Re: upregulation to reverse downregualtion???

June 6, 2012

if you want to deplete serotonin you can use feverfewi took one pill,it some what helped but it caused unbearable anxiety. cyrophetadine is also serotonin antagonist.

June 6, 2012

thanks but an antagonist wont work the way I'm looking for. I need a sustained

depletion all around for a more complete up regulation. An antagonist like

feverfew will cause more desensitisation especially at the 5HT2A receptor which

resists up regulation. Slight increases and decreases in one transmitter wont

cause the massive up regulation needed to reverse desensitisation.

Like the MDMA example when your brain is exhausted of all transmitters.

I found the herbal supplement rauwolfia serpentina, it would need to be taken

for a few weeks to start up regulation i think.

I think maybe we are going the wrong way around this manipulating and

desensitising more and more receptors leaving the brain in a worse condition.

Sure it may be temporary relief but nothing long term

>

> if you want to deplete serotonin you can use feverfew

> i took one pill,it some what helped but it caused unbearable

> anxiety. cyrophetadine is also serotonin antagonist.

>

June 7, 2012

Hi Man I believe your theory , after quiting paxil ,which i took for 6 years i recovered after 3-4 months. Anxiety ans sexual pleasure came back. Than after 6 months I made a big mistake and tool lexapro because the shrink wanted me to, and now pssd.

To: SSRIsex Sent: Wednesday, June 6, 2012 12:47:17 AM Subject: upregulation to reverse downregualtion???

We know that there is serotonin receptor down regulation due to overexposure to serotonin.

We know that there is serotonin receptor up regulation in people with chronically low levels of serotonin (such as suicidal and those that are clinically depressed).

Makes sense right? Too much of it, reduce the sensitivity. Not enough of it, increase the sensitivity.

Low levels actually making one more sensitive to drugs and high levels making one more tolerant.

In this case we have become so tolerant that we are tolerant to our own natural levels of serotonin.

Technically the serotonin receptors should up regulate on withdrawal of the drug but why should they if they are feeling the right amount of serotonin? They only up regulate if they are required to up regulate if the brain is feeling a lack of stimulation.

For example MDMA users will experience a huge influx of serotonin followed by down regulation and then massive serotonin depletion in the following weeks followed by a responsive up regulation. This is shown in studies with rats.

Ssris however work in a different fashion however jamming unnatural amounts in the synapse which our brains cannot immediately respond to which accounts for "start up" effects of massive down regulation in the first few weeks until the brain adapts. This explains why people may only get sexual dysfunction after multiple ssri exposures. Some people may get the same effect after one exposure- possible low receptor number to start with. And possible some individuals can go on and off the drugs with very little side effects due to naturally low serotonin- therefore receptor levels will bounce back.

So question is why aren't we trying to cause a sustained depletion of neurotransmitters to encourage up regulation of receptors???

As far as I can see there is only one drug that can cause this, a drug for high blood pressure Reserpine? Any thoughts on this?

Studies show it increases the response to other drugs such as lsd.

June 11, 2012

Hi Kirby Some shrinks think AD's upregulate receptors. I took suchlow doses, that's the killer. My sexual dysfunction consist of low low, libido it's but still there, numb genitals, however dull skin around the body also, fingertips, hands, sensative areas don't feel the same, also muted orgasm . The only thing I can get is an erection . The crazy thing is my anxiety is extremely low and my ocd is also really mild, I feel very close to flat however I can still laugh sometimes however I can't cry . I remember when I quit paxil after 5-6 years and weaned off super slowly, I recovered slowly but surely and after 3-4 months sexual pleasure and axiety was back like crazy, the old me was back , I even felt the ocd coming back as the weeks went by.

Peace, Adam To: SSRIsex Sent: Monday, June 11, 2012 11:24:02 AM Subject: Re: upregulation to reverse downregualtion???

Desensitising receptors MAY (or may not) reduce anxiety. Anxiety is not just caused by serotonin receptors, they may have nothing to do with it, your shrink will not be able to prove this because in short nobody can, we're not that advanced in understanding the brain. ADS make some people anxious as hell, depends on your brain chemistry and what has gone wrong- these drugs take a stab in the dark which can go wrong oh so often. The serotonin receptors are responsible for many a function in the body, dulling and down regulating them all would be like removing your soul. Who's to say anxiety isn't caused by a million other different mechanisms in the brain? Basically what I'm saying is down regulation is one of the major things causing persistent side effects -otherwise antagonists would have the ability to prevent and block certain symptoms. The idea is to cause a state in the brain where it would want to up regulate the receptors to reach a

new homeostatic set point instead of this new one created with antidepressants. Serotonin/dopamine depletion would not be a pleasant experience but it would make the brain respond/reverse the changes hopefully. I can only find one drug that does this however.

>

> >Ã‚

> >Hi Man

> >Ã‚

> >I believe your theory , after quiting paxil ,which i took for 6 years i recovered afterÃ‚ 3-4 months. Anxiety ans sexual pleasure came back. Than after 6 months I made a big mistake and tool lexapro because the shrink wanted me to, and now pssd.

