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Neurobiology of Sexual Response in Men and Women

By David L. Rowland, PhD


CNS Spectr. 2006;11:8(Suppl 9):6-12

This supplement is sponsored by GlaxoSmithKline

Faculty Affiliations and Disclosures

Dr. Rowland is professor of psychology and dean of graduate studies at Valparaiso University and senior associate in the Department of Population and Family Health Sciences in the Bloomberg School of Public Health at Johns Hopkins University.

Disclosure: Dr. Rowland has recently served as a consultant to Johnson & Johnson and Pfizer.

Submitted for publication: May 22, 2006; Accepted June 16, 2006.

Please direct all correspondence to: David L. Rowland, PhD, Valparaiso University, Department of Psychology, Valparaiso IN, 46383; Tel: 219-464-5446; Fax: 219-464-5381; E-mail:

Focus Points


• Human sexual response comprises several phases, typically distinguished as desire, arousal, and orgasm.
• The neurophysiologic systems underlying these components are not well understood.
• Sexual response is regulated through somatic and autonomic, peripheral and central nervous system pathways, and these pathways are modulated by steroid and peptide hormones.
• Serotonergic and dopaminergic systems are primarily involved in central regulation of sexual response, but cholinergic, γ-aminobutyric acidergic, nitergic, and other systems may also play a role.
• Adrenergic, cholinergic, and nitergic systems are responsible for mediating peripheral vascular responses that enable vaginal and penile response. These systems are also involved in orgasmic response.
• Disruption of hormonal, neural, or vascular integrity is likely to interfere with normal sexual functioning, although psychological and relationship factors play important roles as well.


Sexual desire, arousal, and orgasm are mediated by complex—and as yet not fully understood—interactions of the somatic and autonomic nervous systems, operating at cerebral, spinal, and peripheral levels. Furthermore, neural activity within these systems is modulated by the presence of steroid and peptide hormones, which affect male and female response differentially. At the central level, dopaminergic and serotonergic systems appear to play a significant role in various components of sexual response, although adrenergic, cholinergic, nitergic, γ-aminobutyric acidergic, and other neuropeptide transmitter systems may contribute as well. At the peripheral level, adrenergic, cholinergic, and nitergic activation mechanisms control vascular changes that underlie vaginal lubrication and penile erection. In addition, these systems respond to descending brain and spinal influences that generate orgasmic response. Disruption of endocrine, neural, or vascular response—caused by aging, disease, surgery, or medication—has the potential to lead to sexual inadequacy. At the same time, psychological and relationship factors play an important role in healthy sexual response and may enhance or impair sexual functioning.   


Various models of sexual arousal and response have been proposed over the past century. In their description of the “sexual response cycle,” Masters and Johnson1 distinguished the sequential phases of sexual excitement, plateau, orgasm, and resolution, which corresponded to specific genital changes including increased blood flow, the muscular contractions of orgasm, and the deactivation that follows. The model’s strong focus on genital response and the semantic problem of using discrete labels for a physiologically continuous process were significant limitations.2,3 

Later, Kaplan’s4 model of sexual response, incorporating the three components of desire, excitement, and orgasm, showed the interdependence among the response phases. For example, problems with orgasm could result from insufficient arousal; or problems with arousal might be seated in the desire phase. This triphasic model has had strong appeal because its components coincide with problems typically encountered by clinicians: lack of interest in sex, inability to become aroused (eg, get an erection or show vaginal lubrication), or difficulty with orgasm (eg, premature ejaculation, delayed orgasm, or anorgasmia).5 Since these initial conceptualizations, distinctions between “spontaneous” desire and “stimulus-driven” desire or “arousability” (ie, desire aroused by stimuli such as  the behavior and appearance of the partner) have been proposed. Whereas the former seems more typical of men, the latter may be more significant for women.6

Among the challenges for any model is that of identifying the underlying physiologic mechanisms of desire, arousal, and orgasm. In some instances, identification of supporting anatomic structures and neurophysiologic events has been quite successful, eg, with respect to the local mechanisms involved in penile erection and vaginal lubrication. In others, the relationships are elusive; for example, a comprehensive understanding of the physiology underlying sexual desire and orgasmic response does not yet exist.

Neurobiological systems are involved in sexual response in 3 ways:

(1) Physiologic input systems ensure sexual readiness (arousability) or induce sexual arousal itself. These systems convey information about general environmental conditions or context (is it the right time, the right place, the right mate?) or transmit specific sensory stimulation from a potential mate. In humans, the role of these systems is typically subtle and varies substantially between the sexes and among individuals.

