Estrogen receptor alpha (ERalpha) participates in the neuroendocrine regulation of male sexual behavior, primarily in brain areas located in the limbic system. Males of many species present a long-term inhibition of sexual behavior after several ejaculations, known as sexual satiety. It has been shown that androgen receptor density is reduced 24 h after a single ejaculation or mating to satiety, in the medial preoptic area, nucleus accumbens and ventromedial hypothalamus . The aim of this study was to analyze if the density of ERalpha was also modified 24 h after a single ejaculation or mating to satiety. Sexual satiety was associated with an increased ERalpha density in the anteromedial bed nucleus of the stria terminalis (BSTMA), ventrolateral septum (LSV), posterodorsal medial amygdala (MePD), medial preoptic area (MPA) and nucleus accumbens core (NAc). A single ejaculation was related to an increase in ERalpha density in the BSTMA and MePD. ERalpha density in the arcuate (Arc) and ventromedial hypothalamic nuclei (VMN), and serum estradiol levels remained unchanged 24 h after one ejaculation or mating to satiety. These data suggest a relationship between sexual activity and an increase in the expression of ERalpha (estrogenic receptor) in specific brain areas, independently of estradiol levels in systemic circulation .
Male sexual behavior is regulated by limbic areas like the medial preoptic nucleus (MPN), the bed nucleus of the stria terminalis (BST), the nucleus accumbens (nAcc) and the ventromedial hypothalamic nucleus (VMN). Neurons in these brain areas are rich in androgen receptors (AR) and express FOS-immunoreactivity in response to mating. In many species sexual satiation, a state of sexual behavior inhibition, is attained after multiple ejaculations. The mechanisms underlying sexual satiation are largely unknown. In this study we show that sexual activity reduces androgen receptor immunoreactivity (AR-ir) in some of the brain areas associated with the control of male sexual behavior , but not in others. Thus, one ejaculation reduced the AR-ir in the MPN and nAcc, but not in the BST and VMN. Copulation to satiation, on the other hand, reduced AR-ir in the MPN, nAcc and VMN, and not in the BST. The AR-ir reduction observed in the MPN of sexually satiated rats was drastic when compared to that of animals ejaculating once. Serum androgen levels did not vary after one ejaculation or copulation to exhaustion. These data reveal that sexual activity reduces AR in specific brain areas and suggest the possibility that such a reduction underlies the sexual inhibition that characterizes sexual satiety.
The present article reviews the current findings on the interesting phenomenon of sexual satiety. Knut Larsson in 1956 reported on the development of sexual exhaustion in the male rat after repeated copulation. We have studied the process and found the following results. (1) One day after 4 hours of ad libitum copulation, two-thirds of the population showed complete inhibition of sexual behavior, while the other third displayed a single ejaculatory series from which they did not recover. (2) Several pharmacological treatments, including 8-OH-DPAT, yohimbine, naloxone and naltrexone, reverse this sexual satiety, indicating that the noradrenergic, serotonergic and opiate systems are involved in this process. Indeed, direct neurochemical determinations showed changes in various neurotransmitters during sexual exhaustion. (3) Given enough stimulation, by changing the stimulus female, sexual satiety was prevented, suggesting that there are motivational components of the sexual inhibition that characterizes sexual exhaustion. (4) The GABA antagonist bicuculline, or the electrical stimulation of the medial preoptic area, did not reverse sexual exhaustion. These data suggest, on the one hand, that sexual exhaustion and the postejaculatory interval (which is shortened by bicuculline administration) are not mediated by similar mechanisms and, on the other, that the medial preoptic area does not regulate sexual satiety. (5) The androgen receptor density in brain areas closely related to the expression of masculine sexual behavior, such as the medial preoptic nucleus, was drastically reduced in sexually exhausted animals . Such reduction was specific to certain brain areas and was not related to changes in the levels of androgens. These results suggest that changes in brain androgen receptors account for the inhibition of sexual behavior present during sexual exhaustion. (6) The recovery process of sexual satiety after 4 hours of ad libitum copulation reveals that, after 4 days, only 63% of the males are able to show sexual behavior while after 7 days all animals display copulatory activity.
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This current study examined the effect of a 3-week period of sexual abstinence on the neuroendocrine response to masturbation-induced orgasm. Hormonal and cardiovascular parameters were examined in ten healthy adult men during sexual arousal and masturbation-induced orgasm. Blood was drawn continuously and cardiovascular parameters were constantly monitored. This procedure was conducted for each participant twice, both before and after a 3-week period of sexual abstinence. Plasma was subsequently analysed for concentrations of adrenaline, noradrenaline, cortisol, prolactin, luteinizing hormone and testosterone concentrations. Orgasm increased blood pressure, heart rate, plasma catecholamines and prolactin . These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence . These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.
