Neurobiology Of Sexual Behavior Research Paper

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During the second half of the twentieth century, interdisciplinary research efforts have generated considerable information about the physiological mechanisms that control mammalian reproductive behaviors. The approach has used field and laboratory studies with animals to elucidate general principles that are beginning to be assimilated by the social sciences as they toil to understand the sexual and parental behaviors of our own species. What follows is a review of basic research on sexual behavior, sexual differentiation, and maternal functions in mammals including humans.

1. Sexual Behavior

Mammalian sexual behavior is facilitated in males and females by the hormonal secretions of the testes and ovaries, respectively. In females the display of sexual behavior shows cycles closely associated with fluctuations in the hormonal output of the ovaries. In many species, including rodents commonly used in laboratory experiments, the cyclic display of behavior includes both changes in the ability of the female to copulate as well as her motivation or desire to engage in sexual behavior. In these species intercourse is often physically impossible except during a brief period of optimal hormonal stimulation of central and peripheral tissues. The central effects of ovarian hormones (i.e., estrogen (E) and progesterone (P)) in the facilitation of female sexual behavior are mediated by receptors found in several brain regions including the ventromedial nucleus of the hypothalamus (VMH), the preoptic area, and the midbrain central gray. The effects of E and P on neurons of the VMH appear to be sufficient to facilitate the display of the postural adjustment necessary for copulation in female rats (i.e., the lordosis reflex), and the display of lordosis is prevented by lesions of the VMH (Pfaff et al. 1994). Female rats with VMH lesions can show lordosis if other neural systems that normally inhibit the display of lordosis are also surgically removed (Yamanouchi et al. 1985). The rewarding or reinforcing aspects of female copulation are likely to be mediated by dopaminergic systems that include the nucleus accumbens. The rewarding aspects of female sexuality appear to be activated only when the female can control when and how often she has contact with the male during mating, i.e., when the female can ‘pace’ the copulatory encounter (Erskine 1989).

In sharp contrast with nonprimate species, female monkeys are capable of engaging in sexual behavior at all phases of the ovulatory cycle and after ovariectomy. This fact which of course also applies to women, has been often used to question the importance of ovarian hormones in the modulation of female sexuality in primates. Other work, however, has shown that in spite of having the ability to copulate throughout the menstrual cycle, female monkeys show fluctuations in sexual motivation that are predictable from the pattern of ovarian E production across the cycle. For the behavioral effects of E to be evident, female monkeys must be tested in situations in which they are given the opportunity to choose between avoiding contact with the male or alternatively to approach the male and solicit his attention. In a series of elegant experiments conducted under naturalistic conditions Wallen and associates (Wallen 1990, 2000) have shown that in rhesus females, the willingness to leave an all-female group in order to approach a sexually active male peaks at the time of maximal E production at the end of the follicular phase. Further, under the same conditions, females never approach the male if their ovarian functions are suppressed by pharmacological manipulations. As argued by Wallen, in rhesus females and perhaps also in women, ovarian hormones do not determine the ability to engage in sexual behavior but have salient effects on sexual desire. Almost nothing is known about where E acts in the brain to facilitate sexual motivation in female primates.

In male mammals, castration results in a reduction in sexual behavior and replacement therapy with testosterone (T) or its metabolites restores the behavior to pre castration levels. In nonprimate species both the motivational and performance aspects of male sexuality are affected by lack of T. In men and possibly other primates, lack of T seems to affect sexual motivation more than sexual ability (Wallen 2000). Thus, men with undetectable circulating levels of T can reach full erections when shown visual erotic materials, but report little sexual interest in the absence of T replacement. In men, erectile dysfunction is often due to non endocrine causes such as vascular pathologies or damage to peripheral nerves. In the brain T seems to act primarily in the medial preoptic area (MPOA) to facilitate male sexual behavior, but it is evident that other brain regions as well as the spinal cord and other peripheral sites need hormonal stimulation for the optimal display of sexual behavior in males. Lesions of the MPOA have immediate and profound disruptive effects on male sexual behavior and these effects are remarkably consistent across species. Lesions of the MPOA however do not equally affect all components of male sexual behavior and some of the effects of the lesions are paradoxical. For example, in male rats lesions of the MPOA that virtually abolish male sexual behavior do not seem to affect willingness to work on an operant task when the reward is access to a receptive female. Similarly, male mice continue to show courtship behavior directed to females after receiving large lesions of the MPOA. It has been suggested that lesions of the MPOA selectively affect consummatory aspects of male behavior leaving appetitive or motivational components intact. Not all the data fit this proposed dichotomy. For example rhesus monkeys that show copulatory deficits after MPOA damage do not lose all the consummatory aspects of male behavior; after the lesions the animals are capable of achieving erections and they frequently masturbate to ejaculation (Nelson 2000).