(2) Spinal and brain systems mediate sexual arousal and feelings. In humans, the relevant mechanisms and structures are only now being elucidated through positron emission tomography (PET) and magnetic resonance imaging (MRI) studies.

(3) Finally, physiologic response systems are involved in the internal (autonomic) and external (somatic) responses necessary for preparing and executing a sexual response.

Physiologic Input Mechanisms

Arousability in most nonhuman mammals is largely under the control of the gonadal hormones.7 These hormones, produced by the ovaries and testes, are secreted in response to stimulation originating in the brain and mediated by the pituitary gland and its gonadotropic hormones. In sexually mature females, the secretion of gonadal hormones is sequential, with estrogen dominating during the first half of the reproductive cycle and progesterone during the second half. In males, the secretion of pituitary gonadotropins is tonic rather than cyclic, and the production of androgens is fairly constant over long periods.

The Role of Hormones in Men’s Sexual Response

Testicular hormones, particularly testosterone, contribute to a man’s interest in sex: the removal of these hormones is associated with diminished libido,8 whereas their reinstatement increases nocturnal erections, spontaneous sexual thoughts, and sexual desire. However, men with a deficiency of testosterone may be capable of erectile response,9 suggesting some independence of sexual arousal from testosterone-mediated interest in sex. Moreover, it should not be assumed that a lack of sexual interest in men results only from a lack of testosterone. Many psychological and relationship factors may be accountable, including the perceived level of attractiveness of the partner, feelings of resentment and hostility toward the partner, attempts to exert control over the relationship, and difficulty in dealing with one’s own or a partner’s sexual dysfunction. 

In men, a gradual decline in androgen production is common with aging, particularly beginning around the fifth decade of life. The resulting hypogonadism is associated with diminished sexual interest and, in some instances, decreased erectile function.10 Hyperprolactinemia is another cause of hypogonadism in men. Also at times manifested through a lack of sexual interest and concomitant erectile problems, hyperprolactinemia is usually treated with the dopamine agonist bromocriptine.

The Role of Hormones in Women’s Sexual Response

The role of gonadal hormones in human female sexual response is less clear. In most female primates, ovarian hormones influence but do not control sexual behavior, which may be expressed even when gonadal hormones are minimal. In women, attempts to correlate desire, arousability, and arousal with different phases of the menstrual cycle, during which different hormones dominate, have met with only partial success. In women, both estrogens and androgens may work together to enhance sexual arousal and response.11-13 For example, the administration of estrogen plus small amounts of testosterone to menopausal women provides greater improvement of psychological symptoms (eg, lack of concentration, depression, and fatigue) and sexual dysfunction (eg, impairment of libido, sexual arousal and ability to have an orgasm) than estrogen alone.11,14 However, variability in sexual interest in women, probably even more than in men, is likely to be contextual and partner-based, and relatively independent of biological control systems.

With aging and menopause, women may experience a number of sex-related problems that are directly or indirectly associated with decreased estrogen and androgen production. Sexual desire may be lessened and subjective and physiological aspects of sexual arousal may be affected, the latter because of reduced genital blood flow. Vaginal dryness and consequent discomfort or pain may also interfere with enjoyable intercourse.15

While the specific mechanism through which gonadal hormones might facilitate sexual desire and arousal is unknown, they are probably active at multiple levels. For example, they may “prime” structures in the brain, thereby lowering the threshold to activation in the presence of sexually relevant stimuli. They may also work on spinal and peripheral neural systems: the rise of gonadal hormones during and after puberty may be responsible for “eroticizing” certain types of sensory stimulation—perhaps by transforming somatic sensory stimulation (such as genital touching) into autonomic information. Autonomic activation is generally associated with emotional responding and is necessary for feelings of excitement and arousal.16 Finally, these hormones may affect local mechanisms of penile and vaginal vascular competence. Most important, however, is the realization that sexual response is multifactorial, depending on complex interactions of physiologic, psychological, and relationship factors.