> >

> >To: SSRIsex

> >Sent: Wednesday, June 6, 2012 12:47:17 AM

> >Subject: upregulation to reverse downregualtion???

> >

> >Ã‚

> >We know that there is serotonin receptor down regulation due to overexposure to serotonin.

> >

> >We know that there is serotonin receptor up regulation in people with chronically low levels of serotonin (such as suicidal and those that are clinically depressed).

> >

> >Makes sense right? Too much of it, reduce the sensitivity. Not enough of it, increase the sensitivity.

> >

> >Low levels actually making one more sensitive to drugs and high levels making one more tolerant.

> >

> >In this case we have become so tolerant that we are tolerant to our own natural levels of serotonin.

> >Technically the serotonin receptors should up regulate on withdrawal of the drug but why should they if they are feeling the right amount of serotonin? They only up regulate if they are required to up regulate if the brain is feeling a lack of stimulation.

> >For example MDMA users will experience a huge influx of serotonin followed by down regulation and then massive serotonin depletion in the following weeks followed by a responsive up regulation. This is shown in studies with rats.

> >Ssris however work in a different fashion however jamming unnatural amounts in the synapse which our brains cannot immediately respond to which accounts for "start up" effects of massive down regulation in the first few weeks until the brain adapts. This explains why people may only get sexual dysfunction after multiple ssri exposures. Some people may get the same effect after one exposure- possible low receptor number to start with. And possible some individuals can go on and off the drugs with very little side effects due to naturally low serotonin- therefore receptor levels will bounce back.

> >

> >So question is why aren't we trying to cause a sustained depletion of neurotransmitters to encourage up regulation of receptors???

> >

> >As far as I can see there is only one drug that can cause this, a drug for high blood pressure Reserpine? Any thoughts on this?

> >Studies show it increases the response to other drugs such as lsd.

> >

>

June 11, 2012

haha unluckily lexapro is the most potent ssri of them all and most selective

raising synaptic serotonin to crazy unjustified levels. Small doses would be

still very potent. And yes ssris can up regulate some receptors mostly the 5HT1A

I believe which is meant to account for the therapeutic actions, but for the

most part excessive binding leads to excessive down regulation. From memory I

believe up regulating this receptor leads to an increase in the release of

serotonin leading to would you believe MORE serotonin and MORE down regulation.

Of course this is what is meant to happen say the " experts " . To reverse this you

need to do more then just manipulate levels of one transmitter of the other. It

may give you a little boost but nothing to change receptors. You need your

receptors to not be getting barely any stimulation. Or so the theory goes.

> >

> > >Ã‚Â

> > >Hi Man

> > >Ã‚Â

> > >I believe your theory , after quiting paxil ,which i took for 6 years i

recovered afterÃ‚Â 3-4 months. Anxiety ans sexual pleasure came back. Than

after 6 months I made a big mistake and tool lexapro because the shrink wanted

me to, and now pssd.

> > >

> > > From: kirby.lancaster <kirby.lancaster@>

> > >To: SSRIsex

> > >Sent: Wednesday, June 6, 2012 12:47:17 AM

> > >Subject: upregulation to reverse downregualtion???

> > >

> > >Ã‚Â

> > >We know that there is serotonin receptor down regulation due to

overexposure to serotonin.

> > >

> > >We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

> > >

> > >Makes sense right? Too much of it, reduce the sensitivity. Not enough of

it, increase the sensitivity.

> > >

> > >Low levels actually making one more sensitive to drugs and high levels

making one more tolerant.

> > >

> > >In this case we have become so tolerant that we are tolerant to our own

natural levels of serotonin.

> > >Technically the serotonin receptors should up regulate on withdrawal of the

drug but why should they if they are feeling the right amount of serotonin? They

only up regulate if they are required to up regulate if the brain is feeling a

lack of stimulation.

> > >For example MDMA users will experience a huge influx of serotonin followed

by down regulation and then massive serotonin depletion in the following weeks

followed by a responsive up regulation. This is shown in studies with rats.

> > >Ssris however work in a different fashion however jamming unnatural amounts

in the synapse which our brains cannot immediately respond to which accounts for

" start up " effects of massive down regulation in the first few weeks until the

brain adapts. This explains why people may only get sexual dysfunction after

multiple ssri exposures. Some people may get the same effect after one exposure-

possible low receptor number to start with. And possible some individuals can go

on and off the drugs with very little side effects due to naturally low

serotonin- therefore receptor levels will bounce back.

> > >

> > >So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

> > >

> > >As far as I can see there is only one drug that can cause this, a drug for

high blood pressure Reserpine? Any thoughts on this?

> > >Studies show it increases the response to other drugs such as lsd.

