An erection is a carefully orchestrated series of events controlled by the CNS. We now know that the penis is under the complete control of the CNS, both during sexual arousal and at rest.
The male sexual response reflects a dynamic balance between exciting and inhibiting forces of the autonomic nervous system within the penis and throughout the CNS. The sympathetic component tends to inhibit erections, whereas the parasympathetic system is one of several excitatory pathways. During arousal, excitatory signals can originate in the brain, either by the sight or thought of an appealing sexual partner or by physical genital stimulation. Regardless of the source of these signals, the excitatory nerves in the penis respond by releasing proerectile neurotransmitters such as nitric oxide and acetylcholine. These chemical messengers signal the smooth muscles of the penile arteries to relax and fill with blood, resulting in an erection. The drug sildenafil works directly on the tissue in the penis to keep muscles relaxed and the vessels engorged.
This discovery may have important implications for people who take drugs that enhance levels of serotonin, such as the selective serotonin reuptake inhibitors (SSRIs) that are used to treat depression and other mental health disorders. These drugs often cause sexual dysfunction as a side effect, most commonly delayed or blocked ejaculation in men and a reduced sexual desire and difficulty reaching orgasm in women. The work by McKenna and Marson helps explain how this common and troublesome SSRI side effect may occur. By increasing levels of serotonin in the CNS, the SSRIs may tighten the brain’s built-in controls on erection, ejaculation, and other sexual functions. Interestingly, however, some recent studies also suggest that the inhibiting effects of the SSRIs may actually be helpful for some patients with other types of sexual dysfunction, such as premature ejaculation or inappropriate or excessive sexual urges.
Nothing new here. TEST regulate SERT. = lower serotonin.
High-Dose Testosterone Treatment Increases Serotonin Transporter Binding in Transgender People
One and 4 months of androgen treatment in female-to-male transsexuals increased SERT binding in amygdala, caudate, putamen, and median raphe nucleus. SERT binding increases correlated with treatment-induced increases in testosterone levels, suggesting that testosterone increases SERT expression on the cell surface. Conversely, 4 months of antiandrogen and estrogen treatment in male-to-female transsexuals led to decreases in SERT binding in insula, anterior, and mid-cingulate cortex. Increases in estradiol levels correlated negatively with decreases in regional SERT binding, indicating a protective effect of estradiol against SERT loss.
Last edited by fellow1 on Sun Jan 22, 2023 11:05 pm, edited 1 time in total.
High-Dose Testosterone Treatment Increases Serotonin Transporter Binding in Transgender People
One and 4 months of androgen treatment in female-to-male transsexuals increased SERT binding in amygdala, caudate, putamen, and median raphe nucleus. SERT binding increases correlated with treatment-induced increases in testosterone levels, suggesting that testosterone increases SERT expression on the cell surface. Conversely, 4 months of antiandrogen and estrogen treatment in male-to-female transsexuals led to decreases in SERT binding in insula, anterior, and mid-cingulate cortex. Increases in estradiol levels correlated negatively with decreases in regional SERT binding, indicating a protective effect of estradiol against SERT loss.
Also if you want to increase SERT you can try S. Boulardii probiotic
In a randomized controlled trial by Gu et al. administration of Sb culture supernatant to mice was found to reduce intestinal motility and up-regulate serotonin transporter (SERT) at the mRNA and protein level (58). This likely led to 5-HT cellular influx and enhanced degradation (5) as the Sb supernatant-treated mice exhibited lower concentrations of 5-HT in intestinal tissue (58).