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Is E sexually transmitted?

Ahhh... Behavioural Pharmacology is such a soup. I'd be surprised if you could find a receptor in the brain that if you fucked with, didn't alter ejaculatory responses. There's evidence that 5-HT1 and 5-HT2 receptors play a part, but its very hard to tell how.

It classical idea is that parasympathic nervous system activity (possibley M3 receptor) leads to erection, parasympathic via alpha receptors leads to ejaculation. That makes sense evolutionarily, because you would want to be relatively calm before you busted out the spam javalin, so that say, you didn't try and start fucking in the middle of a fight... but meanwhile, if you were in the groove, and you got a fright, you'd bust your load just before you you ran away.

Meanwhile, the most recent multifactorial explanation I've heard was something like, dopaminergic stimulation causes an activation of the raphe serotonergic neurons which in turn enhances the septo-hippocampal cholinergic pathway and results in expression of penile erection. But don't ask me...


hang on, what was the question again?
 
wow now i know why my girlfriedns pupils always looked gloomy and cuddly like after sex and they were larger pupils too...cool i just learned that
 
this is a shit thread, in my opinion i dont think ud get enough from your saliva to get you high

fuck sake if you could i wouldnt bother buying my drugs - id just find a pillhead to kiss
 
^^ Haha, you think this is a shit thread compared to most of the recent threads? At least in this thread we have some good discussion going about neurochemistry and whatnot.
It's pretty obvious that you aren't likely to get high through bodily fluids, but the second half of the thread that deals with the characterists of an orgasm and how it can be related with feeling high is some good stuff.
 
oh yeah, i know where your coming from with that - i wouldnt have read the whole thread if it was that poo :P it has got some good information, i meant it is shit in the way that if you could get high off swapping spit with a pilled up stranger why would anyone buy theyre drugs
 
So if I ate my semen, I'd waste less of my E?

What a fucking stupid question. The volume of an average guy's ejaculate is only about a teaspoon. Use some common sense FGS; it wouldn't even cause a positive test for the drug.
 
OlympiaMan, that is a stupid question, i think if you ate your semen you might be gay (not that there is anything wrong with it)...

Bilzor, I was wondering how much of mdma makes it through BBB per 100mgs is ingested/insufflated...
 
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C10H12N20 said:
OlympiaMan, that is a stupid question, i think if you ate your semen you might be gay (not that there is anything wrong with it)...

Ever heard of sarcasm?
 
BilZ0r said:
Ahhh... Behavioural Pharmacology is such a soup. I'd be surprised if you could find a receptor in the brain that if you fucked with, didn't alter ejaculatory responses. There's evidence that 5-HT1 and 5-HT2 receptors play a part, but its very hard to tell how...
I couldn't agree more!


mrsumone said:
... Gert Holstege, announced that his brain scans of orgasm resemble the brain scans of a shot of heroin. http://www.jneurosci.org/cgi/content/abstract/23/27/9185
...
Great reference mrsumone!


Folks,

There has been several neurochemical processes described earlier in this thread and spoken in the voice of "fact." I don't mean to sound rude, but there is almost nothing known for certain about the neurochemistry of the human sexual response. All of this talk of certainty, and what in fact actually occurs, is smoke and mirrors (sorry).

If I am being arrogant and am wrong, then please prove it by providing a link to authoritative scientific references available over the net. Citations quoted from books alone don't cut it (sorry). Anything published on this subject will be widely available from authoritative scientific references and journals on the net.

There has been so little done on this topic, and that is because it is almost impossible to get such a study funded. :\

There are some pieces to the puzzle available, especially regarding 5HT receptors, erectile dysfunction and anorgasmia. And part of the reason that is somewhat understood is due to the wide use of SSRIs and the sexual side effects they produce. In fact, what has been gained in understanding from SSRI enduced sexual side effects, has resulted with one drug company currently working on a treatment for PE (premature ejeculation) with an SSRI based compound.

I've been following up just about everything I can come across regarding neurobiology, neuropharmacology and sexual response for quite a number of years. It's really frustrating because so little has been done.

Now if anyone would please help me make an ass out of myself, and provide solid references to these claims showing that they are grounded in scientific fact, I would be forever grateful.

.
 