The view that male sexual behavior results primarily from T action in the MPOA and female sexual behavior from E and P action in the VMH is not without detractors. In a recent study of male sexual behavior in the rat, it was found that androgen antagonists implanted directly into the MPOA did block male sexual behavior as would be expected. However, the most effective site for androgen antagonist blockade was in the VMH! (McGinnis et al. 1996). There is also considerable overlap between the neural systems that are active during female sexual behavior and those that are active in the male during copulation. These studies may indicate that the appetitive aspects of sexual behavior, seeking out a partner, courtship, etc. are under the control of similar neural systems in both sexes (Wersinger et al. 1993).

2. Sexual Differentiation

In addition to the activational effects gonadal hormones have on adult sexual behavior, there is an extensive literature base to show that gonadal hormones also affect the development of brain systems that regulate male and female sexual behavior. These long-lasting effects are often referred to as ‘organizational effects’ to distinguish them from the concurrent facilitative actions that gonadal hormones have in the adult. Organizational hormone actions are thought to occur primarily during the period of sex differentiation of the nervous system. In species with short gestation, such as rats and hamsters, this developmental period occurs around the time of birth, whereas in those species with longer gestation times, such as primates, sex differentiation of the nervous system takes place during fetal development (Nelson 2000).

Normal males are exposed to androgens throughout this early developmental period as a result of the testes becoming active during fetal development. When genetic female rats were treated with T throughout this time they showed significant masculinization of behavior and genital morphology. As adults, these experimental females displayed most of the elements of male sexual behavior including the ejaculatory reflex. When males were deprived of androgens during this time they were less likely to show the consummatory responses associated with masculine copulation. Further, in the absence of androgens during early development, male rodents develop into adults who show most of the elements of female sexual behavior if treated with ovarian hormones. For many laboratory rodents the behavioral masculinizing effects of T treatment result from metabolites of T, namely estradiol and reduced androgens such as dihydrotestosterone. There is good evidence that for some species it is the estrogenic metabolite that is essential for behavioral masculinization.

Ovarian hormones do not appear to play a role in the development of the neural systems that underlie feminine sexual behavior in mammals. When female laboratory rodents, such as the golden hamster, are treated with estrogen during early development they actually show reduced levels of female sexual behavior as adults. However, their levels of male-like behavior, such as mounting receptive females, are increased, findings that are consistent with the concept that estrogen is a masculinizing metabolite of T in males.

The findings on the effects of gonadal hormones during early development of the female are not easily interpreted, because an independent definition of just what is feminine and what is masculine is not available. On the one hand it is clear that if a female rodent is exposed to high levels of androgen throughout early development she will develop a male-like anatomy and will, as an adult, show all the elements of male sexual behavior. On the other hand, female rodents are often exposed to low levels of androgens normally during gestation as a result of developing next to a male in the uterus. These females are often more dominant than other females and less attractive to males (VomSaal 1989). But they still copulate as females and reproduce, suggesting that normal variations in female phenotype may result from normal variation in androgen exposure during development. This variability in female behavior and attractiveness may be an important part of any normal female population. The problem lies in defining the limits of normal female variation resulting from androgen (or estrogen) exposure, as opposed to what androgen effects might be interpreted as masculinization (Fang and Clemens 1999). The criteria for making this distinction have not yet been defined.

Numerous sex differences have been reported for the mammalian nervous system and most of these probably result from the differential exposure to gonadal hormones that occurs during sex differentiation. It also presumed that the sex differences in behavior that we have noted result from these differences in the nervous system of males and females, but few models are available to show a strong correlation between sex differences in the CNS and sex differences in behavior (but see Ulibarri and Yahr 1996). Gonadal hormones can influence the development of the nervous system in a number of ways such as altering anatomical connectivity, neurochemical specificity, or cell survival. For example, while both male and female rats have the same number of nerve cells in the dorsomedial nucleus of the lumbosacral cord prior to sex differentiation, in the absence of androgen many of these cells die in the female, a normal process referred to as ‘apoptosis.’ This differential cell-death rate leaves the adult male rat with a larger dorsomedial nucleus than the female. In some brain regions it is suspected that hormones may actually promote cell death resulting in nuclei that are larger in the female than in the male. There are also numerous examples of sex differences in the peripheral nervous system as well.

For many years sex differences in human behavior were regarded as reflections of differences in how male and female children are reared. However, the accumulation of volumes of work showing that sex differences in non humans are strongly influenced by differential hormone exposure has forced scientists from many fields to re-evaluate the nurture hypothesis. Most would probably now agree to several general statements. 1. The brains of male and female humans are structurally very different. 2. These differences may reflect, at least in part, the different endocrine histories that characterize the development of men and women. 3. Some of the behavioral differences between males and females may result from these differences in their nervous systems. Disagreement occurs when we try to specify how much of one trait or another is due to biological factors and how much to experience, and it must be recognized at the outset that a clean separation of nature from nurture is not possible.

