5-HT1a receptor responsible for PSSD?

[Guest guest]

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.

[Guest guest]

Hi Man Makes some sense, especially the drugs that work the opposite of SSRIs. Are you taking buspar ,and how is it working for you. To: SSRIsex Sent: Saturday, May 12, 2012 3:14:28 PM Subject: 5-HT1a receptor responsible for PSSD?

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.

[Guest guest]

I think you are right, I just started using Buspar for a week and I have been

getting very good results. I've been taking two 5mg a day but I want to take

more. I've shown that article and others to my thyroid dr to spread the word

about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

Yes I am, I'm taking 5mg two times a day and it is going very good thus far. I

also go to a thyroid dr also. After another 3 or so weeks I'm going to see about

bumping it up to 60mg. I read that is the dose that has the most effect. How

much of it do you take. Has it helped you alot?

>

> Hi Man

>  

> Makes some sense, especially the drugs that work the opposite of SSRIs. Are

you taking buspar ,and how is it working for you.

>

>

> ________________________________

>

> To: SSRIsex

> Sent: Saturday, May 12, 2012 3:14:28 PM

> Subject: 5-HT1a receptor responsible for PSSD?

>

>

>

>  

>

> 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.

>

[Guest guest]

What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD?

I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

Sickness, dioreer, cramps. Sent from my BlackBerry® smartphoneSender: SSRIsex Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex Subject: Re: Re: 5-HT1a receptor responsible for PSSD? What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD? I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?>> 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.>

[Guest guest]

Found the following which helps put things into laymens terms. Kind of helped me understand things better.

5-HT1A receptor agonists relieve depression and anxiety. Great! What are they?

by Bill White, Licensed Counselor

"I've heard Viibryd is a 5-HT1A receptor partial agonist. That's supposed to be a good thing, but I have no clue what it means. Help!"

The arrival of Viibryd, an SSRI and 5-HT1A receptor partial agonist, has caused all sorts of hub-bub here on chipur. Most readers are all good with the SSRI piece; however, the 5-HT1A biz throws many for a loop.

It's actually important to know, so we need to discuss it. And the only sane way to handle it is in pieces. Ready?

5-HT

5-HT (5-hydroxytryptamine) is the chemical designation for the neurotransmitter serotonin. It's role in the mood and anxiety disorders is huge.

Receptors & Agonists

For the purposes of our discussion, receptor refers to a neurotransmitter receptor. You'll see one on the receiving neuron (bottom) to the right.

Receptors are present on both postsynaptic and presynaptic neurons – the former being used to receive neurotransmitters, the latter for the purpose of preventing further release of a given neurotransmitter.

Each neurotransmitter has its own receptors. And it's all about efficient electrical signaling.

An agonist is any chemical that binds to a receptor and triggers a response by that cell. A chemical with the opposite action is known as an antagonist.

Oh, partial agonist. Let's not sweat that detail this go-round.

5-HT1A Receptor

A 5-HT1A receptor is a subtype of a 5-HT (serotonin) receptor. In fact, it's the most widespread of the 5-HT receptors.

Amongst other locations, 5-HT1A receptors are found in high densities in the cerebral cortex, hippocampus, and amygdala – all heavily involved in the mood and anxiety disorders.

Activation of 5-HT1A receptors decreases blood pressure and heart rate, and lowers body temperature. Other activation effects include decreased aggression or an increase in calm behavior, increased sociability, inhibition of addictive behavior, and the facilitation of sexual behavior and arousal.

On the other side of the coin, activation of 5-HT1A receptors generates increased impulsivity, inhibition of penile erection, and the impairment of cognition, learning, and memory.

5-HT1A Receptor Agonists

So let's put the pieces together. You may already be familiar with 5-HT1A receptor agonists and not even know it. How 'bout these?

aripiprazole (Abilify), buspirone (BuSpar), clozapine (Clozaril), LSD, nefazodone (Serzone), psilocybin, trazodone (Desyrel), vilazodone (Viibryd), yohimbine, ziprasidone (Geodon)

5-HT1A receptor agonists have traditionally been used in the treatment of mood and anxiety woes.

For example, buspirone (BuSpar) has been a popular anxiety med for a long time.

Just today, Doctor Z. shared in a comment, "Buspirone (Buspar) has been available for years and is a 5HT1A partial agonist. Very inexpensive in generic form. If you're really interested in trying Viibryd, any conventional SSRI combined with Buspirone might be a reasonable and cheap alternative." Click here to head to his website.

Atypical Antipsychotics

You'll notice two atypical antipsychotics (Abilify and Geodon) in our list of 5-HT1A receptor agonists. Don't know about you, but I've seen advertisements for Abilify as an augmentation agent for antidepressants for several years now.

