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    Selective Dopamine Reuptake Inhibitors and Sexual Arousal 
    #1
    Direct dopamine agonists like the anti-Parkinsons drug pramipexole are known aphrodisiacs different from ED drugs like PDE inhibitors. Prami is actually the only drug specifically approved by the US FDA to treat lack of sexual libido ie lack of psychological sexual arousal. Incidentally, it also has the rather embarrassing side-effect of making 80 years old Parkinsons disease patients compulsively masturbating publicly in retirement homes while talking dirty. Or turning old ladies who never gamble in their entire life into compuslive gamblers, sometime gambling away the family house and retirement savings.. Rather strange side-effects of DA agonism!! (google Parkinsons hypersexuality gambling ) or check this out:
    Warn families of risk of sex and gambling addictions with Parkinson's drugs, doctors told The families of Parkinson's sufferers must be warned about dangers of sex and gambling addictions caused by drugs used to treat the disease, doctors have been told.

    New NHS guidelines, due to be released next month, include impulse control disorders for the first time, stating that health professionals should discuss the potential for dramatic change in behaviour with the "family and carers" as well as the patient....
    Note that the effect is not the same as that of ED drugs which target the physical erection aspect. It is the the mental aspect, the arousal phase of sexual behavior originating from the brain. Rats on prami have an increase in humping and jerking off (pardon the term) of at least 200% compared to their sober littermate control [ref].

    Now my question is: Can a selective Dopamine Reuptake Inhibitor (or releaser) have the same effect as direct DA agonists in inducing sexual arousal ? The reason beiing that selective DRIs may not have the other effects of direct DA agonists such as pucking or turning into a big time gambler.. Obviously, it is well known that non-selective SNDRI inhibitors like cocaine have sexual arousing aphrodisiac effects. But with cocaine and related SDRIs, the Serotonergic activity has the paradoxical effect of blocking the sexual arousal effect induced by DA uptake blockade. Kind of like a sexual arousal push-pull between DA push and SERT pull. This is not unexpected since SSRIs are notorious in inducing psychological sexual dysfunction.
    So the question is: would selective DRIs (DRAs) or at least selective DNRI/A have the sexual arousal effect of D2 agonists but without the sexual arousal blocking serotonergic and the emesis (vomiting) inducing effect of direct D2 agonists?
    ps: come to think of it, note that unlike Serotonin and NE, so far in the literature no selective DA releaser DRA has been described afaik .. wonder what kind of pharmacological effect a Selective Dopamine Releaser would have? not a Reuptake inhibitor but a Dopamine Releaser
    Last edited by DotChem; 13-04-2017 at 02:04.
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    #2
    i started pramipexole for its proposed aphrodisiac effects at one point, all it did was make me super sleepy and sedated. how the hell can it work like this, its almost like a benzo. is this unique case??
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    #3
    I was asking in just another thread how there is the effect of sedation with DA agonists - in contrast to their stimulant effect when applied through reuptake blocking.

    Is it not just two roads to the same destination?

    But apparently not.

    Prami is taken for restless leg syndrome, usually at night due to its sedation.

    Where as NDRI's like bupropion, of course, NOT at night, due to it's activation.

    So - I would like this question answered also.
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    #4
    MDPV for the win
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    Bluelighter Cotcha Yankinov's Avatar
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    Quote Originally Posted by JohnBoy2000 View Post
    I was asking in just another thread how there is the effect of sedation with DA agonists - in contrast to their stimulant effect when applied through reuptake blocking.

    Is it not just two roads to the same destination?

    But apparently not.

    Prami is taken for restless leg syndrome, usually at night due to its sedation.

    Where as NDRI's like bupropion, of course, NOT at night, due to it's activation.