Central Mechanisms of Sexual Motivation and Arousal

Distinctions between the desire, cognitive-emotional, arousal, and response aspects of sexuality become blurred at the level of the central nervous system. Even in relatively simple animal models, the interaction of a number of structures is essential for sexual response, as sensory, information-processing, motivational, and motor elements of sexual response are integrated to generate a purposeful action. Furthermore, these structures may themselves be under the influence of modulators; specifically, structures involved in the control of sexual arousal and behavior are often sensitive to the presence of circulating steroid (gonadal and adrenal) hormones.17
In males of many species, several neural structures, particularly the medial preoptic area (MPOA) and other forebrain limbic areas, appear to play a central role in  sexual response. These centers may be responsible for translating sensory input into appropriate behavioral output7; furthermore, they do not operate in isolation but receive input about the organism’s arousal state from the amygdala and about the external environment via cortical structures. Steroid hormones such as testosterone can modulate the activity of the MPOA, as can input from the other brain areas.

The MPOA is also involved in the regulation of sexual behavior in females, but its role is to inhibit sexual receptivity. The important brain structure responsible for activating sexual behavior in females appears to be the ventromedial nucleus (VMN) of the hypothalamus. Removal of this area interferes with sexual response in females and reduces their tendency to approach males. Like the MPOA in the male, the VMN may act by increasing the connection between sexual sensory stimuli and autonomic/ behavioral output.17

The extent to which the preceding findings apply to humans is only now being clarified through research using MRI and PET. Preliminary studies suggest that some of the neural activation during sexual arousal may be shifted from lower brain centers (MPOA and VMH) to higher brain centers in men and women. This pattern is not surprising in view of the fact that sexual response in humans depends more heavily on contextual factors such as the relationship with the sexual partner, social behavior, attitudes, beliefs, and moral codes. In men, changes have been noted in the ventral tegmental area, a midbrain-forebrain region involved in mediating pleasure and reward. Concomitant changes in the frontal, occipital, and temporal lobes have also been noted.18 Generally, these brain regions interpret sensory stimuli and evaluate, choose, and execute motor/behavioral responses. Activity changes in hypothalamic and amygdala areas have also been noted in men. In women, many of these same structures appear to undergo change during arousal and orgasm.19 However, there appears to be less activation of hypothalamic and thalamic regions in women; this may explain the apparent differences between men and women in the response to visual erotic stimuli. 

Neurochemistry of Sexual Response

Given widespread cerebral involvement in sexual response, it is not surprising that multiple neurotransmitter systems appear to contribute to it. However, exactly how and where various transmitters are operative, particularly in humans, are questions still under investigation.

In male rats, moderate doses of dopamine (D1/D2) agonists injected into the MPOA promote erections and copulation. Furthermore, dopamine in the nucleus accumbens has been associated with many reward-related behaviors, including copulation. Injection of the nitric oxide (NO) precursor L-arginine facilitates dopamine release in the MPOA, suggesting a role there for NO as well. Cholinergic nicotinic receptor influences on sexual behavior also appear to be mediated by the MPOA. Oxytocinergic neurons in the paraventricular nucleus (PVN) of the hypothalamus may further mediate erectile response, as do both ascending and descending serotonergic systems in the brainstem. The ascending (cerebral) serotonergic system generally exerts an inhibitory role on rat male sexual activity. However, the fact that different 5-HT receptor subtypes have different effects on sexual function may be related to serotonergic involvement at different levels of the central nervous system—forebrain, brainstem, spinal cord, and autonomic ganglia. Finally, alteration of γ-aminobutyric acid (GABA)ergic neurotransmission affects sexual behavior in rats. Both GABAA and GABAB agonists inhibit sexual behavior, whereas antagonists, at least when injected directly into the MPOA, have prosexual effects. Given the omnibus involvement of the major neurotransmission systems in the expression of sexual behavior in the male rat, it is likely that these systems play at least as complex a role in mediating sexual response in men.20

Specific neurotransmitter involvement in females is less well understood. However, given the overlap in the neural structures mediating male and female sexual response, involvement of similar systems may be assumed. For example, as with males, both the MPOA and PVN appear to have major roles in female sexual function. Furthermore, D1 receptor activation—as well as oxytocin, GABA, and opioid receptor activation—in various hypothalamic centers can increase lordosis (female receptive position) in rats. Likewise, serotonergic systems in the brainstem and upper spinal cord probably mediate orgasmic response in females. Given that drugs affecting serotonergic activity (eg, selective serotonin reuptake inhibitors) and dopaminergic activity (eg, antipsychotics) often interfere with women’s orgasm, these systems are strongly implicated in human female sexual response. In addition, drugs increasing GABA activity (eg, benzodiazepines) result in less satisfying orgasms for women, whereas drugs affecting nitergic (involving NO), adrenergic, and cholinergic systems appear to have minimal effects on human female sexual response.21   