> > >

> >

>

June 12, 2012

Hi Kirby So what do we have to do ,to rebalance our Neurotransmitters, maybe be put into an induced coma so are Neurotransmitters don't work. . I took Lexapro 10 mgs for about 4-5 days and then 5 mgs for close to 2 months. I then quit the 5mgs and started the lowest dose of Luvox the next day, I took that dose for 2-3 days and then dropped down to half of the lowest dose which I took for 1 year, with wellbutrin also. I wonder if I would've weaned of the 5mgs of Lexapro ,if I would still have PSSD, the shrink told me to just go straight on the Luvox considering I was on the lowest dose of Lexapro, however Lexapro froze me more than Luvox and Paxil , I still felt human on paxil and recovered from it. Do yuou think going back on Lexapro 5 mgs and the weaning off

would do anything. Best , Adam To: SSRIsex Sent: Tuesday, June 12, 2012 1:54:51 AM Subject: Re: upregulation to reverse downregualtion???

haha unluckily lexapro is the most potent ssri of them all and most selective raising synaptic serotonin to crazy unjustified levels. Small doses would be still very potent. And yes ssris can up regulate some receptors mostly the 5HT1A I believe which is meant to account for the therapeutic actions, but for the most part excessive binding leads to excessive down regulation. From memory I believe up regulating this receptor leads to an increase in the release of serotonin leading to would you believe MORE serotonin and MORE down regulation. Of course this is what is meant to happen say the "experts". To reverse this you need to do more then just manipulate levels of one transmitter of the other. It may give you a little boost but nothing to change receptors. You need your receptors to not be getting barely any stimulation. Or so the theory goes.

> >

> > >Ãƒâ€šÃ‚

> > >Hi Man

> > >Ãƒâ€šÃ‚

> > >I believe your theory , after quiting paxil ,which i took for 6 years i recovered afterÃƒâ€šÃ‚ 3-4 months. Anxiety ans sexual pleasure came back. Than after 6 months I made a big mistake and tool lexapro because the shrink wanted me to, and now pssd.

> > >

> > > From: kirby.lancaster <kirby.lancaster@>

> > >To: SSRIsex

> > >Sent: Wednesday, June 6, 2012 12:47:17 AM

> > >Subject: upregulation to reverse downregualtion???

> > >

> > >Ãƒâ€šÃ‚

> > >We know that there is serotonin receptor down regulation due to overexposure to serotonin.

> > >

> > >We know that there is serotonin receptor up regulation in people with chronically low levels of serotonin (such as suicidal and those that are clinically depressed).

> > >

> > >Makes sense right? Too much of it, reduce the sensitivity. Not enough of it, increase the sensitivity.

> > >

> > >Low levels actually making one more sensitive to drugs and high levels making one more tolerant.

> > >

> > >In this case we have become so tolerant that we are tolerant to our own natural levels of serotonin.

> > >Technically the serotonin receptors should up regulate on withdrawal of the drug but why should they if they are feeling the right amount of serotonin? They only up regulate if they are required to up regulate if the brain is feeling a lack of stimulation.

> > >For example MDMA users will experience a huge influx of serotonin followed by down regulation and then massive serotonin depletion in the following weeks followed by a responsive up regulation. This is shown in studies with rats.

> > >Ssris however work in a different fashion however jamming unnatural amounts in the synapse which our brains cannot immediately respond to which accounts for "start up" effects of massive down regulation in the first few weeks until the brain adapts. This explains why people may only get sexual dysfunction after multiple ssri exposures. Some people may get the same effect after one exposure- possible low receptor number to start with. And possible some individuals can go on and off the drugs with very little side effects due to naturally low serotonin- therefore receptor levels will bounce back.

> > >

> > >So question is why aren't we trying to cause a sustained depletion of neurotransmitters to encourage up regulation of receptors???

> > >

> > >As far as I can see there is only one drug that can cause this, a drug for high blood pressure Reserpine? Any thoughts on this?

> > >Studies show it increases the response to other drugs such as lsd.

> > >

> >

>

June 12, 2012

The drug you're talking about is very serious, and it's probably not the first

thing I would try.

I did try Cyproheptadine, which lowers serotonin levels at some receptor sites.

Unfortunately, after two weeks, I had severe stomach problems, and had to stop

(lots of Serotonin in the lower intestines). I'm pretty gung ho about solving

this problem, but running to the bathroom with very intense cramps every 10

minutes was a show stopper for me. I was taking a dose so small I could barely

see the sliver of the pill in my hand when I popped it into my mouth.

There are a couple other drugs that do what you're talking about. Unfortunately,

they have all been tried, some by people in this group, with little success.

They can often make things worse.

Please be very careful with the drug you refer to below - Reserpine is indicated

to cause permanent changes in brain chemistry. You're trying to hit a fly on a

glass window with a sledge hammer, without breaking the glass. You probably

won't even hit the fly.

I would try your theory with some other drugs first, and read what other people

have done.

I just tried a drug called Flibanserin, which I obtained from an overseas

supplier. Two tiny doses, and I've gone from 20% of a drive to almost nothing.

