Physiology of prolonged sex: opiate use

[StrawPipes]

Can anyone explain to me how opiates prolong sex be decreasing the urge to ejaculate?

In a physiological sense please.

I'm curious because I've read that some SSRI's are prescribed to treat some sort of premature ejaculation and thought got me thinking; if someone knows why opiates prolong sex than couldn't a drug be synthesized to the act accordingly?

 

[Hammilton]

They decrease CNS activity, dulling sensation.

I haven't bothered to look, but I would imagine that all CNS depressants would produce this effect to some degree. It might be that only those specifically dulling physical sensation (vs. the sedative-hypnotics, some of which actually increase pain) like NMDA antagonists (those with limited DARI activity) would cause this effect.

 

[seep]

Hyperprolactinemia.

Physiological info here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376090/?tool=pmcentrez

and here:

http://www.acnp.org/asset.axd?id=ac72a80f-ddc7-4473-9100-2e6d92a9d845

 

[negrogesic]

Opioids are analgesics and decrease physical sensation. Yes, there are other mechanisms but this is a major one. NMDA antagonists do a similar thing, but add a weird psychological component not present with opioids...

 

[StrawPipes]

So wouldn't it be possible to synthesize some compound for premature ejaculation? Cause I heard or read somewhere (can't remember) that a substantial amount of males suffer from pre-mature ejaculation. And you would think that if their are so many different substances that cause prolonged sex, then couldn't they figure something out that treats that problem specifically and that are not used for other treatments?

Sorry, I'm still learning and it makes me curious if there are drugs specifically for pre-mature ejaculation. I remember reading a post a while back on bluelight and people responded the best way to beat it is just keep doing it with your partner. Well that was the main response. So I'm curiouse if there is a substance synthesized specifically for it.

 

[kolokol1]

Hyperprolactinemia.

Only opiate I've ever taken is codeine but I can tell you're an idiot. The mechanisms suggested in your artiles are retarded. Really the only significant effect of opioids is strongly decreasing oxytocin and generally decreasing other hormones- testosterone, estrogen, LH, etc. From what I understand from your articles- the only mechanism opioids would ever increase prolactin is because they decrease estrogen, and estrogen modulates (decreases) prolactin secretion.

But there's no way most opiates cause increase in prolactin because most opiates, especially the morphine-skeleton ones, are quite strong dopamine agonists. And as you well know dopamine is probably the most powerful thing for decreasing prolactin, dopamine agonists are the treatment for hyperprolactinemia.

 

[Nagelfar]

I always figured the firing mechanism of electrical impulses take more to 'initiate/initialize'; so the spinal reflux that causes orgasm/ejaculation takes more stimulation to fire.

I notice the onset feeling of orgasm, if tried to be reached at certain levels of opiate tolerence, feels more drawn out; sometimes you can "lose it" part way through which is highly frustrating; but the orgasm rush is distinguishable as in slow motion; with portions of it noticeable in the chain of events leading up to actual fluid release....

Mainly orgasm is instantaneous or near so; under opiate influence the build up of the function can be felt from beginning to end; and stopped intentionally or not. A rather interesting state of affairs.

...Interesting especially for understanding yourself as a human body and the intricate warmth feeling building up just prior to orgasm. Sometimes it can be highly more pleasurable to be reached at moderate opiate tolerances. At high tolerances it just seems frustrating; but can be reached, there is little enjoyment because it is more mechanistic in reaching that point and just a chore, due-to / from-the slow, 'less than stroll paced' build up to the orgasm rather than regular running/sprint or middle of the road opiated brisk walk from external stimulation to the onset of orgasm which can be extended pleasure.

 

[seep]

But there's no way most opiates cause increase in prolactin because most opiates, especially the morphine-skeleton ones, are quite strong dopamine agonists. And as you well know dopamine is probably the most powerful thing for decreasing prolactin, dopamine agonists are the treatment for hyperprolactinemia.

One of the most well-known and extensively-documented hormonal effects of acute opiate administration is a sharp spike in serum prolactin, and excess prolactin activity (and all the subsequent androgenic deactivation) is the cause of the sexual side effects brought about by SSRIs. As far as the dopamine-prolactin interplay in chronic opiate use, the Kreek article states:

t has been repeatedly shown in heroin addicts
that the short acting -opioid agonist heroin will cause a
prompt increase in serum prolactin levels, resulting directly
from an abrupt lowering of dopamine levels in the tuberoinfundibular
dopaminergic systems (85).In humans, and to a
greater extent than in rodents, prolactin release is essentially
solely under tonic inhibition by dopaminergic tone in the
tuberoinfundibular dopaminergic system.However, it was
found that during chronic methadone treatment, there is
adaptation or tolerance to this phenomenon, an attenuation,
but not a complete removal or ablation of this response
caused by dopamine lowering and resulting in elevation of
serum prolactin levels (85).Even during long-term methadone
maintenance treatment, as reported in 1978, it was
found that peak plasma levels of the -opiate agonist methadone
are related temporally to the peak plasma levels of
prolactin (85).These findings suggest that the long-acting
opioid methadone administered orally continues to have
an impact at least on the tuberoinfundibular dopaminergic
system, with a lowering of dopaminergic tone, resulting in
a modest increase of prolactin levels, although not exceeding
upper levels of normal. However, that attenuation occurs
suggests that there may be either a lowering of dopaminergic
levels and tone in the turberoinfundibular dopaminergic
system of that region or, alternatively, an attenuation of
responsivity of the -opiate-receptor system.It has been
shown that the -opiate-receptor system similarly plays a
role in modulating prolactin levels in humans (86).In normal
healthy volunteers, dynorphin A causes a prompt rise
in serum prolactin levels, resulting again presumably from
a lowering of dopaminergic tone in the tuberoinfundibular
system (86).This is a , but also a -opioid-receptor effect,
as documented by use of two different opioid antagonists
with different receptor selectivity (86).

Simply put, reward-circuit dopamine stimulation in the mesolimbic pathway is beside the point. The tuberoinfundibular pathway is responsible for prolactin regulation. The relevant feeling should be familiar to anyone whose suffered chronic opioid addiction: it's as if you're constantly in a post-orgasmic sexual refractory period.

 

[wickedlester1]

lortabs hydrocodne also prolong erection you can go like a champ

 

[leungkachong]

This thread is also COMPLETELY missing any information on the relationship between the periaqueductal grey (ie central grey) and sexual arousal/lordosis/etc. I believe that opioids acting here (ie - one of their MAIN sites of action) explains the distinct asexual effects of opioids over other sedatives... much more the hyperprolactinergic effects, especially considering how long it takes for steroid hormones to have their effects via binding to/acting as transcription factors!

I also believe that the sexual arousal and lordosis/ejaculation+erection role of the periaqueductal grey is the best candidate for explaining the extreme increase in nocturnal emmisions in males during withdrawal (rebound hyperactivity in PAG)... as the effect occurs FAR to fast to be accounted for by hormonal pathways.