Heavily involved here is overcoming a characteristic of serotonin-impacting antidepressants (like the SSRIs). It's called therapeutic lag. Simply, it can take some time for them to work.

So an antidepressant regimen that can somehow pick-up 5-HT1A receptor agonistic properties brings faster relief and greater overall efficacy.

That'll Do It

Alrighty, then. A nice thumbnail on 5-HT1A receptor partial agonists. The info may come off like so much bio-babble, but it's really important to have in your back pocket. I mean, why wouldn't you want to know the action of a med you paid for – and aim to swallow?

>> 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.>

[Guest guest]

I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1a

receptor responsible for PSSD?

Sickness, dioreer, cramps. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD?

I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

Back in the day when I was taking Prozac, I was also taking 30mg twice per day

of Buspar. I had a very healthy libido at that time which I never realized was

due to the Buspar but, in hindsight, prior to taking Buspar I had been taking

Clomimprimine with the Prozac and my libido was much, much lower. I quit both

the Prozac and the Buspar at the same time (tapered both) due to elevated liver

enzymes so the PSSD started when both left my system.

Funny thing that I never realized that the Buspar was helping my libido because

I was taking it for Anxiety and not for sexual side effects. It was not until I

was recently reading up on the oxytocin that I saw that buspar and oxytocin has

some similar properties.

> >

> > Hi Man

> >  

> > Makes some sense, especially the drugs that work the opposite of SSRIs. Are

you taking buspar ,and how is it working for you.

> >

> >

> > ________________________________

> > From: troublesome96 <aphagman@>

> > To: SSRIsex

> > Sent: Saturday, May 12, 2012 3:14:28 PM

> > Subject: 5-HT1a receptor responsible for PSSD?

> >

> >

> >

> >  

> >

> > 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.

> >

>

[Guest guest]

Yes they did/do works wonders till you withdraw. But after a course of meds is finshed the sexual problems DON'T come back. Sent from my BlackBerry® smartphoneSender: SSRIsex Date: Mon, 14 May 2012 19:04:08 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex Subject: Re: Re: 5-HT1a receptor responsible for PSSD? I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1areceptor responsible for PSSD? Sickness, dioreer, cramps. Sent from my BlackBerry® smartphoneSender: SSRIsex Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex Subject: Re: Re: 5-HT1a receptor responsible for PSSD? What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD? I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?>> 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.>

[Guest guest]

You are saying that after taking Buspar, then withdrawing, your sexual

dysfunction disappears? What is this theory based on? Personal experience,

research, etc? Sounds good but is it just wishful thinking?

> >

> > 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.

> >

>

[Guest guest]

Hi Mmanning So Buspar can turn the switch back on in the brain and cure PSSD, and you don't have to take it forever. Is that what you're saying. Peace, Adam To: SSRIsex Sent: Tuesday, May 15, 2012 9:17:45 AM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Yes they did/do works wonders till you withdraw. But after a course of meds is finshed the sexual problems DON'T come back. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 19:04:08 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1a

receptor responsible for PSSD?

Sickness, dioreer, cramps. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD?

I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

Hi Adam,I personally found a 3 month course of 5mg buspar 3x a day followed by reduction in doses then stopping completely worked yes. Orginally prescribed for Anxiety my phyc dr said it may help with pssd. I was sceptical but thought it was worth a try. I wouldn't say I'm 100% but at least 80. I'm off all drugs now and aviod aLllcohol Sent from my BlackBerry® smartphoneSender: SSRIsex Date: Tue, 15 May 2012 13:07:13 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex Subject: Re: Re: 5-HT1a receptor responsible for PSSD? Hi Mmanning So Buspar can turn the switch back on in the brain and cure PSSD, and you don't have to take it forever. Is that what you're saying. Peace, Adam To: SSRIsex Sent: Tuesday, May 15, 2012 9:17:45 AM Subject: Re: Re: 5-HT1a receptor responsible for PSSD? Yes they did/do works wonders till you withdraw. But after a course of meds is finshed the sexual problems DON'T come back. Sent from my BlackBerry® smartphoneSender: SSRIsex Date: Mon, 14 May 2012 19:04:08 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex Subject: Re: Re: 5-HT1a receptor responsible for PSSD? I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1areceptor responsible for PSSD? Sickness, dioreer, cramps. Sent from my BlackBerry® smartphoneSender: SSRIsex Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex Subject: Re: Re: 5-HT1a receptor responsible for PSSD? What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD? I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?>> 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.>

[Guest guest]

Hi Mmanning Wow that's cool, 3 times a day you said. I have genital numbness, pleasureless orgasm, lowered libido. Did you have those same problems ? and did the buspar cure them all. Does Buspar make ocd or anxiety worse. From: "mmanning619@..."