I'd kill to be back where I was 3 weeks ago. If you're going to try something

like this, use a dose so small you can barely feel it.

Good luck.

>

> We know that there is serotonin receptor down regulation due to overexposure

to serotonin.

>

> We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

>

> Makes sense right? Too much of it, reduce the sensitivity. Not enough of it,

increase the sensitivity.

>

> Low levels actually making one more sensitive to drugs and high levels making

one more tolerant.

>

> In this case we have become so tolerant that we are tolerant to our own

natural levels of serotonin.

> Technically the serotonin receptors should up regulate on withdrawal of the

drug but why should they if they are feeling the right amount of serotonin? They

only up regulate if they are required to up regulate if the brain is feeling a

lack of stimulation.

> For example MDMA users will experience a huge influx of serotonin followed by

down regulation and then massive serotonin depletion in the following weeks

followed by a responsive up regulation. This is shown in studies with rats.

> Ssris however work in a different fashion however jamming unnatural amounts in

the synapse which our brains cannot immediately respond to which accounts for

" start up " effects of massive down regulation in the first few weeks until the

brain adapts. This explains why people may only get sexual dysfunction after

multiple ssri exposures. Some people may get the same effect after one exposure-

possible low receptor number to start with. And possible some individuals can go

on and off the drugs with very little side effects due to naturally low

serotonin- therefore receptor levels will bounce back.

>

> So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

>

> As far as I can see there is only one drug that can cause this, a drug for

high blood pressure Reserpine? Any thoughts on this?

> Studies show it increases the response to other drugs such as lsd.

>

June 12, 2012

This abstract is an important starting point for understanding how different

serotonin receptors (and their activation/deactivation) increase or decrease

sexual arousal. It's a mice study, of course, so it's just a simple starting

point. You can read it at the link below. The final conclusion of the study is

listed below.

http://www.ncbi.nlm.nih.gov/pubmed/15587814

. . . These results led to the conclusion that 5-HT receptors are involved in

controlling the sexual activation of males. Different types and even subtypes of

the same type of 5-HT receptor had different effects, both inhibitory and

activatory, on activation of the HHTC by receptive females (in other words,

activation of sexual activity in the mice). Blockade of HHTC activation induced

by the presence of females appears to involve 5-HT1A and 5-HT2C receptors, while

activation involves 5-HT2A and 5-HT3 receptors.

> > >

> > > >Ã‚Â

> > > >Hi Man

> > > >Ã‚Â

> > > >I believe your theory , after quiting paxil ,which i took for 6 years i

recovered afterÃ‚Â 3-4 months. Anxiety ans sexual pleasure came back. Than

after 6 months I made a big mistake and tool lexapro because the shrink wanted

me to, and now pssd.

> > > >

> > > > From: kirby.lancaster <kirby.lancaster@>

> > > >To: SSRIsex

> > > >Sent: Wednesday, June 6, 2012 12:47:17 AM

> > > >Subject: upregulation to reverse downregualtion???

> > > >

> > > >Ã‚Â

> > > >We know that there is serotonin receptor down regulation due to

overexposure to serotonin.

> > > >

> > > >We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

> > > >

> > > >Makes sense right? Too much of it, reduce the sensitivity. Not enough of

it, increase the sensitivity.

> > > >

> > > >Low levels actually making one more sensitive to drugs and high levels

making one more tolerant.

> > > >

> > > >In this case we have become so tolerant that we are tolerant to our own

natural levels of serotonin.

> > > >Technically the serotonin receptors should up regulate on withdrawal of

the drug but why should they if they are feeling the right amount of serotonin?

They only up regulate if they are required to up regulate if the brain is

feeling a lack of stimulation.

> > > >For example MDMA users will experience a huge influx of serotonin

followed by down regulation and then massive serotonin depletion in the

following weeks followed by a responsive up regulation. This is shown in studies

with rats.

> > > >Ssris however work in a different fashion however jamming unnatural

amounts in the synapse which our brains cannot immediately respond to which

accounts for " start up " effects of massive down regulation in the first few

weeks until the brain adapts. This explains why people may only get sexual

dysfunction after multiple ssri exposures. Some people may get the same effect

after one exposure- possible low receptor number to start with. And possible

some individuals can go on and off the drugs with very little side effects due

to naturally low serotonin- therefore receptor levels will bounce back.

> > > >

> > > >So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

> > > >

> > > >As far as I can see there is only one drug that can cause this, a drug

for high blood pressure Reserpine? Any thoughts on this?

> > > >Studies show it increases the response to other drugs such as lsd.

> > > >

> > >

> >

>

June 13, 2012

I've read a lot about it, studies show things return to normal after drug

administration http://doctorsonly.co.il/wp-content/uploads/2011/12/2010_1_8.pdf

it can cause depression which resolves after discontinuation when transmitters

return to normal and new storage vesicles are formed. You can get it in the form

of Rauwolfia Serpentina. Ghandi used to drink it as a tea and it has sedative

properties. The used to use it at huge dosages in the old days now the dosages

are tiny to avoid the unwanted side effects. Which other drugs have you found

which cause depletion of all other transmitters? I cant find any others.