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Invalid Usename,

I think you bring up a good point, i also think that is why this subject is very interesting... Has anybody seen the movie "Dopamine" by the way? The main hero there is describing chemical processes in the brain in that movie, like he knows exactly what's going on, other than that, i think that movie is intellectually stimulating.
 
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I was hoping that Decibel would have had second thoughts and deleted this post. :\
Decibel said:
^^^ This was pulled directly from my neuroscience text book, minus citations, because that would take too long to type. If anyone really wants those, I'll edit my post and include a bibliography of the cited parts.

"Biological Psycology" 8th. ed.; Kalat, James. W


"In moderate concentrations, dopamine stimulates mostly type D1 and D5 receptors, which facilitate erection of the penis in the male and sexually receptive postures in the female. In higher concentrations, dopamine stimulates type D2 receptors, which lead to orgasm. The effects at D1 and D2 receptors tend to inhibit each other. As a result, the early stages of sexual excitement are characterized by arousal but not orgasm; the late stage is marked by orgasm and then a decrease in arousal.

Whereas dopamine stimulates sexual activity, the neurotransmitter serotonin inhibits it, in part by blocking dopamine release. Many popular antidepressant drugs increase serotonin activity, and one of their side effects is to decrease sexual arousal and impair orgasm."

I will post my stipulations later. Right now, I have to go to class...

...discuss amongst yourself.
~Decibel

Decibel,

I have no idea who you expect to impress with all of this, but you're making all of this crap up. (See me post at the top of this page.) :X

Most of what you are claiming (not only in this post but in the one before that as well) not only hasn't been established in neurophysiology, but you are speaking of neurotransmitter concentrations as if they fit into drug action models. Neurotransmitters are not drugs, and speaking of them as if they are amounts to being pretty clueless about all of this. 8(


"Many popular antidepressant drugs increase serotonin activity, and one of their side effects is to decrease sexual arousal and impair orgasm."

Give me a break! 8)

Not only is this utter crap, but it isn't even close to what is known to be actually occurring. VelocideX has even provided some useful scientific references in this thread related to the clinical side effect of SSRIs, and I've included others in my paper on Viagra and MDMA.


I think what amazes me the most is that you are claiming to have found all of this "information" ("information" which is currently beyond the limits of established neurophysiology), came out of an undergrad textbook on "Biological Psycology" (it's spelled "psychology" with an "h", BTW).

What did you intend to gain by making something like this up and claiming it was in one of your text books? Did you actually want everyone who accepted it to carry with them a false understanding of neuroscience??? :|


.
 
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Yes, you know, Invalid, because I really don't have anything better to do than fawn for your complete and absolute approval with every waking moment of my day. That is all I do. No. Really.

I will admit that my posts are written matter-of-factly, and for that I apologize. In truth, everything I've written has to be my perception of our subject matter's inner workings. Without a full working lab and years upon years of research and experience, we are all, for the most part, spitting out what we've heard or learned before. If what I said was incorrect, invalid, etc. why. wasn't. it. addressed. when. I. wrote. it.

And on top of that, I posted hoping for intelligent discussion, whether or not I was correct. I didn't expect you to wonderfully attack everything I posted, accuse me of trying to impress someone when really I was hoping to learn about the subject at hand (while attempting to add what I could to the conversation), and still not explain to me why my posts were incorrect.

And I'll scan those pages out of my textbook for you. Yes, it's an undergrad textbook, but does that mean that the basics of what is contained inside are any less valid than if those basics were then stated in a professional resource manual or something of the likes?
~Decibel
 
I have no reason to doubt that the disputed citation came from the source stated. Unfortunately, the edition which is cited is currently discharged from my university libraries, so I can not personally verify the claim.

The statement "Many popular antidepressant drugs increase serotonin activity, and one of their side effects is to decrease sexual arousal and impair orgasm" is absolutely correct.

When it comes to what have been termed neuromodulators, it is common to speak of concentration dependent effects, especially when talking about dopamine. To cite from a very not-undergraduate text book, the 4th ed of Psychopharmacology: "It is noteworthy that dopamine binds to the D3, D4, and D5 receptors with nanomolar or submicromolar affinity constants, while its corresponding constants for the D1 and D2 receptors are in the micromolar ranges".