    So - I would like this question answered also.
    DA agonists may act differently in Parkinson's patients because they may not have as many autoreceptors for prami to bind to. Those dopamine releasing/autoreceptor expressing cells have degenerated but there are still dopamine receptors expressed post synaptically on ie GABA cells for prami to act upon. While in a normal person prami may act on autoreceptors to reduce presynaptic dopamine release.
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    Quote Originally Posted by asecin View Post
    i started pramipexole for its proposed aphrodisiac effects at one point, all it did was make me super sleepy and sedated. how the hell can it work like this, its almost like a benzo. is this unique case??
    No, that's one of the most common side-effects. You probably took too much, didn't taper up, and took it at the wrong time of day.
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    #7
    Personally I found that both NDRIs (Ritalin & EPH (which is supposedly more selective for DA)) and releasing agents (speed, MPA, thiopropamine) effectively annihilated both my sex drive and my ability to get an erection. I realise I may be an unusual case compared to the usual/expected response, but I never got any pro-sexual effects at all from these types of drugs.
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    #8
    Quote Originally Posted by asecin View Post
    i started pramipexole for its proposed aphrodisiac effects at one point, all it did was make me super sleepy and sedated. how the hell can it work like this, its almost like a benzo. is this unique case??
    Yes, Pramipexole is quite sedating at therapeutic doses ie within the range for dopaminergic effect (eg to treat PD, RLS or for sexual effect). And that is because the drug has a pretty dirty pharmacology binding bunch of targets in addition to Dopamine receptors. So it may not be the best for recreational sex.

    A good alternative would be Ropinirole or even Piridibil. Both are D2/D3 agonists with better profile than prami. AFAIK they are not sedating, and have the same sexual effects as prami. Ropinirole is sometimes prescribed "off-label" to treat sexual dysfunction induced by SSRIs use. Keep in mind though Ropirinole or Priribedil are not officially approved for their sexual effect; only for treatment of PD or RLS. They both have the same hypersexual or compuslive gambling effect as prami in PD. A word of caution: as I mentioned, in PD patients at least, some develop hypersexuality but other develop compulsive gambling while on the drug. Other develops both: like this Frenchman PD patient who sued the company GSK maker of Ropinirole and won: he claims he will engage in compulsive promiscuous sex non stop and gamble excessively while on the medication until he stopped using the drug. Whether it worked for non-PD persons, I don't know (AFAIK no study has looked at the sexual effect of DA agonist in non-Parkinsons individuals...So proceed with caution!
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    #9
    Is anything known about residual compulsions after stopping direct dopamine agonists?
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    #10
    Quote Originally Posted by asecin View Post
    i started pramipexole for its proposed aphrodisiac effects at one point, all it did was make me super sleepy and sedated. how the hell can it work like this, its almost like a benzo. is this unique case??
    Dopamine agonists are known for producing somnolence, which is different from sedation, or even drowsiness IME although its often compared to it. And I've taken my fair share of dopamine agonists, and while for me, they reduce the refractory period and make it easy to get an erection(which sometimes won't go away, not to the degree of viagra or something though) but they never made me compulsively seek out sex(but can make it GREAT) or masturbation, I don't know what the literature says about this but from what I have seen the compulsive behaviors described above are anecdotal and usually involve elderly patients.(I know the literature says they can produce compulsive behaviors, but to the degree and how outside social norms the actions are seem to involve the elderly more often, I don't know if this is because of changes in the dopamine system of elderly patients or a simpe lack of inhibition)
    Last edited by Coolwhip; 20-04-2017 at 12:59.
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    #11
    Quote Originally Posted by immad View Post
    Is anything known about residual compulsions after stopping direct dopamine agonists?
    afaik the compulsive behavior stops with cessation of DA agonists therapy and revert to baseline. At least with Parkinson's disease patients whose partners report the matter to the treating physician since they're the only one who can tell the difference between the compulsion and baseline. When it comes to sex, quite delicate issues!
    M: "euhh.. doc! I can't take it anymore (no pun intended!), J has gone incredibly wild since his last visit..
    Doc: Wild? how so .."
    M: see doc, we use to have sex 3-4 times a week..but J is now wanting like 4 times a day sex every single day ..blablabla you get the point..)

