re: ritanserin, pimavanserin, and lumateperone SLS

Posted by undopaminergic on September 14, 2021, at 7:26:05

In reply to Re: ritanserin, pimavanserin, and lumateperone undopaminergic, posted by SLS on September 13, 2021, at 14:52:09

> Hi.

Hi.

> > Last time I checked, I only found one inverse agonist at 5-HT2C, and that was sertindole (Serdolect). I tried it and had to quit due to extreme nasal congestion.
>
> Wasn't there a major problem with sertindole?

Personally, I wouldn't call it major, but it can produce some QT-interval prolongation (more so than most other antipsychotics), which could be potentially lethal in a few particularly sensitive individuals. I had to take an ECG before starting it.

> For me, nasal congestion is an effect that I am guessing is noradrenergic. Imipramine, desipramine, protriptyline, and a few others. I don't think it happened with amphetamines, but probably methylphenidate (Ritalin). Oh, it just occurred to me that the anticholinergic properties of the oral agents, like some TCAs, might cause it, too, but I'm not sure. Anticholinergics are used *topically* to treat congestion.
>

Noradrenergic alpha-1 agonists are used in nasal decongestants (drops or spray). They cause blood vessels to constrict.

Other adrenergics, at least pseudoephedrine, are used orally for nasal congestion.

Anticholinergics are used topically (drops or sprays) to treat runny nose (rhinorrhea), not congestion directly.

> What did you think of Trintellix?

After the failure of lurasidone (which I'm still taking), I'm less interested in vortioxetine. Lurasidone is a high affinity serotonin 5-HT7 antagonist (vortioxetine is too; a bit lower affinity). However, unlike lurasidone, vortioxetine also antagonises serotonin 5-HT3 receptors, so it may still be worth a try, but first asenapine, and then maybe a switch from trimipramine to clomipramine. Clomipramine is probably the most powerful antidepressant that is not a MAOI.

> It made me loopy, despite a couple of neurons firing in the beginning of treatment. Big brain-fog ...
>

Isn't it supposed to do the opposite? (Treat cognitive impairment?)

> and a hint of derealization. However, I think it set up the brain for an almost tragic reaction to the subsequent switch to Effexor. I can't begin to describe how excruciating my reaction was, except to say that I had committed myself to give in to the inevitabilty of committing suicide when I arrived home from a trip to Minnesota to visit a friend of mine. I didn't dare do it in her house, so I decided to wait until I got home. I stopped the Effexor and was okay to travel in a few days. I have taken Effexor at least a handful of times with some benefit. Suicide never entered my mind while taking it.
>

Venlafaxine (Effexor) was a candidate among sertraline and clomipramine, but Dr. Gillman's writings have convinced me that I'm better off with clomipramine. He writes that sertraline is a stronger antagonist at the dopamine transporter than venlafaxine is at the noradrenaline transporter. His evidence for this is compelling, in particular the fact that venlafaxine does not attenuate the tyramine pressor effect.

> Why do I go off on these tangents?
>
> Sorry.

No problem.

-undopaminergic


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poster:undopaminergic thread:1116890
URL: http://www.dr-bob.org/babble/20210723/msgs/1116935.html