Peripheral Autonomic and Somatic (Motor) Responses

The somatic sensorimotor nervous system responds to information about the environment (visual, auditory, tactile, etc.) and innervates striate muscles involved in voluntary motor responses. In contrast, the autonomic nervous system (ANS) is involved primarily in the control of involuntary internal smooth muscle responses, including erection and vaginal lubrication. But sexual arousal and response require the activation of both systems, and their integrated functioning is complex and not well understood.16

It can be said that during sexual arousal the ANS is activated via somatosensory stimulation to prepare the organism for sexual behavior. Activation of the ANS is responsible for mediating extragenital smooth muscle changes, which are similar across the sexes, such as increased blood pressure, transient increases in heart rate, vasocongestion in the breast and pelvic regions, and, ultimately, an overall increase in muscle tension. Genital changes, although different, tend to follow parallel courses in men and women.

Mechanisms of Erection and Ejaculation

Both divisions of the ANS, sympathetic and parasympathetic, are involved in arousal and activation of the genitals. The traditional functional classification of these systems (ie, a homeostatic or regulatory role for the parasympathetic component and an emergency/arousal role for the sympathetic component) does not necessarily extend to activation of the genitals. Thus, the parasympathetic and sympathetic components of the ANS both appear to contribute to sexual excitement, penile erection, and ejaculation16,22 Stimulation of parasympathetic fibers of the pelvic nerve arising from the sacral area of the spinal cord can generate an erection. Recent studies, however, suggest a possible role for the sympathetic nervous system in erection as well, since blockage of this system produces penile engorgement and erection.

The ANS influences erectile tissue through changes in the dynamics of blood flow of the pudendal arteries. Erection is the result of increased arterial flow through vasodilation and shunting of the arterial blood away from immediate venal flow into the cavernous spaces of the penis. This increase in arterial flow initially occurs without an increase in blood pressure and therefore is probably the result of relaxation of the smooth muscle of the arterial walls. When full erection occurs and intracavernosal pressure is increased, small blood vessels are compressed against the relatively unyielding walls of the tunica albuginea, and the resulting blockage decreases venal outflow.

The erectile mechanisms operating at the level of the smooth muscle cells in the penis are complex. At the extracellular level, neurotransmitters, hormones, and locally released substances from penile tissue both originate and modulate the biochemical signals that produce erection. At the cell membrane and the intracellular level, second messenger molecules (eg, cGMP or cAMP) and ions carry the signal via the action of receptor proteins or enzyme pathways. At the intercellular level, the ion channels and gap junctions propagate the signal from one cell to the next. The cumulative input of these factors in response to an erectile stimulus then produces a coordinated physiological response in the penis.

The above processes are regulated primarily by the central and peripheral nervous system through the activity of adrenergic, cholinergic, and nonadrenergic, noncholinergic neurotransmitters. In addition to neurologic control, factors released locally from the corporal tissue of the penis help maintain a tonic flaccid state through vascular constriction. Enzymatic pathways (eg, phosphodiesterase) within the muscle cell may inactivate signal transduction pathways across the cell membrane to suppress erectile function. Interfering with this erection-inhibiting system using PD5 inhibitors (eg, sildenafil) can thus facilitate erectile response.23

Ejaculation is the efferent (motor) component of a reflex process resulting from sensory stimulation of the coronal region of the penis. At the genital level, ejaculation involves two steps: (1) seminal emission and bladder neck closure; and (2) forced expulsion of fluid,16 and requires involvement of the sympathetic, parasympathetic, and somatic motor systems. During the first stage, semen is deposited in the urethral tract and the bladder neck closes to prevent urine from mixing in the urethral tract and semen from flowing back toward the bladder. Sympathetic a-adrenergic mediation of this response has long been known, but recent pharmacologic studies suggest that cholinergic parasympathetic fibers may be involved as well.24

The deposition of semen in the urethral tract serves as a partial trigger for the spasmodic (clonic) contractions of expulsion—a complex process that involves involuntary contraction of striate muscles normally under voluntary control. The initial trigger for the ejaculatory sequence is under the control of brain and spinal systems and is related to the man’s level of sexual excitement and arousal, as evidenced by the effect on the ejaculatory response of centrally acting dopaminergic and serotonergic drugs.16 Furthermore, there is evidence to suggest that the posterior pituitary hormone oxytocin may facilitate these contractions.25 Exactly what makes these rapid contractions so rewarding is unknown, although dopamine release in brain reward centers, the ventral tegmental and nucleus accumbens, is evident in rats during copulation.