The purpose of this study is to gain understanding of the relationship between ejaculation and serum testosterone level in men. The serum testosterone concentrations of 28 volunteers were investigated daily during abstinence periods after ejaculation for two phases. The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak. Ejaculation is the precondition and beginning of the special periodic serum testosterone level variations, which would not occur without ejaculation. The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum. These data are the first to document the phenomenon of the periodic change in serum testosterone level; the correlation between ejaculation and periodic change in the serum testosterone level, and the pattern and characteristics of the periodic change.
Research points to an association between testosterone (T) and partnering in some women and men, and this association has been interpreted as an effect of either relationship status (i.e. differences in relationship status lead to differences in T) or relationship orientation (i.e. T is associated with the likelihood of entering relationships). To address whether physical partner presence was associated with decreased T, we examined T levels in people ( 72 women; 49 men ) who were single, in long-distance relationships, or in same-city relationships. No participants were using exogenous hormones, including hormonal contraceptives. Participants provided a saliva sample and responded to questions about their relationship status. Single men had higher T than long-distance and same-city partnered men , which supports the relationship orientation interpretation. In contrast, same-city partnered women had lower T than single women and women in long-distance relationships , which supports the relationship status interpretation. We conclude that physical partner presence is not necessary to see an association between partnering and hormones in men (since same-city and long-distance partnered men had similar T levels), but may be necessary in women (since same-city partnered women had lower T than long-distance partnered women).
Masturbation is pointless for most guys with PFS symptoms usually dictate that it is not possible to get errect without Chemical assistance i.e viagra also masturbation gives no pleasure if anything its just a reminder of our issues and further more many do not feel the urge I myself can’t remember the last time it must be years ago. I would sooner save whats in the tank for the misses .
Yes some are lucky it doesn’t hit them between the legs as hard as others but the ones it does get do tend to be stuck with persistent sexual issues . I just can’t get my head around how the symptoms persist even years after the drug is discontinued I suppose only science is going answer this question…
I did a 90 day NoFap this summer and felt much better during that period. Libido was higher, my voice became deeper and my confidence was back. But as soon as I started to masturbate and have sex again my libido decreased, morning erections disappeared and the confidence was gone.
So upregulation seemed to help you at it “should” be for most guys. Other NoFap guys become asexual for weeks to months, then have insane libido and confidence after the flatline. Either way, this proves that extreme alterations in fapping habits are playing a major role in androgen signaling
The studies on PFS have confirmed that the androgen receptors in the body are upregulated.
While some upregulation is considered desirable, the PFS upregulation is likely excessive and with the combination of lowered DHT and/or increase in DHT following cessation of 5ARi, something was thrown out of balance in the receptor or signaling pathway.
Some have hypothesized that downregulating the receptors could address the upregulation that has occurred. It appears as though masturbation has the potential of downregulating the receptors.
That’s generally been my experience. Often I’ll watch porn and fap with a weak erection and low pleasure. If I try a second time it is often a harder erection and I feel more dopamine.
Back in the day I used to often get sleepy and feel a gaba surge on a slow lazy Saturday when I’d rub one off. I’d take a nap and then wake up to rub one off again when I felt the urge. That happened once about two months ago. For a few
minutes i escaped prison and I was in heaven on Earth again
That’s what confusing me. We should have upregulated AR but for me while on NoFap I was feeling much better. But as soon as I started to have sex/masturbate most of my symptoms are back again. How is this possible?
It makes sense because it’s similar to how some people feel better taking AA’s again. NoFap will upregulate and push the AR’s even more. It’s like a temporary band-aid that can make the cut worse in the long run.
If fapping makes you feel like crap, maybe if you keep doing it the body will adjust. Who knows though, this is all so complex and experimental.
Back in the day, i could enjoy masturbating and watching porn so much, no matter how much i stressed or depressed, it was always yield the same stable enjoyable experience.
I was eating unhealthy didn’t care my health, yet every masturbation was like god sent beautiful… Now we are trying to best set and setting to enjoy a mild orgasm. Pfs sucks. Worst man made disease on planet earth. Wish we got cancer and died soon. At least this shit would be over without this pain and constant struggle…
I used to be so excited on Saturday morning. I’d get out of bed and couldn’t wait to drop my boxers and jerk my morning wood to Porn and go on a dopamine adventure for clips for my fetishes. I’d often have such strong urges that I’d do this before I pissed. Those were the days.