Encyclopedia of Sexuality and Gender

Living Edition
| Editors: Amy D. Lykins


  • Robert L MeiselEmail author
  • Laura E Been
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-59531-3_10-1



The historical origins of dopamine as a regulator of sexuality came from patient reports in conjunction with neurological (e.g., Parkinson’s disease) or endocrine (e.g., hyperprolactinemia) disorders of dopamine dysregulation. More detailed studies in humans and other animals identified a broad range of effects of dopamine neurotransmission on each of the components of sexual behavior, i.e., libido, sexual arousal, and orgasm. Moreover, through there are nuanced differences between males and females, dopamine has essentially the same effects in both biological sexes. Simply seeing a congruent potential sexual partner will activate one of the main dopamine pathways (the mesocorticolimbic dopamine system) in males and females. Arousal leading up to sexual intercourse also activates the mesocorticolimbic dopamine system, whereas hypothalamic dopamine is more associated with intercourse itself. Orgasm, which may signal the termination of copulation, is followed by a decrease in dopamine signaling. Most studies to date have focused on cis-gendered heterosexual men and women, highlighting a need for more studies on people with differing sexual orientations and gender identities. At the same time, commonalities in the role of dopamine from the existing data might predict that these general principles will apply broadly.


A role for dopamine in sexual function originated with reports that Parkinson’s patients express low levels of sexual desire, and that therapeutic L-DOPA treatments increased their interest in sex (Bronner, Royter, Korczyn, & Giladi, 2004). Because Parkinson’s disease follows from a loss of dopamine neurons, and L-DOPA to a degree can alleviate the loss of dopamine, the idea was that dopamine might underlie sexual behavior in people. A secondary source came from a disease state in men in which abnormally elevated prolactin, a hormone released from the pituitary gland, impaired sexual function. This condition was treatable in men given bromocriptine, both directly through the actions of bromocriptine on dopamine neurotransmission and indirectly through dopamine inhibition of prolactin release. These types of observations from different clinical conditions formed the basis for more directed research into dopamine regulation of sexual function in both males and females.

As with many neurotransmitters, dopamine pathways in the brain and spinal cord are organized by discrete cell groups, each of which then sends projections to well-defined targets (Klein et al., 2019). The distinct dopamine pathways are conceptualized to be associated with different behavioral properties which then can map onto elements of copulation in both males and females. There are three phases of the sexual response common to all animals: libido, sexual arousal (including engaging in sexual activity itself), and orgasm (Georgiadis & Kringelbach, 2012). Dopamine neurotransmission is involved in all three phases, though to differing degrees. Adding complexity to the system, dopamine acts on its target neurons through different variants of the dopamine receptor (Klein et al., 2019). There are two families of receptor with the dopamine D1 family (D1 and D5 receptor subtypes) generally activating neurons, and the dopamine D2 family (D2, D3, and D4 receptor subtypes) mediating inhibition. Despite this complexity of circuits and receptors, some principles have emerged from both the human and animal literatures linking dopamine to sexual function.

Animal models often provide a basis for testing hypotheses about the biological regulation of human behaviors (Kim et al., 2013). Colloquially we think of people having sex for pleasure (a psychological process mediated by dopamine), whereas animals have sex for the primary purpose of reproduction. Some of the basis for this erroneous view comes from our own experiences where couples rarely have babies, yet we assume they have sex at a much higher rate. Human data support this common notion with less than 1% of heterosexual encounters resulting in pregnancy. For animals, contraception is not an option meaning that the vast majority of matings produce offspring. In spite of the differences in the percentage of fertile matings between people and animals, it has become clear that all mammals engage in sexual behavior for pleasure, with pregnancy and the birth of offspring a biological consequence of that initial motivation for sex.

In this section, we will provide an overview of the role of dopamine in each of the three phases of sexual response. Our approach is to synthesize the literature from humans and animal models, pulling out common principles and themes. In doing so, we aim to highlight how dopamine action in the brain influences sexual behavior in across sexes, genders, and species.

