TABLE 2.

Neurochemical and hormonal regulation of ejaculation.

Neurotransmitter/hormone	Effect
Dopamine	Stimulates ejaculation through D2-like receptors (D2, D3, and D4 receptors, mainly D3)
Serotonin	Inhibits ejaculation in the brain and stimulates it in the spine through the receptors 5HT, with 1A, 1B, and 2C
Nitric oxide	Inhibits ejaculation through reduction of seminal vesicle contraction and seminal emission
Oxytocin	Synthesized in the supraoptic and PVN of the hypothalamus and released from the posterior pituitary gland
	Augments powerful epididymal contractions and sperm motility
	Acts in the CNS to stimulate ejaculation
Prolactin	Secreted from the pituitary gland
	Hyperprolactinemia has a marked inhibitory effect on male sexual desire, through inhibition of GnRH  (therefore T production) and dopamine production
Thyroid hormones	Hypothyroidism and hyperthyroidism are associated with delayed and premature ejaculation, respectively
Glucocorticoids	Cortisol levels are elevated after ejaculation in animal studies
	No change in cortisol levels in humans
	Replacement of cortisol in Addison disease improves sexual function including orgasm
Estrogens	Regulates the emission phase of ejaculation through the regulation of epididymal contractility, luminal fluid  reabsorption, and sperm concentration
Androgens	Low levels are associated with delayed ejaculation, whereas high levels are associated with premature ejaculation
	Facilitates the control of the ejaculatory reflex through its androgen receptors in the MPOA and other  areas in the CNS
	Pelvic floor muscles involved in ejaculation are androgen dependent

Note: CNS = central nervous system; MPOA = medial preoptic area; PVN = paraventricular nucleus.