Perhaps, I should have corrected/clarified myself on an earlier posting.
From Stephen Stahl's Essential Psychopharmacology textbook, there are three stages of the sexual response:
- involving a desire for sex or sex drive
2. Arousal (erection
, lubrication, swelling) - involving signaling the sex organs into action.
From what I know so far:
Libido is increased by increased dopamine levels in the mesolimbic dopamine reward centers of the brain (note the specificity of localization). Increases in other areas may or may not negatively affect libido. Libido is decreased by increased prolactin levels - though dopamine itself reduces prolactin levels. Serotonin in the brain may reduce libido, by reducing dopamine levels among other effects. However, when anxious or stressed, a small increase in serotonin may help libido by reducing the perception of stress and by reducing anxiety (thus the usefulness of serotonin reuptake inhibitors in premature ejaculation). Acetylcholine (via interneurons) reduces dopamine release from dopaminergic neurons, and thus may reduce libido. Blocking NMDA glutamate receptors may increase dopamine levels. Increase norepinephrine levels (another stimulant neurotransmitter) may increase libido in some people, though excessive norepinephrine may reduce libido (since norepinephrine is a signal for stress). GABA is involved with libido. Increased GABA levels may reduce anxiety/stress, leading to increased libido. Excessively high GABA activity sedates - reducing libido. Increased histamine levels may potentially improve libido (Histamine is a stimulant neurotransmitter like dopamine and norepinephrine). However excessive histamine may trigger anxiety, anger, irritability, agitation, insomnia, and stress - reducing libido.
Arousal involves transforming the sex drive into a signal from the brain to activate the genitals. Acetylcholine is involved in transmitting the signal through the parasympathetic nerves to the genitals. Nitric oxide (formed from L-arginine by Nitric Oxide Synthetase in nerves) is then released, activates the intracellular enzyme guanylyl cyclase, which then makes cyclic guanylate monophoasphate (cGMP), which relaxes vascular smooth muscle, opens blood flow, and causes and erection. cGMP's actions are terminated by Phosphodiesterase
Orgasm/ejaculation involves norepinephrine, which transmits signals through the sympathetic nervous system to the genitals, to trigger orgasm and ejaculation. Serotonin signals from the brain through the spine, to the genitals inhibit orgasm.
Blocking phosphodiesterase using Viagra
helps maintain blood flow into the penis, maintaining an erection.
Prostaglandin E1 (Caverject), via injection to the penis, can relax vascular smooth muscle like nitric oxide, and can thus be used to obtain an erection, even if the nervous system is not signaling properly (e.g. impaired transmission due to diabetes).
Wellbutrin in some people may improve libido by increasing norepinephrine level in the brain - depending on the dose. In my experience, high doses can impair libido - possibly by activating the adrenal glands (since norepinephrine is the signal for stress from the brain to the adrenals), causing an increase in cortisol, which causes transient insulin resistance, which reduces testosterone
production, which then reduces dopamine levels.