Role of neurotransmitters in sexual function--论文代写范文精选

女性的性功能系统导致血流增加。羟色胺行为在中央和周边受体。血清素下调和多巴胺减少活动,导致性欲减退。此外,血清素的激活受体对性机能产生影响。激活的受体亚型降低，促进行为的发生。下面的paper代写范文进行详述。

Abstract
Nitric oxide, serotonin, dopamine, epinephrine, norepinephrine, acetylcholine, histamine, GABA are all implicated to have roles in sexual function. Neurotransmitters act both within the brain and in peripheral organs, and therefore may play complex and interacting roles in promoting and facilitating sexual functioning.

(a) Nitric oxide (endothelial relaxing factor) 
Nitric oxide (NO) is an essential component in the production of penile, and possibly, clitoral vasocongestion and tumescence. The release of NO by cholinergic and non-cholinergic nerves appears to be the major contribution of the parasympathetic nervous system.(38) As described above, NO is now understood to be the most significant mediator of vascular smooth muscle relaxation, responsible for engorgement of erectile tissue in men and women. Sexual stimulation leads to NO production that in turn stimulates the release of guanylate cyclase. Guanylate cyclase converts guanosine triphosphate to cGMP and cGMP produces relaxation of the smooth muscles of the penile arteries and corpus cavernosum resulting in increased blood flow into the penis.(39) Some evidence suggests that this may also occur in the clitoris.(40) Normally, cGMP is metabolized by cyclic nucleotide phosphodiestrase isozymes into gunanosine 5'- monophosphate. As long as sexual stimulation continues, cGMP production and metabolism remain balanced and penile or clitoral tumescence is sustained.(41) Erectile dysfunction can result when this process is not working normally or when it is partially or completely disrupted. (5)

(b) Vasoactive Intestinal Polypeptide (VIP) VIP has been less well understood but is shown to colocalize with NO is nerves to genital blood vessels and smooth muscle. In women, systemic administration and local subepithelial injection of VIP result in increased vaginal blood flow and lubrication.(9) In addition, sexual arousal raises the level of VIP found in the plasma. In men VIP also co-localizes with NO and has been shown to play an important role in erection.(5) 

(c) Serotonin 
Serotonin acts at both central and peripheral receptors in the mediation of sexual function. (5) Centrally, serotonin appears to downregulate and diminish levels of mesolimbic dopaminergic activity and to elevate prolactin, resulting in decreased libido.(42,43) In addition, serotonergic activation of different receptor subtypes has differential effects on sexual functioning. Activation of receptor subtype IA lowers the thershold for ejaculations, while activation of 2A , 1B or IC inhibits sexual behaviours and stimulation of 2C facilitates behaviour in animal models.(44) Peripherally, at spinal or end-organ receptors, serotonin has inhibitory effects on ejaculation in animals.(45) Also serotonin tends to cause problems with orgasm and desire more than arousal itself. Serotonin even acts on the smooth muscles of the genitals possibly inhibiting the muscular contractions that characterize orgasm.(5) Further, serotonin acts at peripheral nerves, where it appears to affect the flow of genital sensory information. Lastly, serotonin may delay orgasm through pre-synaptic inhibition of adrenergic transmission.(45) 

(d) Dopamine
All the four major dopaminergic CNS pathways are proposed to play a role in sexual behavior. The incertohypothalamic pathway stimulation increases all phases of male rat sexual behaviour and induces penile erection. In female rats it induces sexually receptive posture called lardosis. The mesolimbic pathway is involved in the anticipatory phase of sexual activity associated with motivation and sexual reward. The nigrostriatal pathway is important in the motor behaviour required for consummatory sexual activity in male rats. Lastly the tubero infudibular pathway appears to play a role in baseline sexual interest as opposed to more acute behavioural changes.(5,46,47) Regarding relationship between dopamine and prolactin, it remains unclear whether hyperprolactinemia itself is causative or acts as a surrogate marker for decreased dopmine. A recent F-MRI study demonstrated an increase in blood flow to specific dopaminergic and other brain structures when 17 college men and women viewed pictures of people they love and are sexually attracted to.(48) (e) Epinephrine Plasma levels of epinephrine have been shown to increase prior to viewing an erotic film, slowly increase during masturbation, peak at orgasm, and return to baseline level within several minutes of orgasm.(49) 

The epinephrine and norepinephrine metabolite, vanillylmandelic acid, increases prior to intercourse and continue to be elevated over baseline upto 23 hours following sexual activity.(50) (f) Norepinephrine In men, blood plasma NE levels were positively correlated with arousal and erection during masturbation and sexual activity, increased upto 12-fold at orgasm and declined to baseline levels within 2 minutes of reaching orgasm.(51,52) Studies suggest that NE is also active during the sexual response cycle of women. Blood plasma levels of NE increased during masturbation peaked at orgasm, and slowly declined following orgasm in normally functioning women.(49,52) 
(g) Acetylcholine 
Erection occurs when the smooth muscles of the corpus cavernosum relax permitting increased blood flow into the penile tissue. The human corpus cavernosum is innervated by cholinergic nerves and contains cholinergic receptors suggesting endogenous cholinergic activity in the penile tissue.(53,54) Acetylcholine (Ach) appears to play a less direct role in sexual functioning that is largely a function of maintaining the balance of cholinergic and sympathetic input at the genital level.(5) Ach antagonist, atropine showed no effect on either vaginal vasocongestion or orgasm in women and large doses were insufficient to block penile erection in men,(9) though in vitro administration of Ach to pre-contracted corpus cavernosum induced smooth muscle relaxation.(7) Thus Ach is sufficient to produce vasocongestion, but not essential for this effect.

(h) Histamine Very little is known about the role of histamine in facilitating sexual functioning, but evidence suggests that activity at both H2 and H3 receptors in the penis can cause erection.(56) There are a few case reports of decreased desire in both men and women taking cimetidine (H2 antagonist), the mechanism of which may be, decreased peripheral response to testosterone (7) or decreased metabolism of estradiol leading to gynaecomastia in men.(57) 

Gama aminobutyric acid (GABA) 
GABA enhancing benzodiazepine use has been implicated in case reports of decreased libido, erectile dysfunction and anorgasmia.(58) While mechanisms are poorly understood, it is hypothesised that centrally mediated sedation and peripheral muscle relaxation may be responsible.(5) Apart from the above mentioned ones, many other putative neurotransmitters, including argininevasopressin, angiotensin II, substance P, neuropeptide-Y, a-MSH, Gn RH are involved in sexual functioning, but there is little research into their precise role.(59)

Conclusion
Sexual function is a complex phenomenon involving an orchestra of chemical elements ranging from small molecules like nitric oxide to peptides like oxytocin. We are aware that derangements of various hormones and neurotransmitters are involved in sexual dysfunction but their precise role is not known. Further, putative neurotransmitters are gaining more implications in sexual dysfunction. Deeper investigation into these areas will no doubt reveal greater insight about sexual functioning which in turn assists in efficient management of sexual dysfunction(paper代写)

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