Posted by undopaminergic on March 7, 2022, at 16:31:20
In reply to Re: Testosterone sollution complete/partial remission? » undopaminergic, posted by SLS on March 7, 2022, at 6:22:20
> Hi, UD.
>Hi, SLS.
> > > > The possible HPA axis dysfunction was one of the reasons I started trimipramine. It reduces cortisol levels, and when it starts to wear off, the cortisol rises again. I take most of the dose at night, in an attempt to normalise the cortisol concentration curve.
>
> That's a really interesting strategy. I didn't know that about trimipramine.
>
> What's your best guess as to why trimipramine has value as an antidepressant? What mechanisms do you think might be involved?/
>The histamine H1-receptor antagonism is of course somewhat useful for sleep. The serotonin 5-HT2A-receptor antagonism may somewhat increase dopamine release in the prefrontal cortex. However, a particularly unusual effect of trimipramine, and apparently unique in an antidepressant, is the histamine H2-receptor antagonism. Famotidine, a selective H2-antagonist, has shown promise in the treatment of the negative (aka. deficit) symptoms of schizophrenia:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1188579/
which is relevant because these symptoms overlap a great deal with depression.I have unsuccessfully tried to elicit feedback (any comment) here on the histamine H2-antagonism. So, I have to say it is only my hunch that this effect is highly significant in the antidepressant mechanism of action of trimipramine.
-undopaminergic
poster:undopaminergic
thread:1118871
URL: http://www.dr-bob.org/babble/20220128/msgs/1118911.html