To: SSRIsex Sent: Tuesday, May 15, 2012 4:30:14 PM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Hi Adam,I personally found a 3 month course of 5mg buspar 3x a day followed by reduction in doses then stopping completely worked yes. Orginally prescribed for Anxiety my phyc dr said it may help with pssd. I was sceptical but thought it was worth a try. I wouldn't say I'm 100% but at least 80. I'm off all drugs now and aviod aLllcohol Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Tue, 15 May 2012 13:07:13 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Hi Mmanning So Buspar can turn the switch back on in the brain and cure PSSD, and you don't have to take it forever. Is that what you're saying. Peace, Adam To: SSRIsex Sent:

Tuesday, May 15, 2012 9:17:45 AM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Yes they did/do works wonders till you withdraw. But after a course of meds is finshed the sexual problems DON'T come back. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 19:04:08 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1a

receptor responsible for PSSD?

Sickness, dioreer, cramps. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD?

I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

Hi Mmanning I once tried wellbutrin, in high doses taken with Luvox it helped a little however, I was wired, at 150mgs it did nothing. To: SSRIsex Sent: Tuesday, May 15, 2012 4:30:14 PM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Hi Adam,I personally found a 3 month course of 5mg buspar 3x a day followed by reduction in doses then stopping completely worked yes. Orginally prescribed for Anxiety my phyc dr said it may help with pssd. I was sceptical but thought it was worth a try. I wouldn't say I'm 100% but at least 80. I'm off all drugs now and aviod aLllcohol Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Tue, 15 May 2012 13:07:13 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Hi Mmanning So Buspar can turn the switch back on in the brain and cure PSSD, and you don't have to take it forever. Is that what you're saying. Peace, Adam To: SSRIsex Sent:

Tuesday, May 15, 2012 9:17:45 AM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Yes they did/do works wonders till you withdraw. But after a course of meds is finshed the sexual problems DON'T come back. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 19:04:08 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1a

receptor responsible for PSSD?

Sickness, dioreer, cramps. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD?

I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

How long have you been off? And, have there been fluctuations since quitting or

have you consistently been at 80%.

> >

> > 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.

> >

>

[Guest guest]

Hi Man Are you taking a high dose of Buspar, I want to try it however I don't want to effect recovery. Wellbutrin did dick all for me. If I use it I don't want to use if for long. To: SSRIsex

Sent: Tuesday, May 15, 2012 4:30:14 PM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Hi Adam,I personally found a 3 month course of 5mg buspar 3x a day followed by reduction in doses then stopping completely worked yes. Orginally prescribed for Anxiety my phyc dr said it may help with pssd. I was sceptical but thought it was worth a try. I wouldn't say I'm 100% but at least 80. I'm off all drugs now and aviod aLllcohol Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Tue, 15 May 2012 13:07:13 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Hi Mmanning So Buspar can turn the switch back on in the brain and cure PSSD, and you don't have to take it forever. Is that what you're saying. Peace, Adam To: SSRIsex Sent:

Tuesday, May 15, 2012 9:17:45 AM Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

Yes they did/do works wonders till you withdraw. But after a course of meds is finshed the sexual problems DON'T come back. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 19:04:08 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

I mean will your sexual benefits will go away To: SSRIsex Sent: Monday, May 14, 2012 9:31:45 PM Subject: Re: Re: 5-HT1a

receptor responsible for PSSD?

Sickness, dioreer, cramps. Sent from my BlackBerry® smartphone

Sender: SSRIsex

Date: Mon, 14 May 2012 13:38:16 -0700 (PDT)To: SSRIsex <SSRIsex >ReplyTo: SSRIsex

Subject: Re: Re: 5-HT1a receptor responsible for PSSD?

What happens when you guys quit the buspar. To: SSRIsex Sent: Sunday, May 13, 2012 9:52:00 PM Subject: Re: 5-HT1a receptor responsible for PSSD?

I think you are right, I just started using Buspar for a week and I have been getting very good results. I've been taking two 5mg a day but I want to take more. I've shown that article and others to my thyroid dr to spread the word about this. How many mgs are you on?

>

> 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.

>

[Guest guest]

Hello people!Wikipedia has a lot of info about AD`s and other drugs.From my research i found this drugs to have potential to fight pssd.Bupropion ( i have tried, and its good against pssd but i´m allergic. My hands' skin start to fell...)BuspironeRopiniroleOxitocynCiticolineCyproheptadine.Anyone who knows others drugs please share the info.The next one i'm going to try is buspirone.WE WILL WIN THIS WAR!!!