Consumer & Behavioral Neuroscience
So last night I attended Science On Tap in Philadelphia at National Mechanics. First, I love that place! It’s super cool and comfortable with great drinks and food (ps… brunch there is delicious as well if you get a chance). Originally a bank (Mechanics National in 1837), it’s been through a lot of changes.
Last night SciCurious spoke about “Prozac, Welbutrin, and Zoloft: The Alphabet Soup of Antidepressants”. Good stuff. Great talk and great discussion afterward.
And one of the questions from the crowd sparked my brain since it didn’t get a chance to be answered.
What causes sexual dysfunction as a side effect of antidepressants?
I’m no expert in serotonin or sex. But it got me interested in seeing what was out there on the subject. And my previous experience in industry also involved a bit of research on increasing sexual desire… so it piqued my interest.
SciCurious had spoken of the drug targets and possible causes for depression… most revolving around the release and recycling of the neurotransmitter serotonin.
– Some antidepressant medications work by targeting levels of serotonin and other neurotransmitters in the synapses.
SciCurious had also talked about how serotonin is not just located in the brain. in my own work, I know that serotonin is much involved in the gut (where it was originally discovered) and plays a big role in our feeding behavior (which may explain the sometimes extreme effects that SSRI – selective serotonin reuptake inhibitors – can have on appetite).
Does it have a function on the sex organs?
First: erection is not a prerequisite for ejaculation, and each of these sexual responses can exist without the other. Penile erection is a vascular event controlled by the autonomic nervous system. The pelvic plexus represents a junction for efferent nerves to the structures involved in erection and ejaculation. The spinal cord contains three sets of neurons (thoracolumbar sympathetic, sacral parasympathetic, and somatic) innervating the sexual organs involved in erection and ejaculation. The presence of cerebral descending pathways to spinal erection and ejaculation centers tell us that the brain has both an excitatory or inhibitory effect on these processes. Sympathetic pathways are anti-erectile, sacral parasympathetic pathways are pro-erectile, and contraction of the perineal striated muscles upon activity of the pudendal nerves improves penile rigidity. Brain structures that control the spinal command for erection and ejaculation are part of a larger network that is dedicated to regulating sexual responses. Sensory information from the genitals is a potent activator of pro-erectile spinal neurons and elicits reflexive erections. Neurophysiological and pharmacological research has elucidated that dopamine and serotonin have key roles in controlling erection and ejaculation. Nitric oxide, which can be colocalized with VIP and acetylcholine, is the main proerectile neurotransmitter and noradrenaline is considered to be the major antierectile agent. Reflexive erection elicited by recruitment of penile afferents involves both autonomic and somatic efferents. This reflex is mediated at the spinal cord level and modulated by supraspinal influences. Serotonergic pathways originating in the raphe nuclei may mediate inhibitory control on reflexive erections. The hypothalamic medial preoptic area is an important integrating center and dopamine may regulate penile erection at this level.
Erectile dysfunction (ED) is sexual dysfunction characterized by the inability to develop or maintain an erection during sexual performance. There are psychological factors contributing to the dysfunction that stem from thoughts or emotions unrelated to physiology, but it’s rare. Two external causes (or rather, easy to fix causes) of ED are arsenic poisoning from water or potassium deficiency. Viagra is a phosphodiesterase type 5 inhibitor often used to treat ED. It blocks the degradative action of phosphodiesterase type 5 on cyclic GMP in the smooth muscle cells lining the blood vessels supplying the corpus cavernosum of the penis causing an erection. Viagra is the most effective of available treatments. And although the actions it takes are recognized as being at the penis, there is some evidence of central brain effects as well. Recently local sildenafil administration was shown to enhance extracellular dopamine AND serotonin in the nucleus accumbens in the brain.
A recent fMRI study compared the brains of men taking either SSRIs (known to contribute to sexual dysfunction) or Bupropion, a norepinephrine and dopamine reuptake inhibitor, that is often recommended as an alternative treatment without adverse effects concerning sexual arousal and libido.
