Posted by Caleb462 on June 24, 2003, at 22:24:31
In reply to Re: Caleb/Others, Re: Calling; Correction, posted by rod on June 24, 2003, at 14:27:51
> > > > > > "BuSpar lowers the genetically elevated 5HT1 receptor that causes persistent worry, and is aggravated by SSRI's. Those with post traumatic stress disorder appear to have an elevated 5HT-2 receptor that can be worsened by BuSpar and also need Remeron, usually only for a few months".
> > > > > >
> > > > > > >>>>>>>>>>One more (of many) examples of where Doc Heller says that Buspar lowers 5HT1a site (that's his quote, I chopped off the person's lengthy question just to save space)
> > > > > >
> > > > > > Caleb "Perhaps he means that adding Buspar will quicken the process of 5-HT1a desensitization. Yes, that is probably what he means... I guess?"
> > > > > >
> > > > > > >>>>>>>>> no, that's not what he means dude, he says that ssri's raise the 5HT1a site that causes those problems for some and that Buspar lowers (he even said "blocks" in some responses) that site....later!
> > > > > >
> > > > > >
> > > > > >
> > > > >
> > > > > Well, Buspar is a partial agonist at 5-HT1a... and so perhaps could block serotonin from getting to that site. However, that makes no difference since buspar itself acts like serotonin by ACTIVATING the 5-HT1a site. 5-HT1a receptors will respond in the same manner after repeated treatment to either an SSRI or Buspar. I'm no expert... I could be wrong, but what he's saying doesn't seem to make any sense.
> > > > >
> > > >
> > > >
> > > > I think you are right, this doesn't seem to make sense.
> > > > Base on my personal opinion:
> > > > Both, Buspar and the ssris, downregulate (desensitization) the 1a receptor by stimulating this site, through different mechanisms (direct or by blocking the reuptake pump). Progolnged stimulation causes downregulation.
> > > > But the huge digfference ist that the ssris cause a disruption in dopamine efflux at the beginning of treatment and Buspar is also a D2 Agonist (its acting like dopamine; not blocking)
> > > > So I think the reason why Buspar is good for ssri induced anxiety, at the beginning of treatment, is because Buspar somewhat compensates the decreased dopamine efflux by directly stimulation this site (d2).
> > > > thats my personal opinion.
> > > >
> > > > Roland
> > >
> > > well, I really thought Buspar acts like an agonist, but I re-checked this and it turned out to be wrong. It acts like an antagonist (blocker). So just forget my above post. sorry.
> > > I dont know how it works.
> >
> > I believe the idea is that it primarily blocks pre-synaptic D2 receptors, therfore increasing DA release.
>
>
> maybe, I looked at a previous thread:
> "Buspar: dopamine agonist or antagonist? (Eliz?)"
> http://www.dr-bob.org/babble/20030624/msgs/236668.html
>
> I really have no real clue how this drug works. I dont even know what *partial* agonist means. I dont think it stands for the selectivity towards a specific receptor subtype. maybe the answer lies within this term. the poeple from the mentioned thread also dont really know whats going on.I've always been a bit confused by the term myself. Here is a definition I found -
Partial agonist = a compound which possesses affinity for a receptor, but unlike a full agonist, will elicit only a small degree of the pharmacological response peculiar to the nature of the receptor involved, even if a high proportion of receptors are occupied by the compound.
poster:Caleb462
thread:236166
URL: http://www.dr-bob.org/babble/20030624/msgs/236797.html