Libido. We can think of libido in terms of sexual desire, which is thought of as “wanting sex” in motivational terms. Sexual desire reflects a general and ongoing interest in sex, which is represented intrinsically as an intersection of internal physiological drives and stimuli/events in world around us (Kim et al., 2013). In our daily activities, we can simply be thinking about sex or we may be in a situation (e.g., a party) in which familiar or unfamiliar people stimulate the desire for sex. Sexual desire is a direct result of our experiences, which under healthy circumstances utilizes a feed-forward neural system which maintains or enhances sexual interest.

The dopamine circuit most closely related to sexual desire is the mesocorticolimbic pathway. The cell group (termed “ventral tegmentum”) for this pathway resides in the midbrain (meso; think of it as located about halfway between your nose and base of the skull). These neurons send their connections forward to a brain region termed the “nucleus accumbens,” a part of the limbic system which controls emotion and arousal. The ventral tegmentum also sends connections to the prefrontal cortex (cortico), which is involved in emotion and arousal, as well as decision making. Collectively this dopamine circuit is key to arousal and emotions generated by thinking about sex (i.e., desire), determining who we find sexually arousing, and making decisions about whether to act on those desires. Below we review the evidence for the involvement of the mesocorticolimbic dopamine system in desire in humans and animals.

Functional brain imaging studies of sexual behavior in humans are relatively rare and are mostly descriptive rather than mechanistic. Neuroimaging studies intending to measure sexual desire or motivation have primarily used passive viewing paradigms in which subjects are shown photos or videos of sexual content (Georgiadis & Kringelbach, 2012). Humans are very sensitive to their preferred sexual stimuli. Even when visual sexual stimuli are presented subliminally, they can induce measurable responses in brain areas associated with motivation. Few studies have addressed the question of whether sexual preference (orientation) gives rise to differences in activity induced by visual sexual stimuli. However, the evidence so far suggests there are not differences in neural responses to visual sexual stimuli between same sex-oriented versus opposite sex-oriented individuals; both are more sensitive to their preferred sexual stimuli and show similar magnitude brain responses to visual sexual stimuli. Very few studies have examined other common variations in sexual preference.

The passive viewing paradigm has been used most commonly to measure brain responses to visual sexual stimuli in cis-gendered heterosexual men. Across studies, the most consistent finding is that the mesocorticolimbic pathway, and in particular the ventral striatum (including the nucleus accumbens), is activated when sexual images are presented for relatively short durations (Ferretti et al., 2005). In contrast, visual sexual stimuli presented for longer than 30 s rarely yield measureable mesolimbic activity, suggesting that mesolimbic dopamine activity may be associated primarily with initial sexual motivation or sexual wanting. This idea is supported by data from a pharmacological study in which the neural responses to subliminally-presented visual sexual stimuli were sensitive to manipulation of dopamine levels in heterosexual men. Specifically, treatment with the dopamine agonist L-DOPA enhanced activation of the nucleus accumbens in response to subliminally-presented sexual stimuli. In contrast, treatment with the dopamine antagonist haloperidol, which blocks dopamine actions, decreased neural activity in the nucleus accumbens in response to subliminally-presented sexual stimuli.

The passive viewing of visual sexual stimuli presumably measures the neural response to unconditioned sexual stimuli, but it is worth noting that these neural responses can be conditioned as well. For instance, one study paired geometric shapes with the presentation of either visual sexual stimuli or neutral visual stimuli (Klucken et al., 2009). Eventually, the geometric shapes associated with the visual sexual stimuli caused activation in same brain areas as the visual sexual stimuli (e.g., midbrain and ventral striatum) when they were presented alone, and some subjects even reported experiencing sexual desire in response to presentation of the conditioned shape stimuli. This is important for two reasons: (1) It underscores the idea that the mesolimbic circuitry that responds to sexual stimuli is in no way specific to sexual stimuli. Rather, this pathway can be activated by a variety of motivating stimuli, unconditioned or conditioned. (2) The mesolimbic pathway must interact with other neural systems in order to direct libido towards appropriate targets and execute the motor programs required for the transition from libido to arousal and mating.