Enhancement of serotonergic and noradrenergic/dopaminergic neurotransmission led to differential effects in the subjective experiences of sexual functioning accompanied by opposite drug effects on local neural activities upon erotic stimulation. Overall, most brain activations elicited by erotic movies were reduced under paroxetine but not under bupropion. Particularly, under paroxetine, neural activities decreased in the ventral striatum, midbrain, and distinct areas along the cingulate gyrus. These regions have already been described by others to mediate aspects of motivational and emotional processes related to sexual behavior, although their specific role awaits further research. The combined noradrenalin/dopamine reuptake inhibitor bupropion showed opposite fMRI effects and was associated with a prolonged and increased activation of brain regions previously related to the processing of rewarding and salient stimuli. If clinically possible, this suggests enhancement of dopaminergic transmission as a plausible add-on treatment to counteract the side effects of antidepressant SSRI medication on sexual functioning that impose a high risk on medication adherence and hence therapeutic success.
So that means that there is hope to get around the sexual dysfunction side effect, and it implicates brain regions that involved in the processing of motivational (ventral striatum), emotional, and autonomic components of erotic stimulation (anterior cingulate) show a reduced responsiveness under paroxetine.
Increased serotonin means it takes longer for ejaculation, if at all. And low does the opposite.
It’s a bit more difficult to pin point here for many reasons. While the clitoris does become erect during sexual arousal, it’s not obvious as in men. And most treatment has to do with adding lubricants or inducing orgasm. The female orgasm lasts, on average, approximately 20 seconds, and consists of a series of muscular contractions in the pelvic area that includes the vagina, the uterus and the anus. It is preceded by erection of the clitoris and moistening of the opening of the vagina. Historically, women were medically diagnosed with female hysteria, – faintness, nervousness, insomnia, fluid retention, heaviness in abdomen, muscle spasm, shortness of breath, irritability, loss of appetite for food or sex, and “a tendency to cause trouble”. Women considered suffering from the condition would sometimes undergo “pelvic massage” by the doctor until the woman experienced “hysterical paroxysm” or an orgasm. Paroxysm was regarded as a medical treatment, and not a sexual release or pleasure. This, however, stopped being considered a disorder in the 1920s.
During stimulation, the parts of the female brain responsible for processing fear, anxiety and behavioral control relax and reduce in activity. This peaks at orgasm when the female brain’s emotion centers are effectively closed down in a trance-like state.
About 15% of women report difficulties with orgasm, 10% have never climaxed, and 40–50% have either complained about sexual dissatisfaction or experienced difficulty becoming sexually aroused at some point in their lives. If orgasm is desired, anorgasmia may be attributed to an inability to relax, or “let go.” It seems to be closely associated with performance pressure and an unwillingness to pursue pleasure, as separate from the other person’s satisfaction.Experts say that women worry so much about the pleasure of their partner that they become anxious, which manifests as impatience with the delay of orgasm for them.
I don’t know, sounds like a cop out to me. But that is what the experts say. So one might think that then antidepressants would increase sexual interest in women? Right?
Well, there’s a study for that.
Fluoxetine is an SSRI that is known to have the sexual dysfunction side effect, especially for women. And it turns out that the 5-HT(1A) receptor has been implicated in this sexual dysfunction in rats. Treatment with fluoxetine inhibits lordosis (sexual pose) behavior in both Fischer and Sprague-Dawley female rats and may involve effects of the SSRI in addition to activation of the 5-HT(1A) receptor.
(okay, maybe a disturbing image, apologies)
Back to serotonin and sex:
Interestingly, last year news hit the “wires” that serotonin was a sex bomb that made mice hypersexual and maybe even bisexual. But of course, it’s never that simple. And SciCurious commented on that here. I especially liked her critique of the papers possible confounds… like ceiling effects, etc.
A paper back in 2008 found that women have a greater number of the most common serotonin receptors than men. They also show that women have lower levels of the protein that transports serotonin back into the nerve cells that secrete it. It is this protein that the most common antidepressants (SSRIs) block. So… does that mean that women are already at a disadvantage to men in sex drive… and even worse when given SSRIs?
Remains to be seen. So much research waits to be done. And not everything needs to be drug led. Behavior can play a large part in recovering sex drive as well.
It’s not just a problem with antidepressants either. The majority of sex being had out there is what is known as “maintenance sex” , or sex without desire. And while it can be physically arousing, it’s described as less fulfilling, because arousal doesn’t always mean desire. Sensate focus techniques and sexual counseling with sex therapists are still the leading treatments for this kind of disorder.
Sexual dysfunction is common with major depressive disorder. It’s not a symptom of major depressive disorder exactly, but decreased sexual desire and arousal may be characteristics associated with depression-related anhedonia. Sexual dysfunction is also a common side effect of treatment with serotonergic antidepressants and may be a reason that patients on SSRIs and other serotonergic medications discontinue treatment prematurely.
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