Now while this disagrees with what Kalat is reported to have written, it still reinforces the ideas behind concentration dependent effects of neurotransmitters. Indeed, one should look at Hoyer et al., 1994 and their congress on serotonin subtypes published in Reviews in Pharmacology if you want to see some nearly 50 fold differences in affinities.

Indeed, with volume transmission a nearly universally accepted phenomena, it is part of innate physics of the system that diffusion will produce a gradient of dopamine from a single point source which will reach several tens of µM and last for several hundreds of ms. Hence, concentrations of dopamine must change.

Meanwhile, if you have actual proof that the 8th ed. of Biological Psychology doesn't say that, then submit it.
 
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BilZ0r,

I'm far less concerned about the implied neurochemical actions being described through a drug action model, than I am the claim that human sexual function has been established to this degree in neurophysiology.

No I don't have access to the book. And my "proof" is in the fact that almost nothing is known about the neurophysiology of sexual function, and far from what Decibel claims to be available in his undergrad book.

In fact, one of the neurophysiologists I worked with from NIH is now over at Pfizer. I'm certain that he'd love to know these "established" findings on the neurochemistry of human sexuality. They're looking for a neurochemical approach that will reliably produce an increase in sexual arousal. I last winter when I spoke with him they weren't having much luck.

Show me, show me where human sexual function is understood to this degree in neurophysiology. This isn't something so trival that the established references and journals couldn't be bothered to include. Quite the opposite.

8)
 
Invalid Usename:
It is always interesting when academic world meets business world. Having worked with venture capitalists i can say that scientists are always ahead of business people by like 20 years. Scientists always claim things like they exist for a fact and business people always bitch how scientists are outthere and do not understand how the real world works. The reality I think is that both you and Decibel are probably right. I am sure there are theories and studies that show how the sexual function works, but it is definitely not sufficient for commercial (real world) application.

I bet you your friend at Pfizer is racking his brain over this competing drug:

http://psa-rising.com/wiredbird/abbott-uprimaj0601.htm

...works as dopamine agonist.

Seems like Abbott guys found a way to put science to real life. BTW my friend tried it and he says it worked great.
 
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C10H12N20,

Abbott has been working with this for a while, and were in Phase III trials of the drug back in late 2001. I don't personally know anyone over at Abbott, but I'd bet that they aren't completely sure why it works on ED in some patients.


The thing is, if anyone can just make any wild claims they want to, especially when they aren't consistent with the current science, then the quality of information here goes down to the level of supermarket tabloids: eye witness claims about alien crafts see at Area 51, a "secret third strand" on the DNA chain that everybody missed and "the government" is hiding from us, just name it. 8(

I'm not involved in the business world, my perspective is from government public health research. I also spent some time working in several antidepressant research projects specifically in a government neurophysiology lab. And I have far more than a passing interest in how the human sexual response is mapped neurologically. There's hardly a damn thing known about it, and mention sexuality when you are trying to get such a project funded and you end up getting shut out. It's only been since the new ED treatments have made such a big hit on the market that pharmaceutical have started investing is such research. All of their findings remain outside of established science, and in the realm of proprietary information.

Pfizer just did an extensive study, which they completed earlier this year, that involved PET imaging of the limbic during sexual arousal. They found that the male and female sexual response was rather different and involved different regions. But other than some vague references in the public media (essencially Pfizer thumbing their noses at the competition), all of the study is maintained as strictly proprietary information owned by Pfizer.
 
Invalid Usename,
Correct me if I am wrong, but that is how antidepressant R&D works: throw it on the wall and see if it sticks. Most of the prescribing info for antidepressants says "exact mechanism of action is UNKNOWN"... I am not even sure if we know exactly all of the 5HT subreceptor functions, because I keep seeing different (inconsistent) descriptions... I doubt pharmaceutical companies do either... So in that regard I hear you loud in clear, there is just theories, but on the other hand, we still have drugs that are based just on theories and trials (but no mechanism known) and we got some people benefiting from these drugs. So I guess after all, we dont have to know everything exactly for things to work. At the end if we did know everything about us, then we would "see the world through creator's eyes"...

I am really getting excited about shit you guys are talking about here, I might go back to school and get some degree in neuroscience in addition to my MBA... Anybody has advice on what is like the major to take to learn all this shit you talk about...
 
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