Animal models can provide insight into the neural mechanisms of libido in humans (Kim et al., 2013). Although animals cannot completely model some of the higher order cognitive functions associated with libido in humans, many of the same brain regions are activated in response to sexual motivation in humans and animals, and dopamine plays a prominent role across species. Generally, drugs that increase dopamine activity in animals facilitate sex behavior, whereas drugs that inhibit dopamine activity reduce sexual behavior, although considering dopamine receptor subtypes adds a level of nuance to these generalities. For example, in male rats, D2/D3 dopamine agonist drugs increase noncontact erections in response to an inaccessible female. These types of erections are thought to be analogous to “psychogenic” erections in men, i.e., erections that arise from audiovisual stimuli or fantasy and reflect sexual motivation. Dopamine agonist drugs also increase general activity in anticipation of copulation in male rats, possibly reflecting an increase in sexual excitement or motivation. In Japanese quail, another well-studied animal model of sexual behavior, D2 agonists increase the amount of time that males will spend viewing a receptive female, a proxy for sexual attraction in this highly-visual avian species. In contrast, D1 and D2 antagonists decrease the number of approaches to a goal zone where males could observe a female (Ball & Balthazart, 2011).

Recently, variation in the gene sequences for proteins related to dopamine function have been correlated with individual differences in libido. In one case, variation in gene sequences for the dopamine transporter was analyzed. The dopamine transporter eliminates dopamine from the synapse (the point of communication between nerve cells), terminating the dopamine signal. Variations in this gene can affect the strength of the dopamine signal if it affects the ability of the dopamine transporter to turn off dopamine signaling. Genetic variations in the dopamine transporter that reduce transporter function thereby increasing dopamine signaling correlate with higher numbers of sexual partners (a measure of libido) for men carrying this variant, but not for women. Gene variants for the dopamine D4 receptor have also been identified. In this instance, different variants were associated with either higher or lower sexual desire in both men and women. These findings are intriguing, but limited in that the functional significance of the D4 variants with respect to dopamine activity is not known.

Sexual Arousal. Most of what we know about dopamine regulation of sexual behavior comes from its role in sexual arousal. During sex, the mesocorticolimbic system is activated in conjunction with ongoing sexual arousal. The effects of dopamine here are linked to whether there is a pleasurable outcome to sex. These effects of dopamine can underlie both sexual function and dysfunction. Put another way, it is just as easy to learn that sex is not pleasurable as it is pleasurable, and unpleasant learned associations can lead to states of hypoactive sexual desire. The performance of sexual behavior is associated to a greater degree with regions of the hypothalamus (Braunstein, 2011), a structure located on the floor of the brain in front of (i.e., rostral to) the midbrain. The hypothalamus receives inputs from dopamine cell groups, though these inputs are more diffuse than the localized mesocorticolimbic projections.

Simply engaging in sex does not constitute sexual arousal, nor is it necessarily pleasurable. Animal studies clearly demonstrate this dissociation. Dopamine is elevated in the nucleus accumbens of female rodents during sex behavior. This elevation in dopamine is especially pronounced if the female can initiate and control the pacing of the sexual interaction. Under these circumstances, the elevation in dopamine during sex establishes the pleasurable and rewarding consequences of sex. Nucleus accumbens dopamine inputs do not regulate the expression of sexual behavior. Indeed, female rodents with interruption to dopamine activation of the nucleus accumbens can still engage in sexual activity. However, females do not initiate sexual interactions with males and these sexual interactions do not produce a pleasurable outcome (that is, they are not rewarding). In the extreme, female rodents in which the nucleus accumbens is damaged will aggressively try to fight off the male’s attempts to mount, although if the male is actually able to mount the female, she will display the characteristic sexual posture for that animal species. With lesser degrees of antagonism of dopamine signaling the female is more passive, seemingly willing to respond sexually to the male’s mounts. However, behavioral data suggest that these sexual interactions are not rewarding for the female. In these circumstances, repeated sexual experiences for the female do not increase the likelihood that she will initiate future sexual interactions with the male. This absence of a feed-forward facilitation of initiating sexual interactions with the male may provide an animal model for instances of low sexual desire in women.