Mechanisms of Vaginal Lubrication and Female Orgasm

As in men, sympathetic, parasympathetic, and somatic pathways innervating the genital region—in women, particularly the vagina and clitoris26—mediate the response to sexual stimulation. Sympathetic and parasympathetic nerves connect via the pelvic and pudendal nerves, and their stimulation can increase blood flow to and affect smooth muscle tone in the vagina. Somatic pathways are responsible for controlling striate muscles around the vaginal opening and in the pelvic and abdominal areas.

During sexual arousal, vaginal smooth muscle shows a gradual increase in tone. In addition, autonomic input stimulates blood flow to the vagina through vasodilation; increased capillary flow, and the engorgement of the lining of the vaginal wall as well as the labia and clitoris with blood, stimulate vaginal lubrication. At the peak of sexual arousal all the capillaries are open and the flow is maximal.26 As with erectile response in men, α-adrenergic antagonists such as phentolamine cause vasodilation and increased vaginal blood flow in women, suggesting that decreased sympathetic tone, along with concomitant increases in parasympathetic activity, mediates this response.

As in men, the trigger for orgasm is unknown but probably involves accumulating afferent input. Undoubtedly both pelvic and genital structures (clitoris, uterus, cervix, etc.) contribute to the overall experience of orgasm in women. Clearly, the clitoris and, possibly, the periurethral glans (area below the clitoris surrounding the urethra) are homologous to the penis and are the locus of orgasm for most women. As in men, peripherally mediated genital and orgasmic responses are under the control of brain and spinal mechanisms; alteration of central monoaminergic systems frequently interferes with orgasmic response in women. Furthermore, since ovarian hormones contribute to vaginal tissue response, women’s genital responsivity is influenced by hormonal changes that occur with aging and various pathologies.

There is ongoing debate regarding the function of orgasm in women. Hypotheses include preparation of the uterus for impregnation, facilitated transport of sperm toward the uterus, or even dissipation of vasocongestion in the vaginal region. Given these sex differences in structure and function related to orgasm as well as the brain structures involved, the mechanisms of orgasm may be sufficiently dissimilar in women and men so that the experience of orgasm is different as well. Furthermore, 15% to 42% of women may experience multiple orgasms in rapid succession.27 In contrast, multiple orgasm in men is still viewed as “case study” material, although recent research suggests that a subpopulation of men may be capable of achieving multiple orgasms.28


Sexual response involves interacting systems of physiologic input, maintaining arousability and producing arousal by transmitting general information about external conditions as well as specific sensory stimuli; spinal and cerebral input, inducing a state of central activation and arousal; and physiologic response, both autonomic and somatic, preparing and executing the climactic phase of the sexual response cycle. In humans, arousability is influenced by the gonadal hormones, but variations in sexual desire are more likely to be due to psychosocial than to biological factors. In humans, responsibility for mediating arousal appears to be partly shifted from lower (limbic) to higher brain centers, and some of the brain structures that regulate arousal appear to be activated to differing degrees in men and women.

Somatic, sympathetic, and parasympathetic neural pathways are involved in the mechanisms of arousal and orgasm. Central regulation of sexual response primarily involves serotonergic and dopaminergic pathways, although several other neurotransmitter systems also take part. Adrenergic, cholinergic, and nitergic mechanisms mediate the peripheral vascular responses of penile erection and vaginal lubrication. In both men and women, decreased sympathetic tone and increased parasympathetic activity appear to be responsible for increased genital blood flow during sexual arousal, and orgasm may be triggered by a reflex response to accumulating afferent input. However, local differences in structure and function, together with differences in the relative involvement of some brain centers, suggest that there are differences, as well as common elements, in the way the cycle of arousal and orgasm is subjectively experienced by men and by women.