Antagonists are not really guaranteed to up regulate anything and sometimes down

regulate further. This is exhausting.

> >

> > We know that there is serotonin receptor down regulation due to overexposure

to serotonin.

> >

> > We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

> >

> > Makes sense right? Too much of it, reduce the sensitivity. Not enough of it,

increase the sensitivity.

> >

> > Low levels actually making one more sensitive to drugs and high levels

making one more tolerant.

> >

> > In this case we have become so tolerant that we are tolerant to our own

natural levels of serotonin.

> > Technically the serotonin receptors should up regulate on withdrawal of the

drug but why should they if they are feeling the right amount of serotonin? They

only up regulate if they are required to up regulate if the brain is feeling a

lack of stimulation.

> > For example MDMA users will experience a huge influx of serotonin followed

by down regulation and then massive serotonin depletion in the following weeks

followed by a responsive up regulation. This is shown in studies with rats.

> > Ssris however work in a different fashion however jamming unnatural amounts

in the synapse which our brains cannot immediately respond to which accounts for

" start up " effects of massive down regulation in the first few weeks until the

brain adapts. This explains why people may only get sexual dysfunction after

multiple ssri exposures. Some people may get the same effect after one exposure-

possible low receptor number to start with. And possible some individuals can go

on and off the drugs with very little side effects due to naturally low

serotonin- therefore receptor levels will bounce back.

> >

> > So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

> >

> > As far as I can see there is only one drug that can cause this, a drug for

high blood pressure Reserpine? Any thoughts on this?

> > Studies show it increases the response to other drugs such as lsd.

> >

>

June 19, 2012

I know what you're saying my friend. I don't know anything else that could

potentially drop all the transmitters. The kind of re-boot you're talking about

though . . . I don't know. After my experience with a tiny tiny dose of one

substance that effects only one neurotransmitter - Flibanserin - I'm pretty

scared to touch anything else.

I will share what I've been looking at with a strong caution to anybody that

wants to mess with these neurotransmitters. Please be very careful. Just go in

knowing that anything that messes with these neurotransmitters could potentially

cause more damage. I don't want to be responsible for making things worse for

anybody.

That said, I will say I have found one thing that does make a big difference -

mythylphenidate (Ritalin). Get a high dose of adderall or concerta into your

system and I promise you'll notice some difference in sexual pleasure and

desire. Mehtylphenidate is a 5HT2A receptor agonist, as listed below. It does

help. Beyond that, I don't know of anything yet that actually reverses this

awful condition. If you're daring, though, read on . . .

My research points me toward a couple of things (which I will probably try, when

I get up the nerve again). If we assume Serotonin transmitters are involved, the

question essentially is: which serotonin receptors should we mess with, and do

we want to use an " agonist " or an " antagonist " on that particular receptor? If

you look at a couple of the most directly relevant rat studies, they point

toward using a combination of the following:

5HT1A receptor antagonist (Lecozotan looks the most promising)

5HT2A receptor agonist (usually stimulants, mostly illegal)

5HT2C receptor antagonist

Summary of rat study #1, with study abstract below . . .

1A agonist - blocked activation of sexual activity(Flibanserin - bad)

1A/1B agonist mixture - blocked activation of sexual activity

1A Antagonist " blocked the blocking " of the 1A agonist (Lecozotan - promising)

1B agonist - no effect

1B/2C agonist mixture - blocked activation of sexual activity

2A antagonist - blocked activation of sexual activity (Flibanserin - bad)

5HT3 antagonist - blocked activation of sexual activity(though raised initial

plasma)

Abstract of study #1

Placing of receptive females in the sector of a cage separated by a partition

preventing physical contact but allowing sight and olfaction induced increases

in blood testosterone levels in male mice. The selective agonist of 5-HT1A

receptors 8-OH-DPAT (0.1 mg/kg) and the mixed 5-HT1A/1B receptor agonist

eltoprazine (3.0 and 10.0 mg/kg) blocked the activatory effect of presentation

of females on the hypothalamohypophyseal-testicular complex (HHTC) in males,

while the 5-HT1A receptor antagonist p-MPPI (0.2 mg/kg) prevented the inhibitory

effects of 8-OH-DPAT and eltoprazine. The 5-HT1B receptor agonist CGS-12066A

(1.0 and 2.0 mg/kg) had no effect, while the mixed 5-HT1B/2C agonist TFMPP (5.0

mg/kg) blocked the increase in blood testosterone in males in response to

presentation of females. The 5-HT2A receptor antagonist ketanserin (1.0 and 2.0

mg/kg) prevented the increase in testosterone induced by the presence of

females. The 5-HT3 receptor antagonist ondansetron (0.05 and 0.1 mg/kg)

increased the initial plasma testosterone level but blocked activation of the

HHTC induced by the presence of receptive females. These results led to the

conclusion that 5-HT receptors are involved in controlling the sexual activation

of males. Different types and even subtypes of the same type of 5-HT receptor

had different effects, both inhibitory and activatory, on activation of the HHTC

by receptive females. Blockade of HHTC activation induced by the presence of

females appears to involve 5-HT1A and 5-HT2C receptors, while activation

involves 5-HT2A and 5-HT3 receptors.

