Re: 5-HT1a receptor responsible for PSSD?

[Guest guest]

Has anybody out there ever gotten a hold of Flibanserin?

These " partial agonists " (such as Buspar, and many others) seem to be productive

for some people, though I've never had a lot of success myself with Buspar in

terms of reversing PSSD (and I've tried almost everything else on the list of

drugs that work as partial agonists of the 5HT1A Receptor, with no real success

- sorry for the downer). I'm intrigued by the notion of a full " agonist " for

this receptor, which is what Flibanserin claims to be. I know the FDA shut it

down here in the U.S., but it's not been tried for folks with our particular

problem as far as I know. I'd really like to give it a whirl, but there just

doesn't seem to be any way to get my desperate little hands on it. Do they still

sell it in Germany?

I guess in the final analysis, it's a long shot that this drug will work,

especially when the partial agonists haven't, but hey, I'm an optimist . . .

Anybody out there ever been able to experiment with this drug for this

particular problem? I'd love to hear your tale.

Thanks,

>

> Ever since my experience on Buspar it got me thinking that this receptor

is responsible for some of our PSSD.

> First of all, I came across this statement on wikipedia, " 5-HT1A

autoreceptor desensitization and increased 5-HT1A receptor postsynaptic

activation via general increases in serotonin levels by serotonin precursor

supplementation, serotonin reuptake inhibition, or monoamine oxidase

inhibition " . This one was on the wikipedia site for PSSD--- " Treatment with

fluoxetine (Prozac) has been shown to cause persistent desensitization of 5HT1A

receptors after removal of the SSRI in rats.[31] These long-term adaptive

changes in 5-HT receptors, as well as more complex, global changes, are thought

to be mediated through alterations of gene expression. "

> Also, " 5-HT1A receptor agonists decrease blood pressure and heart rate

via a central mechanism. " --- I believe my heart rate is faster than it should

be, and I have read that other people on this site have said that their resting

heart rate seems to be faster than usual.

> Also " 5-HT1A receptor activation has been shown to increase dopamine

release in the medial prefrontal cortex, striatum, and hippocampus "

>

> Other effects of 5-HT1A activation that have been observed in scientific

research include:

> Decreased aggression

> Increased sociability

> Decreased impulsivity

> Inhibition of drug-seeking behavior

> Facilitation of sex drive and arousal

> Inhibition of penile erection

> Diminished food intake

> Prolongation of REM sleep latency

> Reversal of opioid-induced respiratory depression.

>

> 5-HT1A receptor activation induces the secretion of various hormones including

cortisol, corticosterone, adrenocorticotropic hormone (ACTH), oxytocin,

prolactin, growth hormone, and & #946;-endorphin.

>

> I found this interesting but I don't know entirely what it means--- The

autoreceptors must first densensitize before the concentration of extracellular

serotonin in the synapse can become elevated appreciably. Though the

responsiveness of the autoreceptors is somewhat reduced with chronic treatment,

they still remain effective at constraining large increases in extracellular

serotonin concentrations. For this reason, serotonin reuptake inhibitors that

also have 5-HT1A receptor antagonistic or partial agonistic properties such as

vilazodone and SB-649,915 are currently being investigated as novel

antidepressants with a faster onset of action and greater efficacy than many of

those currently available.

>

>

> Lastly, you can look at some of the drugs out there that target this receptor.

Buspar has been known to counter sexual side effects. Viibryd is a new drug that

targets the 5HT-1a receptor and it claims to have " little/no sexual side

effects " . Look up the drug Flibanserin. It was a drug that was being developed

to treat Hypoactive Sexual Disorder. It never came out, but it was a " 5-HT1A

receptor agonist and 5-HT2A receptor antagonist that had initially been

investigated as an antidepressant. "

>

>

>

> What do you think? I'm not a scientist, but it all seems to be correlated to

me.

>