1. Masters WH, Johnson VE. Human Sexual Response. Boston, MA: Little, Brown; 1966.
2. Rosen RC, Beck JG. Patterns of Sexual Arousal: Psychophysiological Processes and Clinical Applications. New York, NY: Guilford Press; 1988.
3. Robinson P. The Modernization of Sex.  New York, NY: Harper & Row; 1976.
4. Kaplan HS. The New Sex Therapy.  New York, NY: Brunner/Mazel; 1974.
5. Diagnostic and Statistical Manual of Mental Disorders. 4th ed text rev. Washington, DC: American Psychiatric Association; 2000.
6. Basson R. A model of women’s sexual arousal. J Sex Marital Ther. 2002;28:1-10.
7. Pfaus JG, Kippin TE, Coria-Avila G. What can animal models tell us about human sexual response? Annu Rev Sex Res. 2003;14:1-63.
8.  Bancroft J. Human Sexuality and Its Problems. Edinburgh: Churchill Livingstone; 1989.
9. Davidson JM, Myers L. Endocrine factors in sexual psychophysiology. In: Rosen R, Beck G, eds. Patterns of Sexual Arousal: Psychophysiological Processes and Clinical Applications. New York, NY: The Guilford Press; 1988:158-186.
10. Morales A, Buvat J, Gooren L, et al. Endocrine aspects of men’s sexual dysfunction. In: Lue TF, Basson R, Rosen R, et al, eds. Sexual Medicine: Sexual Dysfunction in Men and Women. 2nd International Consultation on Sexual Dysfunctions. Paris: Health Publications; 2004:345-382.
11. Grio R, Cellura A, Porpiglia M, Geranio R, Piacentino R. Sexuality in menopause: Importance of adequate replacement therapy. Minerva Gynecol. 1999;51(3):59-62.  
12. Davis SR. Testosterone deficiency in women. J Reprod Med. 2001;46:291-296.
13. Wallen K. Sex and context: hormones and primate sexual motivation. Horm Behav. 2001;40:339-357.
14. Sherwin BB, Gelfand MM, Brender W. Androgen enhances motivation of females: a prospective crossover study of sex steroid administration in the surgical menopause. Psychosom Med. 1985;47:339-351.
15. Davis SR, Guay AT, Shifren JL, et al. Endocrine aspects of female sexual dysfunction. In: Lue TF, Basson R, Rosen R, et al, eds. Sexual Medicine: Sexual Dysfunction in Men and Women. 2nd International Consultation on  Sexual Dysfunctions. Paris: Health Publications; 2004:749-782.
16. Motofei IG, Rowland DL. Neurophysiology of ejaculation: developing perspectives. BJU Int. 2005;96:1333-1339.
17. Pfaff DW, Schwartz-Giblin S. Cellular mechanisms of female reproductive behaviors. Knobil E, Neill J, eds. The Physiology of Reproduction. New York, NY: Raven Press; 1988:1487-1568.
18. Stoléru S, Grégoire MC, Gérard D, et al.  Neuroanatomical correlates of visually evoked sexual arousal in human males. Arch Sex Behav. 1999;28:1-21.
19. Karama S, Lecours AR., Leroux JM, et al. Areas of brain activation in males and females during viewing of erotic film excerpts. Hum Brain Map. 2002:16;1-13.
20. Saenz de Tajeda I, Angulo J, Cellek N, et al. Physiology of erectile function and pathophysiology of erectile dysfunction. In: Lue TF, Basson R, Rosen R et al, eds. Sexual Medicine: Sexual Dysfunction in Men and Women. 2nd International Consultation Sexual Dysfunctions. Paris: Health Publications; 2004:289-343.
21. Meston C, Levin R, Sipski M, et al. Women’s orgasm. Annu Rev Sex Res. 2004;15:173-257.
22. Rowland DL, Burnett A. Pharmacotherapy in the treatment of male sexual dysfunction. J Sex Res. 2000;37:226-243.
23.    Padma-Nathan H, Christ G, Adaikan G, et al. Pharmacotherapy for erectile dysfunction. In: Lue TF, Basson R, Rosen R, et al, eds. Sexual Medicine: Sexual Dysfunctions in Men and Women. 2nd International Consultation Sexual Dysfunctions. Paris: Health Publications; 2004:505-565.
24. Giuliano F, Clement P. Neuroanatomy and physiology of ejaculation. Annu Rev Sex Res. 2005;16:190-216.
25. Carmichael MS, Humbert R, Dixen J, et al. Oxytocin increase in human sexual response. J Clin Endocrinol Metab. 1987;64:27-31.
26. Levin RJ. Sexual arousal—its physiological role in human reproduction. Annu Rev Sex Res. 2005;16:154-189.
27. Darling CA, Davidson JK, Jennings DA. The female sexual response revisited: understanding the multiorgasmic experience in women. Arch Sex Behav. 1991;20:527-540.
28. Dunn ME, Trost JE. Male multiple orgasms: A descriptive study. Arch Sex Behav. 1989;18:377-388.


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