Among mammals, the ventromedial nucleus of the hypothalamus is a critical regulatory center for circuits controlling the expression of the female sex behavior postures. Studies of hypothalamic damage in women support a similar involvement of the ventromedial nucleus in sexual behavior, though the examples are few with the interpretations prone to criticism. Dopamine neurotransmission in the ventromedial hypothalamus affects the expression of female sexual behavior in animals through a set of unusual biochemical interactions in neurons in this region. The ovarian hormones estradiol and progesterone are released in the bloodstream through which they circulate to the brain. In the ventromedial hypothalamus, these hormones alter the structure of the neurons to increase their dendrites, increasing the number of active connections on these cells. In addition, the hormones alter the biochemical properties of the neurons such that the neurons are more likely to increase their level of excitability. This increased excitability of the nerve cells along with increased excitatory inputs produces a greater flow-through of information activating the larger neural circuit directly responsible for the expression of female sexual behavior.

Dopamine is involved in the interaction between ovarian hormones and neuronal excitability in the ventromedial hypothalamus via an intersection of dopamine-triggered biochemical pathways with receptors for progesterone in these cells. Dopamine stimulates the D1 receptors on the surface of ventromedial hypothalamic neurons, thus triggering biochemical changes within the neurons. These biochemical changes in turn switch the progesterone receptor into its activated state, even in the absence of progesterone. In this way, dopamine potentiates the activity of progesterone receptors and the consequent effects on the throughput of excitation through the ventromedial hypothalamus, resulting in the expression of female sexual behavior. The important question of whether this process also occurs in the ventromedial hypothalamus of women does not have an answer at this time.

In men, systemic manipulations of dopamine affect several aspects of sexual arousal. Dopamine agonists stimulate sexual behavior, especially in circumstances where baseline expression of these behaviors is low. For example, apomorphine (a general dopamine agonist) stimulates erection in men with erectile dysfunction. In contrast, dopamine antagonists including antipsychotic drugs disrupt several aspects of sexual behavior. Potential neural loci for this dopamine action during sexual arousal/copulation are difficult to investigate using functional imaging due to ethical considerations, as well as methodological limitations. Data from partnered stimulation studies, in which a sexual partner manually stimulates a subject from outside the scanner, may provide the most naturalistic approximation of neural activity during sexual arousal.

As expected, genital stimulation activates the somatosensory cortex (a brain region responding to touch) rather than the mesolimbic areas activated by visual sexual stimuli. However, partnered stimulation can activate other dopamine-sensitive areas such as the ventral pallidum and the insular cortex. Further, data from partnered stimulation studies point to the hypothalamus as a critical target for dopamine action during sexual arousal in men (Brunetti et al., 2008). Imaging data suggest that activity in the hypothalamus is broadly associated with sexual arousal and penile tumescence. More specifically, activity in the lateral hypothalamus is correlated with penile tumescence, whereas activity in the anteroventral hypothalamus was correlated with penile detumescence after stimulation ended. It is notable that this pattern of activation maps onto data in rodents that shows that these same hypothalamic regions regulate arousal and de-arousal states.

Whereas the human literature on the neurobiological underpinnings of sexual arousal is relatively sparse, the animal literature is extensive and rich. Systemic manipulations of dopamine in animals follow the same pattern as in humans: activating dopamine generally facilitates sex behavior and inhibiting dopamine generally reduces sex behavior. In male rats, systemic treatment with apomorphine stimulates erection. Similarly, systemic administration of L-DPOA reduces the number of intromissions (penile insertions) required for ejaculation and decreases the latency to achieve an ejaculation. Treatment with a D2-selective agonist can activate copulation in sexually inactive male rats and reduce ejaculatory threshold in sexually-active male rats. In contrast, systemic treatment with dopamine antagonist drugs increases the latency for male rats to initiate mating behaviors, and decreases the efficiency with which males mate (e.g., the number of times the males achieve penile insertion). Finally, antipsychotic drugs which block dopamine receptors decrease the number of ejaculations in male rats. It is clear from the literature in male rats that systemic manipulations of dopamine have a profound effect on male sexual arousal.