    I am not sure if any study has looked specifically at the long term effect of DA agonits on Compulsive behavior. And that's because DA therapy for PD patients is chronic so there is no control group to compare to. So it is hard to tell what might happen with non-PD people occasionally using DA agonists for recreational sex


    Quote Originally Posted by Coolwhip View Post
    ...I don't know what the literature says about this but from what I have seen the compulsive behaviors described above are anecdotal and usually involve elderly patients.(I know the literature says they can produce compulsive behaviors, but to the degree and how outside social norms the actions are seem to involve the elderly more often, I don't know if this is because of changes in the dopamine system of elderly patients or a simpe lack of inhibition)

    In fact it is more than anecdotal; it is pretty well documented. And actually, it is more prevalent with younger PD patients rather than olders!!
    Prevalence of hypersexual behavior in Parkinson’s disease patients: Not restricted to males and dopamine agonist use

    Abstract: This study investigates the prevalence and demographic characteristics of hypersexuality in Parkinson’s disease (PD). Impulse control disorders in PD patients have been associated with dopamine agonist therapy. Moreover, hypersexuality and pathological gambling have been associated with males, while females may be inherently thought to be more likely to participate in compulsive shopping and binge-eating behaviors. In this study, a screening mail-in survey was sent to all PD patients at a single Movement Disorders Center. One hundred forty one of 400 (35.3 %research packets were returned completed. Fifteen of 141 patients met initial screening criteria for hypersexual behavior. After detailed interview, only 6/141 (4.3 % of PD patients met criteria for pathologic hypersexual behavior. These behaviors included: compulsive masturbation, prostitution, and paraphilias. Patients with a younger age of PD onset were more likely to exhibit hypersexual behavior. Unlike previous report, no significant association was found between hypersexuality and gender or dopamine agonist use. Rather, this study suggests that physicians should be vigilant for hypersexual behavior in all PD patients, regardless of gender and PD medication regimen. Ultimately, given the innate sensitivity of the topic and survey limitations, it is very likely that hypersexual behavior in our cohort, as it is in the general PD population, has been under-reported. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840579/
    Note that much of the clinical studies are looking at Pathological Compulsion on DA agonist as opposed to non-Pathological compulsive behavior. I mean, if somebody with no history of excessive sexual libido suddenly start craving sex and masturbating every 10-15min non-stop for 24 hours straight while taking the drug now that's pathological! On the other hand, nobody would pay any attention if someone who use to have daily sex is now having sex twice a day on DA agonist (a huge 100% increase but nothing to worry about, isnt it? So it wont show on the statistics reported in these studies.


    here are few more studies that are specific on the hypersexual side-effect of the drugs
    Pramipexole and Compulsive Masturbation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880944/
    The role of dopamine in risk taking: a specific look at Parkinson’s disease and gambling https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038955/
    A Case of Sleep Masturbation Related to Dopamine Agonist Therapy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3466025/

    Keep in mind, these are underestimated since hardly patients will respond to survey and admits they engage in compulsive sex or gambling. Actually they may not even connect the behavior to the drug (DA agonist) use. Usually, only the patient partner or people close to him/her will be aware of the change in behevior.
    And once again. keep in mind all the studies are for the effect of DA agonist on Parkinson's Disease patients.

    EDIT: One more study looking at the prevalence of hypersexuality among PD patients:

    Frequency of New-Onset Pathologic Compulsive Gambling or Hypersexuality After Drug Treatment of Idiopathic Parkinson Disease https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665974/
    Abstract:

    OBJECTIVE: To determine the frequency of new-onset compulsive gambling or hypersexuality among regional patients with Parkinson disease (PD), ascertaining the relationship of these behaviors to PD drug use.


    PATIENTS AND METHODS: We retrospectively reviewed the medical records of patients from 7 rural southeastern Minnesota counties who had at least 1 neurology appointment for PD between July 1, 2004, and June 30, 2006. The main outcome measure was compulsive gambling or hypersexuality developing after parkinsonism onset, including the temporal relationship to PD drug use.


