A Closer Look at the Biological Basis of Women s Sexual Desire and Arousability Part 1

The neuroendocrine basis of sexual interest is poorly understood. The consequences on sexuality of medications with known or partly identified mechanisms of action suggest that more than 30 neurotransmitters, peptides, and hormones are embedded in the sexual reaction. Currently, the most clinically profound include noradrenaline, dopamine, oxytocin, and serotonin via 5HT1A and 5HT2C receptors all considered to be prosexual. Serotonin acting via most 5HT receptor sites, prolactin, and GABA, are considered sexually negative. The role of dopamine has been inquired especially in rodents. Dopaminergic input from the ventral tegmental area, particularly to the nucleus accumbens and forebrain is significant for cognitive and advantage processes. Dopamine administration into the nuclear accumbens has been found to stimulate the anticipatory phase (or appetitive phase) of a sexual activity. The paraventricular nucleus and the medial preoptic area of the hypothalamus regulate the anticipatory/motivational phases of rat copulation as well as the physiological changes of genital engorgement. Introducing a male hamster increases the dopamine in the nucleus accumbens in the female hamster along with her raised sexual activity. Even in animals, the outcomes of experience can be seen there is more 50 Basson dopamine accumulation and for a longer time period in female hamsters that are sexually experienced than in those who are sexually naive. In oophorized female hamsters, progesterone administration after estrogen priming leads to enhanced numbers of sex hormone receptors in the medial preoptic area. Interestingly, dopamine administration has the same effect as does environmental change namely the presence of a male hamster.

Brain imaging of women during sexual arousal evidences activation of areas involved in cognitive appraisal of the stimuli, namely the orbital frontal and anterior cingulate areas, and other areas involved in the emotional reaction to arousal including the rostral anterior cingulate. The latter and the posterior hypothalamus also imaged, are involved in the organization and perception of genital physiological reactions. Of interest, areas in the basal ganglia and temporal lobes that had shown activity in the nonsexually aroused state are no longer imaged during arousal, suggesting that they are involved in stimulating inhibition.

Hormones can be measured during the sexual reaction, but these determinations may contemplate the outcome of sexual response rather than cause (e.g., oxytocin increases with arousal and prolactin increases after orgasm).

Estrogen is acknowledged to affect mood and sleep and so its essential action may indirectly influence sexual response. That postmenopausal estrogen therapy causes improvement in well being, sleep, and vasomotor symptoms, is demonstrate based, but there are few scientific data to suggest that sexual benefit is afforded by relief of these particular symptoms. The role of androgen in women's sexual desire and arousability is currently under investigation. Although there is consensus that androgens are needed for sexual response, scientific study of androgen therapy with physiological amounts of androgen is only just beginning. It is also confusing whether the aromatization of testosterone to estradiol within the cell is essential, or whether instead or in addition, activation of the androgen receptor is necessary. Areas of high density androgen receptors in women's brains also have high aromatase activity. Thus, the whole question of whether any benefit of testosterone administration to women is actually due to getting estrogen more available (by decreasing SHBG) continues unsolved. The major androgens include the proandrogens, dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione, plus testosterone (T), and dehydrotestosterone (DHT). Output of adrenal androgen falls from the early 30s forward. Ovarian androstenedione is systematically reduced in mid- and later life. Studies are less conclusive regarding ovarian T production after natural menopause, with evidence of both decreased and raised production. Two recent small studies have shown a gradual decrease of T in women through their 40s with loss of mid-cycle peaks of T and androstenedione. Studies across the menopause transition demonstrate either a minimal decrease or even an increase. Contempt further reduction in adrenal androgen, in some women there may be enhanced production of ovarian T through the next two decades. On the other hand, some women show very low levels of ovarian production given the T levels in a large group of older women, after natural or surgical menopause were similar. Both of these groups of women were getting estrogen therapy.

About The Author

David Crawford is the CEO and owner of a guaranteed penis enlargement company known as Male Enhancement Group which is dedicated to researching and comparing male enhancement products in order to determine which male enhancement product is safer and more effective than other products on the market. Copyright 2010 David Crawford of guide to penis enlargement This article may be freely distributed if this resource box stays attached.

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