Summary of rat study #2 with abstract below . . .

2A antagonists - blocked activation of sexual activity.

2C antagonist - activated sexual activity (Cyproheptadine - painful side effects

for me - bad stomach trouble)

2A/2C nonselective antagonist - no effect

Abstract

The role of 5-HT2A and 5-HT2C subtypes of serotonergic receptors in the control

of sexual behavior and plasma testosterone regulation was studied in male CBA

mice exposed to a sexually receptive female separated by a transparent

partition. Introduction of the receptive female induced sexual motivation and

arousal in males, as evidenced by a prolonged time spent at the partition,

unsuccessful attempts to step across it and a significant increase in plasma

testosterone levels. Administration of 5-HT2A receptor antagonists ketanserin

(1.0 and 2.0 mg/kg i.p.) or cyproheptadine (1.0 and 2.0 mg/kg i.p.) diminished

the behavioral components and prevented the hormonal components of male sexual

arousal. Administration of the selective 5-HT2C antagonist RS 102221 (1.0 and

2.0 mg/kg) considerably increased the time spent by males at the partition (p <

0.001) and, at the dose of 2.0 mg/kg, increased plasma testosterone levels (p <

0.01). Administration of ritanserin - a nonselective 5-HT2A/2C antagonist and,

to a smaller degree, 5-HT2B antagonist - at doses of 0.1 and 0.5 mg/kg did not

significantly influence male behavior and the activating effect of the presence

of a female on the hypothalamo-pituitary-testicular system, although it

increased resting testosterone levels (p < 0.05). The present findings suggest

that 5-HT2A/5-HT2C receptors may be involved in the neural control of male

sexual motivation and arousal, presumably by exerting reciprocal facilitative

(5-HT2A) or suppressive (5-HT2C) influences.

According to these studies, to stimulate sex drive you would want a combination

of the following. Examples of each are listed below (Wikipedia).

1 - HT1A receptor antagonist (Lecozotan looks the most promising)

2 - 5HT2A receptor agonist (usually stimulants, mostly illegal)

3 - 5HT2C receptor antagonist

1A receptor antagonist . . .

Alprenolol - non-selective beta blocker as well as 5-HT1A receptor antagonist,

used in the treatment of angina pectoris.

Asenapine - high affinity (pKi) for numerous receptors, including the serotonin

5-HT1A (8.6), 5-HT1B (8.4), 5-HT2A (10.2), 5-HT2B (9.8), 5-HT2C (10.5), 5-HT5A

(8.8), 5-HT6 (9.5), and 5-HT7 (9.9) receptors, the adrenergic & #945;1 (8.9),

& #945;2A (8.9), & #945;2B(9.5), and & #945;2C (8.9) receptors, the dopamine D1

(8.9), D2 (8.9), D3 (9.4), and D4 (9.0) receptors, and the histamine H1 (9.0)

and H2 (8.2) receptors. Partial agonist at the 5-HT1A receptors.[3] At all other

targets Asenapine is an antagonist

BMY 7378 - weak partial agonist/antagonist

Cyanopindolol - both a & #946;1 adrenoreceptor antagonist and a 5-HT1A receptor

antagonist

Iodocyanopindolol - & #946;1 adrenoreceptor antagonist and a 5-HT1A receptor

antagonist

Lecozotan - selective 5-HT1A receptor antagonist[3] which enhances the

potassium-stimulated release of acetylcholine and glutamate.[4]

Methiothepin - antagonist at various serotonin and dopamine receptors.

NAN-190 - previously believed to act as a selective 5-HT1A receptor antagonist,

but a subsequent discovery showed that it also potently blocks the

& #945;2-adrenergic receptor.[1]

Nebivolol - & #946;1 receptor blocker with nitric oxide-potentiating

vasodilatory effect used in treatment of hypertension and, in Europe, also for

left ventricular failure.

Oxprenolol - Oxprenolol is a lipophilic beta blocker which passes the

blood–brain barrier more easily than water soluble beta blockers. As such, it is

associated with a higher incidence of CNS-related side effects than hydrophilic

ligands such as atenolol,sotalol and nadolol.[1]

Pindolol - Pindolol is a nonselective beta blocker with partial beta-adrenergic

receptor agonist activity. It possesses ISA (Intrinsic Sympathomimetic

Activity). This means that pindolol, particularly in high doses, exerts effects

like epinephrine orisoprenaline (increased pulse rate, increased blood pressure,

bronchodilation), but these effects are limited. Pindolol also shows membrane

stabilizing effects like quinidine, possibly accounting for its antiarrhythmic

effects. It also functions as a 5-HT1A receptor weak partial agonist /

antagonist.