In animals, the primary site of dopamine action for male sexual arousal is the medial preoptic area of the hypothalamus (Will, Hull, & Dominguez, 2014). As in the ventral striatum, levels of extracellular dopamine increase in the medial preoptic area of both male rats and Japanese quail in anticipation of mating and during mating. Lesions of the medial preoptic area eliminate or impair male copulatory behavior in every species studied, of which there have been many. In addition, site-specific injections of dopamine altering drugs into the medial preoptic area mirror the effects of systemic manipulations. For example, injections of apomorphine into the medial preoptic area facilitate copulatory behavior and increase the number of erections in male rats. On the other hand, injections of cis-flupenthixol (a nonspecific dopamine antagonist) directly into the medial preoptic area reduce sexual motivation (as measured by approaches to a goal box containing a female mating partner), reduce the number of male rats that successfully copulate, and impair copulatory performance in the remaining males that did copulate. In male Japanese quail, injections of both D1 and D2 antagonists into the medial preoptic area attenuate multiple aspects of male sexual behavior including the inhibition of rhythmic cloacal sphincter movements (a measure of sexual arousal in birds) as well as consummatory sexual behaviors.

The medial preoptic area is well-situated to regulate sexual arousal in several ways. First, the medial preoptic area sends direct projections to the ventral tegmental area, suggesting it can interface with libido/motivation. Second, the medial preoptic area is the major integrative center for gonadal hormones such as testosterone. In fact, studies from male rats show that gonadal hormones modulate dopamine action in the medial preoptic area. Testosterone generally enhances dopamine release in the medial preoptic area, and removing the natural source of circulating testosterone via castration impairs dopamine release in the medial preoptic area in response to a female sexual partner. The mechanism by which testosterone regulates dopamine release in the medial preoptic area depends on increased production of nitric oxide, the molecular target of pro-erectile drugs (e.g., Viagra). It is important to note that testosterone is a hormone that can easily be converted into estradiol (an estrogen) or dihydrotestosterone (a potent androgen). These products of testosterone also impact dopamine signaling in the medial preoptic area. When castrated male rats (who have no circulating testosterone) are treated with estradiol, it increases baseline levels of extracellular dopamine in the medial preoptic area, but does not rescue the characteristic increase in dopamine in response to a female. However, treatment with both estradiol and dihydrotestosterone in castrated males allows for a dopamine response to an inaccessible female. Oddly, testosterone may influence basal level of dopamine in the medial preoptic area via estrogen receptors, but activation of androgen receptors appears to be critical for males to display the typical dopamine response to a female along with the accompanying sexual arousal.

The distinction between the roles of preoptic dopamine in desire versus arousal may depend on the subtype of dopamine receptor involved, or possibly the ratio of different receptor subtypes (Will et al., 2014). Site-specific injections of the D1 agonist THP into the medial preoptic area increase the number of erections in response to physical stimulation in male rats, suggesting that D1 activity in the medial preoptic area modulates the physiological manifestation of erections. D1 activation may also increase sexual arousal more broadly via the sensitization of sexual stimuli. In male rats, repeated sexual experience leads to a facilitation of sex behavior that is correlated with an increase in medial preopotic area biochemical markers of D1 activation. Moreover, simply exposing a male rat to an inaccessible female mating partner for 7 days prior to copulation enhances copulatory behavior on the 8th day. However, injection of a D1 antagonist prior to each of the seven exposures prevents this behavioral effect. In contrast to D1 receptors, D2 activity in the medial preoptic area may mediate the transition from erection to ejaculation. Taken together, these data suggest activation of D1 receptors in the medial preoptic area may be more critical for sexual desire, whereas activation of D2 receptors in the medial preoptic area may be critical for arousal and ejaculation. The balance of activity at these two receptors may signal the appropriate action at different points in the mating episode.