Most of the evidence for biological factors operating to produce sex differences in human behavior comes from clinical or field psychology studies. A number of syndromes involve variation in androgen or estrogen levels during early development: congenital adrenal hyperplasia (CAH) is a syndrome in which the adrenal gland produces more androgen than normal. Turners Syndrome is characterized by regression of the ovaries and reduced levels of androgen and E from an early age. Hypogonadism is a condition where boys are exposed to lower than normal levels of androgen. There are also populations of girls and boys who were exposed to the synthetic estrogen, diethylstilbestrol (DES) during fetal development as well as populations whose mothers were treated with androgenic-like hormones during pregnancy. A number of studies point to a change in girls play behavior as a result of exposure to androgens during fetal development. CAH girls or girls exposed to exogenous androgenic compounds are often found to show an increased preference for playing with toys preferred by boys and less likely to play with toys preferred by untreated girls. These androgen-exposed girls also are more likely to be regarded as ‘tomboys’ than their untreated sibs or controls and engage in more rough and tumble play than controls (Hines 1993). Some have argued that variation in androgen or E levels during early development may affect sexual orientation, but a general consensus on this point has not been reached at this time.

3. Maternal Functions

For rodents, especially in the case of the laboratory rat, the endocrine and neural mechanisms responsible for the onset and maintenance of maternal behavior are relatively well understood (Numan 1994). This understanding has stemmed to a large extent from the careful description of behaviors shown by maternal rats; these behaviors are easy to identify and to quantify in the laboratory. Such a rich and objective behavioral description is often lacking for other species including our own. In rats, all components of maternal care of the young (except milk production) can be induced in the absence of the hormonal changes that normally accompany pregnancy, parturition, and lactation. Thus, virgin female rats become maternal if they are repeatedly exposed to pups of the right age, a process referred to as sensitization. Hormones, nevertheless, play a critical role in the facilitation of maternal behavior and are necessary for the coordination of maternal care and the arrival of the litter. Using different experimental paradigms, several laboratories have identified E as the principal hormone in the facilitation of maternal behavior. When administered systemically or when delivered directly into the MPOA, E triggers the display of maternal behavior under many experimental conditions. Prolactin from the anterior pituitary or a prolactin-like factor from the placenta also play a role, albeit secondary, in the facilitation of maternal functions; administration of prolactin or analogs of this hormone enhances the activational effects of E on maternal behavior. Also, mice lacking functional prolactin receptors show poor maternal care. Other peptides and steroids have been implicated in the support of maternal functions (Nelson 2000). For example, central infusions of oxytocin facilitate maternal behavior under some conditions and the effects of P on food intake and fuel partitioning are crucial to meet the energetic challenges of pregnancy and lactation (Wade and Schneider 1992).

The integrity of the MPOA is necessary for the display of normal maternal behavior. Damage of the MPOA using conventional lesions or chemical lesions that spare fibers of passage interferes with normal maternal behavior under several endocrine conditions. Similar behavioral deficits are seen after knife cuts that interrupt the lateral connections of the MPOA. Cuts that interrupt other connections of the MPOA do not reproduce the behavioral deficits seen after complete lesions (Numan 1994). Normally, male rats do not participate in the care of the young, but exposing males to pups for several days can induce components of maternal behavior. Compared to females, adult males require more days of sensitization with pups and tend to show less robust maternal behavior. This sex difference is not evident before puberty (Stern 1987) suggesting that sexual differentiation of behavior may not be completed until after sexual maturation. When males are induced to care for the pups, the behavior is sensitive to the disruptive effects of lesions of the MPOA. Since MPOA damage affects both male sexual behavior and the display of maternal care, it is possible that there is partial overlap between the neural circuits that support these two behavioral functions. Alternatively, MPOA lesions may affect more fundamental aspects of the behavioral repertoire of the animals, and such a deficit then becomes evident in different ways under different social conditions. The effects of MPOA lesions in females are also complex and not fully understood. In addition to affecting maternal functions MPOA damage results in a facilitation of the lordosis reflex concurrently with a reduction in the females’ willingness to approach a sexually active male in testing situations that permit female pacing. Finegrained analyses of the functional anatomy of the MPOA are needed to further elucidate the precise role of this area in mammalian reproductive functions.

Studies of monogamous mammalian species where males and females remain together after mating offer the opportunity to study paternal care as well as social bonding between parents and between parents and offspring. One promising model is that of the prairie vole in which both the female and the male care for the young (DeVries and Villalba 1999). Studies of these monogamous rodents suggest that bonding of the female to the male and to her young may be enhanced by oxytocin, a peptide hormone synthesized in the hypothalamus and secreted by the posterior pituitary. In the male, paternal care appears to result, not from oxytocin, but from another hypothalamic hormone, vasopressin. In addition to these posterior pituitary hormones investigators have found evidence for a role of the endogenous opiates in strengthening the bond between mother and offspring (Keverne et al. 1999).


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