Ejaculation Threshold Hypothesis

In order to understand the suggested biological variation of the IELT in relation to the serotonergic system, delaying effects of SSRIs and suggested genetics, Waldinger and co-workers have proposed the existence of a threshold of the IELT (5,49).

In the case of a low setpoint of the threshold, men can only sustain a small amount of sexual arousal prior to ejaculation. Whatever these men do or fantasize during intercourse, any control of ejaculation remains marginal and these men ejaculate easily even when they are not fully aroused. The low threshold is assumed to be associated with a low 5-HT neurotransmission and probably a hypofunction of the 5-HT2C receptor and/or a hyperfunction of the 5-HT1A receptor, as mentioned earlier.

In the case of a higher setpoint, men will experience more control over their ejaculation time. They can sustain more sexual arousal before ejaculating. In these men, 5-HT neurotransmission varies around a normal or averaged level and the 5-HT2C receptor functions normally. The mean and range values of the setpoints that are considered to be normal or averaged are not known. These men have the neurobiological ability to voluntarily decide to get an ejaculation quickly or after a longer duration of intercourse.

In case of a high or very high setpoint, men may experience difficulty in ejaculating or cannot get an ejaculation even when fully sexually aroused. At a high setpoint, 5-HT neurotransmission is supposed to be increased, the 5-HT2C receptor sensitivity is enhanced, and/or the 5-HT1A receptor sensitivity is decreased.

According to this threshold hypothesis, it appears to be the level of 5-HT2C and 5-HT1A receptor activation that determines the setpoint and associated ejaculation latency time of an individual man. In case of men with premature ejaculation or any man using serotonergic antidepressants, the SSRIs and clomipramine activate the 5-HT2C receptor and therefore switch the setpoint to a higher level leading to a delay in ejaculation. The effects of SSRIs on the setpoint appear to be individually determined; some men respond with extreme delay whereas others only experience a small delay at the same dose of the drug. Moreover, cessation of treatment results in a uniform reset of the setpoint within 3-5 days to the lower individually determined reference level, which is assumed genetically determined.

It is speculated that the threshold is mediated by serotonin neurotransmission and 5-HT receptors in the brainstem or spinal cord and may consist of serotonergic fibers that inhibit neurons that convey somatosensory information from the genitals. It is suggested that SSRIs enhance the inhibitory effects of these serotonergic neurons. However, also the cerebral cortex may mediate inhibitory impulses, but currently this has not been demonstrated. Apart from a suggested SSRI-induced increased inhibition of sensory input, the SSRIs might also delay ejaculation by interfering with spinal cord motoneurons of peripheral neurons that inhibit the internal genitals. Further studies are needed to unravel this important and intriguing question.

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