Orgasm. Orgasms in people are subjectively intense sexual sensations that mark the termination of the sexual response cycle. Physiologically, orgasms are triggered by the spinal cord and autonomic nervous system. The subjective sensations of orgasm are accompanied by rhythmic contractions of the pelvic floor muscles and anus in both men and women, and seminal emission (i.e., ejaculation) in men. These physiological responses terminate rapidly once orgasm is triggered, signaling the beginning of a sexual refractory period which can vary in time considerably among individual men and women. We of course cannot determine whether animals experience the subjective feelings associated with orgasm, though we know that they have the same physiological responses, including a sexual refractory period (Pfaus et al., 2016). The subjective experience aside, the commonality between the physiological response and underlying nervous system control of orgasm has led to the view that orgasm is an evolutionarily conserved response that may serve different functions among animal species (Pavličev & Wagner, 2016).

The neurobiology of human orgasm is difficult to study because of the unpredictable and uncontrolled nature of orgasm. In men, studies using partnered manual stimulation during functional imaging suggest that the mesocorticolimbic pathway is activated during ejaculation. These findings do not map entirely onto data from studies that measure dopamine release during sexual behavior in male rodents. In male rats, dopamine release decreases in limbic and hypothalamic regions during ejaculation. This decline lasts through the refractory period during which sexual behavior is inhibited. With time, dopamine levels gradually increase and arousing stimuli can again activate copulation. Interestingly, in sexually exhausted male rats that are unable to copulate, mesolimbic dopamine remains at pre-copulatory levels even when a new female is introduced, suggesting that mesolimbic dopamine may be necessary for the initiation of copulatory behavior. It is possible that interspecies differences in mating patterns may explain the discrepancy between data from humans and rodents; in men, the refractory period is long compared to male rats who have refractory periods lasting only a few minutes. As such, mesolimbic dopamine may need be more dynamic in rats to signal the timing for mating resumption, a consideration that is less important in human men.

Imaging studies in women have identified changes in the activity of the prefrontal cortex accompanying orgasm, which is the primary link between orgasm and the dopamine system. In these studies, measurements of brain activity were made through a period of genital stimulation leading to orgasm, which was confirmed by measuring contractions of the pelvic floor muscles. Elevations of prefrontal cortex activity during sexual stimulation decreased rapidly upon orgasm. The degree to which these changes in activity in the prefrontal cortex (and by extension changes in dopamine) are related to a sexual refractory period following orgasm in women is not known.


Data from humans and nonhuman animals demonstrate that dopamine action in the brain is a key mediator of sexual behavior in both males and females. Dopamine neurotransmission is involved in libido, sexual arousal (including sexual activity), and orgasm, although its role in orgasm is less well defined.

The major regions involved in libido and sexual arousal are the mesolimbic pathway and hypothalamus. Unconditioned or conditioned sexual cues activate the mesolimbic dopamine pathway, which links sexual desire to its rewarding outcome. The result is that motivation and action are directed towards opportunities for sexual interactions. As such, mesolimbic dopamine activity is associated with both libido and sexual arousal/activity. Hypothalamic dopamine is likewise activated during both sexual desire and during sexual behavior. In particular, activation of D1 and D2 dopamine receptor subtypes in the preoptic area of the hypothalamus may underlie its role in sexual desire and sexual arousal, respectively. Importantly, the hypothalamus projects to the ventral tegmentum, providing a clear mechanism by which the two systems can coordinate dopamine action in order to dynamically regulate the response to sexual cues prior to and during mating.

Although there are many parallels between sexual behavior and its underlying neurobiology between humans and nonhuman animals, human sexual behavior is unique in its variability. Future studies examining the neurobiology of sexual behavior in humans would benefit from examining populations outside of cis-gendered heterosexual men and women to identify areas of commonality and divergence among people with differing identities.



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© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Department of NeuroscienceUniversity of MinnesotaMinneapolisUSA
  2. 2.Department of PsychologyHaverford CollegeHaverfordUSA