Propanolol - Beta Blocker

Robalzotan - selective antagonist at the 5-HT1A receptor.[1] It was shown to

completely reverse the autoreceptor-mediated inhibition of serotonin release

induced by the administration of selective serotonin reuptake inhibitors like

citalopram in rodent studies.

S15535 -

Spiperone

TFMPP

UH-301

WAY-100,135

WAY-100,635

Mefway

2A Agonist . . .

2C-B - psycheuledic drug

5-MeO-DMT - psycheuledic drug

BZP - Benzylpiperazine (BZP) is a recreational drug with euphoric, stimulant

properties. The effects produced by BZP are comparable to those produced by

amphetamine. Adverse effects have been reported following its use including

acute psychosis,renal toxicity, and seizures.[2] No deaths have been reported

following a sole ingestion of BZP, although there have been at least two deaths

from the combination of BZP and MDMA. Its sale is banned in a few countries,

including Australia, New Zealand, the United States, the Republic of Ireland,

the United Kingdom, Romania and other parts of Europe.[3][4] However, its legal

status is currently less restrictive in some other countries such as Canada,

with investigations and regulations pending under European Union laws.

Bufotenin - Bufotenin (also known as bufotenine and cebilcin), or

5-hydroxy-N,N-dimethyltryptamine (5-OH-DMT), is a tryptamine related to the

neurotransmitter serotonin. It is an alkaloid found in the skin of some species

of toads; in mushrooms, higher plants, and mammals.[1]

The name bufotenin originates from the Bufo genus of toads, which includes

several species of psychoactive toads, most notably Bufo alvarius, that secrete

bufotoxins from their parotoid glands.[2] Bufotenin is similar in chemical

structure to the psychedelics psilocin (4-HO-DMT), 5-MeO-DMT, and DMT, chemicals

which also occur in some of the same fungus, plant, and animal species as

bufotenin. The psychoactivity of bufotenin has been disputed, though recent

studies suggest it is similar in nature to 5-MeO-DMT.

DMT - N,N-Dimethyltryptamine (DMT) is a naturally occurring psychedelic compound

of the tryptamine family. Its presence is widespread throughout the plant

kingdom.[3][4] DMT occurs in trace amounts in mammals, including humans, where

it may putatively function as a trace amine neurotransmitter.[5] It is

originally derived from the essential amino acid tryptophan and ultimately

produced by the enzyme INMT during normal metabolism.[6] The significance of its

widespread natural presence remains undetermined. Structurally, DMT is analogous

to the neurotransmitter serotonin (5-HT), the hormone melatonin, and other

psychedelic tryptamines, such as 5-MeO-DMT, bufotenin, and psilocin (the active

metabolite of psilocybin).

When ingested, DMT acts as a psychedelic drug.[7] Depending on the dose and

method of administration, its subjective effects can range from short-lived

milder psychedelic states to powerful immersive experiences; these are often

described as a total loss of connection to conventional reality with the

encounter of ineffable alien realms.[8] Indigenous Amazonian Amerindian cultures

consume DMT as the primary psychoactive in ayahuasca, a shamanistic brew imbibed

for divinatory and healing purposes. Pharmacologically, ayahuasca combines DMT

with an MAOI, an enzyme inhibitor that allows DMT to be orally active.[9]

DOM -

Ergonovine

Lisuride

LSD

Mescaline

Myristicin

Psilocin

Psilocybin

TFMPP (partial agonist or antagonist)

Yohimbine

2C Antagonist . . .

Agomelatine[33] (antidepressant[33])

Amitriptyline

Asenapine

Clomipramine

Clozapine[33] (antipsychotic[33])

Cyproheptadine

Dimebolin

Eltoprazine

Etoperidone

Fluoxetine

Iloperidone

Ketanserin[33] (antihypertensive[33])

Lisuride

Methysergide[60]

Mianserin

Mirtazapine

Nefazodone

Olanzapine

Quetiapine

Risperidone

Ritanserin

Trazodone

Ziprasidone

> > >

> > > We know that there is serotonin receptor down regulation due to

overexposure to serotonin.

> > >

> > > We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

> > >

> > > Makes sense right? Too much of it, reduce the sensitivity. Not enough of

it, increase the sensitivity.

> > >

> > > Low levels actually making one more sensitive to drugs and high levels

making one more tolerant.

> > >

> > > In this case we have become so tolerant that we are tolerant to our own

natural levels of serotonin.

> > > Technically the serotonin receptors should up regulate on withdrawal of

the drug but why should they if they are feeling the right amount of serotonin?

They only up regulate if they are required to up regulate if the brain is

feeling a lack of stimulation.

> > > For example MDMA users will experience a huge influx of serotonin followed

by down regulation and then massive serotonin depletion in the following weeks

followed by a responsive up regulation. This is shown in studies with rats.