    RESULTS: Of 267 patients with PD who met the study inclusion criteria, new-onset gambling or hypersexuality was documented in 7 (2.6 % )All were among the 66 patients (10.6 % )taking a dopamine agonist. Moreover, all 7 (18.4 were among 38 patients taking therapeutic doses (defined as ≥2 mg of pramipexole or 6 mg of ropinirole daily). Behaviors were clearly pathologic and disabling in 5: 7.6% of all patients taking an agonist and 13.2% of those taking therapeutic doses. Of the 5 patients, 2 had extensive treatment for what was considered a primary psychiatric problem before the agonist connection was recognized.


    CONCLUSION: Among the study patients with PD, new-onset compulsive gambling or hypersexuality was documented in 7 (18.4 % of 38 patients taking therapeutic doses of dopamine agonists but was not found among untreated patients, those taking subtherapeutic agonist doses, or those taking carbidopa/levodopa alone. Behaviors abated with discontinuation of agonist therapy or dose reduction. Because this is a retrospective study, cases may have been missed, and hence this study may reflect an underestimation of the true frequency. Physicians who care for patients taking these drugs should recognize the drug's potential to induce pathologic syndromes that sometimes masquerade as primary psychiatric disease.
    Last edited by DotChem; 20-04-2017 at 21:33.
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    #12
    Clearly I was wrong about it being anecdotal, but I didn't look at those studies too closely, but they all seemed to involve PD patients and I didn't see any clear evidence that it affects young people more than old ones(especially since PD seems to develop in older patients more than young). And I'm no clinician but those some off those studies seemed like small sample sizes, were case studies, or the side effects involved less than 10% or even 5% of patients, some of whom were taking rather large doses.

    I'm not arguing that dopamine agonists can't have those effects, but I'd like to see some double-blind controlled large sample studies involving otherwise healthy individuals before I concur that dopamine agonists are going to cause compulsive sexual behaviors in large portion of the general population taking relatively low doses.
    Last edited by Coolwhip; 21-04-2017 at 18:34.
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    #13
    Is there any indication or research suggesting that direct dopamine agonists could have positive effects on people who were nonresponders are had negative reactions to indirect dopamine agonists (i.e. NDRIs, NDRAs and selective DRIs)?
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    #14
    Bluelighter Cotcha Yankinov's Avatar
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    Quote Originally Posted by Coolwhip View Post
    I'm not arguing that dopamine agonists can't have those effects, but I'd like to see some double-blind controlled large sample studies involving otherwise healthy individuals before I concur that dopamine agonists are going to cause compulsive sexual behaviors in large portion of the general population taking relatively low doses.
    My guess would be that the doses of a DA agonist would have to be above the lower range to cause hypersexuality in a normal person (in order to outpace their autoreceptor activation), whereas most of the binding will be post-synaptic at all doses in Parkinson's patients (who lack autoreceptors and probably have sensitized postsynaptic dopamine receptors anyways)
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    Prami is a strange medication.



    I've used it to lower prolactin in the past. But the side effect most notable was the short refractory periods. I could orgasm then be ready with a hard on less than 1 minute later, it was crazy lol.

    FOR ME, rather than have the sexual urge it was more of just my dick would get hard and wouldn't go down until I orgasmed, then it would come back within a minute. I wasn't overly "in the mood" though..

    Be careful though when first starting it because you need to taper up like .2mg the first few days. I made the mistake of taking .5mg the first time and was wrapped around the toilet about to puke all while having an erection...

    It makes you feel tired but when you try and sleep you just toss and turn and can't ever fall asleep.




