Posted by Questionmark on May 4, 2004, at 16:58:31
In reply to Re: Nardil anticholinergic vs. adrenergic SEs, posted by King Vultan on April 30, 2004, at 12:35:22
Thanks so much to you guys for replying. i learned some new info thanks to yous.
SadPanda, you said,
"Given that MAOI's raise levels of all neurotransmitters, I would say they are procholinergic & proadrenergic to some degree."
i'm pretty sure this is not true, though. i think MAOIs raise the levels of most or all biogenic amines (at least serotonin, DA, NE, and epinephrine), but i'm pretty sure it does not raise levels of Ach (and Ach is not an amine).You also said,
"I know what agonism & antagonism does at some receptors, the ones that differentiate non-MAOI drugs. ie: Alpha 1 NE blockade causes orthostatic hypotention & reflex tachcardia, but what does agonism do?"
Probably the opposite, essentially-- i would imagine. But that's good to know, thank you. One thing i'm pretty confused about is all the adrenergic receptor subtypes and their specific effects.
"Ach-Muscarinic blockade causes memory problems, dry mouth, increased eye ball pressure & constipation, but what does agonism do?, cause drooling & diarrohea? :)"
Actually, yes-- well, excessive/increased salivation and diarrhea at least. That's why withdrawal symptoms from an anticholinergic compound can often include these two (and other) effects."SSRI's raise serotonin which causes extra agonism at all 5-HT receptors. 5-HT1 receptor agonism is believed to be what causes an AD effect. 5-HT2A agonism causes excess REM sleep & vivid dreams, antagonism increases deep sleep & may be anxolytic. 5-HT2C is tied to sexual function, agonism causes anorgasmia, antagonism reverses it & is said to be anxiolytic by some. 5-HT3 agonism causes nausea."
Thanks. The specific actions of 5-HT2A and 5-HT2C receptors are so confusing (and possibly still up in the air to some extent, it seems).
King Vultan (Todd) said,
> "Absolutely. Drugs that increase norepinephrine transmission such as MAOIs, selective NE reuptake inhibitors (Strattera, desipramine), or drugs that increase NE transmission in combination with other neurotransmitters (Effexor, Wellbutrin) can generate "pseudo" anticholinergic effects. These effects are not true anticholinergic effects such as one might get from drugs like amitriptyline or imipramine where you do see substantial blockade of muscarinic acetylcholine receptors but rather, side effects that mimic them from the effects on the noradrenergic system. Stahl "Essential Psychopharmacology" states that "This is not due to direct blockade of muscarinic acetylcholine receptors but to indirect reduction of net parasympathetic tone resulting form increased sympathetic tone. Thus a "pseudo-anticholinergic" syndrome of dry mouth, constipation, and urinary retention may be caused by selective NRIs, even though they have no direct actions on cholinergic receptors. Usually, however, the indirect reduction of cholinergic tone yields milder and shorter lasting symptoms than does direct blockade of muscarinic cholinergic receptors." "That is so helpful and informative. Thank you.
Thank you for your information (and compliment) as well, SLS.
Now does anyone know anything that can be done (aside from a cholinergic, which i would like to try) for these effects, particularly on the adrenergic side of things? Probably not, but i thought i'd ask.
i know that yohimbine helps a good deal with them for me, probably because of the alpha-2 NE antagonism, but one has to be very cautious with this drug, and it's not something i would enjoy trying to take every day either.Thanks again.
poster:Questionmark
thread:341646
URL: http://www.dr-bob.org/babble/20040429/msgs/343329.html