> > > Ssris however work in a different fashion however jamming unnatural

amounts in the synapse which our brains cannot immediately respond to which

accounts for " start up " effects of massive down regulation in the first few

weeks until the brain adapts. This explains why people may only get sexual

dysfunction after multiple ssri exposures. Some people may get the same effect

after one exposure- possible low receptor number to start with. And possible

some individuals can go on and off the drugs with very little side effects due

to naturally low serotonin- therefore receptor levels will bounce back.

> > >

> > > So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

> > >

> > > As far as I can see there is only one drug that can cause this, a drug for

high blood pressure Reserpine? Any thoughts on this?

> > > Studies show it increases the response to other drugs such as lsd.

> > >

> >

>

June 19, 2012

Hi, Have you tried any of these drugs.

> > > >

> > > > We know that there is serotonin receptor down regulation due to

overexposure to serotonin.

> > > >

> > > > We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

> > > >

> > > > Makes sense right? Too much of it, reduce the sensitivity. Not enough of

it, increase the sensitivity.

> > > >

> > > > Low levels actually making one more sensitive to drugs and high levels

making one more tolerant.

> > > >

> > > > In this case we have become so tolerant that we are tolerant to our own

natural levels of serotonin.

> > > > Technically the serotonin receptors should up regulate on withdrawal of

the drug but why should they if they are feeling the right amount of serotonin?

They only up regulate if they are required to up regulate if the brain is

feeling a lack of stimulation.

> > > > For example MDMA users will experience a huge influx of serotonin

followed by down regulation and then massive serotonin depletion in the

following weeks followed by a responsive up regulation. This is shown in studies

with rats.

> > > > Ssris however work in a different fashion however jamming unnatural

amounts in the synapse which our brains cannot immediately respond to which

accounts for " start up " effects of massive down regulation in the first few

weeks until the brain adapts. This explains why people may only get sexual

dysfunction after multiple ssri exposures. Some people may get the same effect

after one exposure- possible low receptor number to start with. And possible

some individuals can go on and off the drugs with very little side effects due

to naturally low serotonin- therefore receptor levels will bounce back.

> > > >

> > > > So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

> > > >

> > > > As far as I can see there is only one drug that can cause this, a drug

for high blood pressure Reserpine? Any thoughts on this?

> > > > Studies show it increases the response to other drugs such as lsd.

> > > >

> > >

> >

>

June 20, 2012

No but Lezozotan is the next on the list. It's ordered and on the way. I'm also

interested in the HT52C antagonist called Latrepirdine (Dimebon). That

combination is the most selective that I can see.

You can buy any of these drugs from China, though I can't vouch for the purity.

Sorry but it's a crap shoot.

Go to www.tradekey.com and type in the chemical you want to purchase. You'll get

40 emails the next day from suppliers who want to sell them to you. Most of

these companies manufacture " intermediate pharmaceutical chemicals. " You can

have something tested for purity here in the states, but it will cost you 2,000.

Take very small doses. Be careful.

Thanks,

Jed

> > > > >

> > > > > We know that there is serotonin receptor down regulation due to

overexposure to serotonin.

> > > > >

> > > > > We know that there is serotonin receptor up regulation in people with

chronically low levels of serotonin (such as suicidal and those that are

clinically depressed).

> > > > >

> > > > > Makes sense right? Too much of it, reduce the sensitivity. Not enough

of it, increase the sensitivity.

> > > > >

> > > > > Low levels actually making one more sensitive to drugs and high levels

making one more tolerant.

> > > > >

> > > > > In this case we have become so tolerant that we are tolerant to our

own natural levels of serotonin.

> > > > > Technically the serotonin receptors should up regulate on withdrawal

of the drug but why should they if they are feeling the right amount of

serotonin? They only up regulate if they are required to up regulate if the

brain is feeling a lack of stimulation.

> > > > > For example MDMA users will experience a huge influx of serotonin

followed by down regulation and then massive serotonin depletion in the

following weeks followed by a responsive up regulation. This is shown in studies

with rats.

> > > > > Ssris however work in a different fashion however jamming unnatural

amounts in the synapse which our brains cannot immediately respond to which

accounts for " start up " effects of massive down regulation in the first few

weeks until the brain adapts. This explains why people may only get sexual

dysfunction after multiple ssri exposures. Some people may get the same effect

after one exposure- possible low receptor number to start with. And possible

some individuals can go on and off the drugs with very little side effects due

to naturally low serotonin- therefore receptor levels will bounce back.

> > > > >

> > > > > So question is why aren't we trying to cause a sustained depletion of

neurotransmitters to encourage up regulation of receptors???

> > > > >

> > > > > As far as I can see there is only one drug that can cause this, a drug

for high blood pressure Reserpine? Any thoughts on this?

> > > > > Studies show it increases the response to other drugs such as lsd.

> > > > >

> > > >

> > >

> >

>

June 20, 2012

You may wan to look at these . . .

Iloperidone

Mianserin (Bolvidon, Depnon, Norval, Tolvon

Mirtazapine (Remeron, Avanza, Zispin)