    Very strange, but your body adjusts quickly.
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    #16
    Quote Originally Posted by Ozle View Post
    Is there any indication or research suggesting that direct dopamine agonists could have positive effects on people who were nonresponders are had negative reactions to indirect dopamine agonists (i.e. NDRIs, NDRAs and selective DRIs)?
    I am not aware of specific studies looking at particular conditions beeing treated but imho the way to look at it is that NDRIs/NDRAs can be seen as as indirect non selective agonists. They increase the neurotrasnmitter (DA, NET or SERT resp.) concentration in the synaptic cleft (or prevent its decrease therein is more accurate) and thus activate the corresponding receptors regardless of the sybtypes. And since, there are a bunch of receptors subtypes for each neurotransmitter and each involved in different neuropsychological responses, the action of the RIs or RAs is to activate ALL the functions without discriminating which receptor subtype is getting activated. For example, there are at least 5 dopamine receptors subtypes with different brain distribution and therefore involvement in different brain functions. So a non-selective DA agonist (such as DRIs) used for sexual effect will also activate emesis (vomit)-inducing dopaminergic DA neurons (D2Rs are responsible for emesis while D4Rs are responsible for the sexual arousal effect of dopaminergics and incidentally also the focus/executive function missing in ADHD according to current literature.. check pubmed for current infos..)

    With Serotonin , it is even worse: there are at least 11 serotonin 5HT receptors subtypes known. So you can imagine the "havoc" that SSRIs can wreak besides their intended indications. Which is why selective serotoneric agonists are beeing developed by BigPharma for a bunch of indications anything from psychedelic 5HT2a agonists to military-grade 5Ht1AR agonists used with soldiers as aggressives (as opposed to 5HT1a antagonists that are serenics basically Chill Pill a bit like ganja..I mean rats on 5HT1a agonists become so aggressive, they would even attack a Cat if it happens to be around...etc

    So IMHO, yes someone who have a bad reaction to NDRIs/RAs can benefit from selective DA agonist. It all depends on the target conditions beeing treated. However, note that some people may not respond because of the polymorphism of the gene expressing the receptor in question. I mean, for example dopamine D2R is notorious in having relatively wide "genetic variability" among populations. So therapy with selective agonists targeting D2 will have to be adjusted to each indivual accordingly (disclaimer: this is no clinical advice am not a physician so pls seek appropriate advice..)

    Now back to sex arousal and DA agonists; It turns out the DA receptor subtypes responsible for the sexual arousal of dopaminergic is the D4. rats dosed D4 selective agonist will have spontaneous erection, increase humping with decrease refractory period similarly to the experience mentioned by @intense with prami.

    Quote Originally Posted by Coolwhip View Post
    I'm not arguing that dopamine agonists can't have those effects, but I'd like to see some double-blind controlled large sample studies involving otherwise healthy individuals before I concur that dopamine agonists are going to cause compulsive sexual behaviors in large portion of the general population taking relatively low doses.
    That would be the ideal: controlled human studies looking at the effect a DA agonist on sexual activity in healthy subjects. The only problem is that such studies won't be taken seriously by regulatory authorities since you are not treating a disease really. Getting sexually turn-on or not is not really a “disease”! I mean unlike erectile dysfunction which can be a pathological condition that can be treated by drugs. But anyway for such studies, you would need tons of money (I mean tons of it). Only Big Pharma can afford and since Big Pharma goes only after blockbusters drugs, I don’t know if the “market” is large enough for their investments!


    But actually, there have been lots of preclinical animal studies on that question (DA agonists as sex aphrodisiacs) paid for by BigPharma. I mean HugePharma including Pfizer and Abbott.. Abbott alone spent $100 of millions of dollars to develop DA agonists precisely as Aphrodisiacs. They came up with this ABT which is a selective dopamine D4R agonist with >60% efficacy. Rats injected with this compound will have spontaneous erection, increase intromission and lower refractory period with less of the other dopaminegric effects of non-selective DA agonists such as vomitting. More studies were done in Germany, Sweden, Italy beside the Abbott studies. Several D4 agonists were developed to treat psychogenic sexual dysfunction (medical term for sexual arousal enhancing drug aka Aphrodisiacs – basically turn-on drugs).

    I am not sure why BigPharma didn't develop further the D4 agonists probably a financial decision lying in wait for the market to turn... but who knows?

