Neurohormonal Changes Following Ejaculation
The primary neurohormonal change following ejaculation is a significant increase in prolactin levels, which is approximately 400% greater after intercourse compared to masturbation, suggesting greater physiological satiety after partnered sexual activity. 1
Physiological Process of Ejaculation
Ejaculation consists of two synchronized phases:
- Emission phase: Involves deposition of seminal fluid into the posterior urethra
- Expulsion phase: Involves rhythmic contractions of pelvic muscles to expel semen
These phases are controlled by:
- Sympathetic nervous system (primary control)
- Parasympathetic nervous system
- Somatic nervous system 2
Key Neurohormonal Changes Post-Ejaculation
Prolactin Response
- Significant prolactin increase occurs after orgasm
- This increase is 4 times greater following intercourse than masturbation
- Functions as a feedback mechanism that decreases arousal through inhibitory central dopaminergic processes
- Serves as a neurohormonal index of sexual satiety 1
Dopamine and Serotonin Pathways
- Dopaminergic pathways are involved in shortening the post-ejaculatory refractory period
- Serotonergic pathways tend to lengthen the duration of the refractory period
- This explains why SSRIs (which increase serotonin levels) can help reduce premature ejaculation 3
Post-Ejaculatory Refractory Period (PERT)
The refractory period after ejaculation involves:
- Decreased sexual arousal and inability to achieve another erection/ejaculation immediately
- Two phases have been identified in animal models:
- Absolute PERT (aPERT): Complete inhibition of erection and ejaculation
- Relative PERT (rPERT): When stronger or novel stimuli can overcome inhibition
However, it's important to note that whether these distinct phases exist in humans remains unexamined 3
Recent Research Findings
Recent research has challenged some long-held beliefs about post-ejaculatory physiology:
Prolactin's role: While prolactin increases after ejaculation, a 2021 study using mouse models found compelling evidence refuting the long-standing hypothesis that prolactin is responsible for establishing the refractory period 4
Sildenafil effects: Research shows that sildenafil (Viagra) appears to:
- Prolong ejaculation latency time
- Extend detumescence time (time to lose erection after ejaculation)
- Improve rigidity quality after ejaculation
- However, it does not significantly shorten the refractory period 5
Clinical Implications
Understanding these neurohormonal changes has important clinical applications:
Treatment of ejaculatory disorders: Knowledge of neurotransmitter involvement has led to pharmacological treatments for premature ejaculation, particularly targeting serotonin pathways 2
Diagnostic considerations: When evaluating patients with ejaculatory complaints, a detailed sexual history is essential, as premature ejaculation is a self-reported diagnosis 6
Treatment prioritization: In patients with concurrent erectile dysfunction (ED) and premature ejaculation, the ED should be treated first, as premature ejaculation may improve when concomitant ED is effectively treated 6
Knowledge Gaps and Future Directions
Despite advances in understanding ejaculation physiology, significant knowledge gaps remain:
- Limited evidence-based data on human PERT mechanisms
- Lack of research on age-related changes in post-ejaculatory physiology
- Need for brain imaging studies to better understand central mechanisms 3
Brain imaging and electromagnetic tomography studies in men of different age groups are needed to advance our understanding of post-ejaculatory neurohormonal changes 3.