    EDIT: this is Abbott compound ABT-724


    this and related benzimidazoles would make nice aphrodisiacs RCs tho. safer, cheap and easy to synthesize and very potent $vendors take notice! It is a selective D4 agonist potent aphrodisiacs (at least in rats) with no side-effects of non-selective agonist like vomiting .. keep in mind rats sex life is not that different from humans' ..
    Last edited by DotChem; 26-04-2017 at 01:49.
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    #17
    so wait, what, D4 is the holy grail for aphrodisia? does cocaine act on d4? that would explain some of that. anyway, its impossible to find any of the ones you mentioned, research chems, that act on d4 any help, idea, of what is reliably possible to obtain available now days that might have some effect on d4, research or drug wise, even herbal stuff if any possibility!?
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    #18
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    Cocaine doesn't have direct effects on DA receptors, it's a reuptake inhibitor...
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    Please read the links above or PM me if I lock your post. Stay Safe. R.I.P. F28
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    #19
    Quote Originally Posted by sekio View Post
    Cocaine doesn't have direct effects on DA receptors, it's a reuptake inhibitor...
    well, it causes extreme aphrodisiac effect in me, maybe i should just concentrate on reuptake inhibitors instead of these exciting D4 agonists. though, im quite a bit too excited after reading dotchem's post
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    #20
    UPDATING this thread CHEMSEX ..for those interested in the mechanism of the sexual effect of Dopamine Reuptake inhibitors/Releasers or Agonists. Here is a study from Italy : It turns out activation of D4 subtypes dopamine receptors is responsible for the sexual effect of stims.. Rats dosed with a selective D4 agonists like this compound ABT-724 would f..k like ...euhh rabbits. The drug increases frequency of intromission, decrease mounting frequency and shorten post refractory period after ejaculation dramatically. In other words, it makes rats incredibly horny!! Incidentally, D4 agonism is also responsible for the nootropic effect of stims so D4s are sort of like the sexual effect of meth + nootropic effect of MPH without all other effects of DA agonists like pucking.. Just pure horniness + intense focused sex !! Pretty clean SEXUAL APHRODISIAC imho for those interesting in the sexual function of stims. Surprising they're not on Chemsex RC market..

    Role of dopamine D4 receptors in copulatory behavior: Studies with selective D4 agonists and antagonists in male rats. Sanna F1, Contini A2, Melis MR3, Argiolas A4. https://www.ncbi.nlm.nih.gov/pubmed/26287845

    Abstract

    Dopamine influences the anticipatory and consummatory phases of sexual behavior, by acting on receptors of the D2 family (D2, D3 and D4) and in particular of the D2 subtype, although evidence for a role of D4 receptors in erectile function and copulatory behavior is also available. In order to clarify such a role of D4 receptors, the effect of selective D4 receptor agonists and antagonists on copulatory behavior of sexually potent male rats in classic copulation tests with a receptive female, was compared with that of apomorphine and haloperidol, a classic dopamine receptor agonist and antagonist, respectively. PD-168,077 (0.05-0.2mg/kg) and ABT-724 (0.01-0.04mg/kg), two selective D4 receptor agonists, given subcutaneously, improved dose-dependently copulatory behavior as shown by the decrease of mount frequency and post ejaculatory interval induced by PD-168,077, and of mount frequency, ejaculation latency, post ejaculatory and inter intromission intervals induced by ABT-724, and by the increase of ejaculation frequency and copulatory efficacy induced by both drugs. Conversely, L-745,870 (1-5mg/kg), a selective D4 receptor antagonist, given intraperitoneally, impaired dose-dependently copulatory behavior, as shown by the increase in intromission and ejaculation latencies, mount frequency, post ejaculatory interval and the decrease in ejaculation frequency and copulatory efficacy induced by this drug. L-745,870 (5mg/kg) administered before PD-168,077 (0.2mg/kg) or ABT-724 (0.04mg/kg), also abolished completely the facilitatory effects of both PD-168,077 and ABT-724 on sexual behavior. These results confirm the involvement of D4 receptors in specific aspects of male rat copulatory behavior that overlap only partially with those influenced by apomorphine and haloperidol.

    Copyright 2015 Elsevier Inc. All rights reserved.


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