premature ejaculation/dopamine

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Study of the link between dopamine transporter gene polymorphisms and response to paroxetin and escitalopram in patients with lifelong premature ejaculation.

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We evaluated the role of dopamine (DA) transporter gene polymorphism in lifelong premature ejaculation (LPE) and its role in determining the response to paroxetine and escitalopram. Eighty consecutive patients and controls were recruited. Sixty of them suffered from LPE. They were divided into two

Effects of the dopamine D3 receptor agonist 7-hydroxy-2-(di-N-propylamino) tetralin in hyperthyroidism-induced premature ejaculation rat model.

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Various factors are involved in the aetiology of premature ejaculation (PE). Hyperthyroidism is one of the causes of acquired PE, but the exact mechanism by which it causes the disorder is not yet understood. The aim of this study was to evaluate the role of the dopaminergic system in

Impact of varicocelectomy on urine dopamine value in patients with premature ejaculation and varicocele.

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Dopamine is an important regulator of male sexual function and behaviour. Decreased levels of this substance have been observed in blood and seminal plasma of infertile men. Hence, this study was carried out to determine the impact of varicocelectomy on 24-hr urine dopamine values in patients with

Stimulation of dopamine autoreceptors elicits "premature ejaculation" in rats.

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Following treatment with dopamine (DA) receptor agonists, such as apomorphine, N-n-propyl-norapomorphine, lisuride and 3-(3-hydroxyphenyl)-N-n-propyl-piperidine (3-PPP) (50, 2.5, 400 and 5000 micrograms/kg, respectively), male rats attain ejaculation with receptive females sooner and after fewer

Relationship between premature ejaculation and genetic polymorphisms of the dopamine transporter gene (SLC6A3).

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OBJECTIVE • To investigate the possible relationships between premature ejaculation (PE) polymorphisms in the dopamine transporter (DAT) gene (SLC6A3, DAT1), which has a polymorphic 40 base pair (40 bp) variable number of tandem repeats (VNTR) sequence in the 3'-untranslated region (3'

The dopamine transporter gene (DAT1) polymorphism is associated with premature ejaculation.

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BACKGROUND Previous research has suggested brain dopamine (DA) neurotransmission to be involved in the control of ejaculation. Furthermore, previous studies indicate a partly hereditary background to premature ejaculation. OBJECTIVE To investigate whether the dopamine transporter gene (DAT1)

The selective D2 dopamine receptor antagonist eticlopride counteracts the ejaculatio praecox induced by the selective D2 dopamine agonist SND 919 in the rat.

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The selective D2 antagonist eticlopride, at a dose (0.01 mg/kg, s.c.) that fails to modify the normal behavior of rats, significantly reversed all the behavioral effects exerted by the selective D2 agonist SND 919 (0.1 mg/kg, i.p.), namely, the stimulation of stretching-yawning, penile erection and

Gene Variants in Premature Ejaculation: Systematic Review and Future Directions

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Introduction: A growing number of genetic association studies have been performed to investigate the association between the genetic susceptibility alleles and the risk of premature ejaculation (PE); however, the results remain

[An update on ejaculation physiology and premature ejaculation definition, prevalence data, and etiology].

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Ejaculation consists of two synchronized phases: a) emission, the contraction of the vas deferens, prostate and seminal vesicles and bladder neck expelling the seminal fluid to the urethra; it is mediated by sympathetic nerves, and b) expulsion, seminal fluid outward propulsion by the rhythmic

Candidate molecule for premature ejaculation, DA-8031: in vivo and in vitro characterization of DA-8031.

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OBJECTIVE To evaluate the efficacy of DA-8031 against premature ejaculation, we performed in vitro and in vivo pharmacologic studies. METHODS We used a monoamine transporter binding affinity assay, receptor binding affinity assay, monoamine reuptake inhibition assay, and serotonin uptake inhibition

Current and Emerging Treatments for Premature Ejaculation.

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BACKGROUND Over the past 20-30 years, the premature ejaculation (PE) treatment paradigm, previously limited to behavioral psychotherapy, has expanded to include drug treatment. Pharmacotherapy for PE predominantly targets the multiple neurotransmitters and receptors involved in the control of

Delay of ejaculation induced by SB-277011, a selective dopamine D3 receptor antagonist, in the rat.

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BACKGROUND Dopamine (DA) plays a key role in different aspects of the male sexual response, including sexual motivation and arousal, penile erection, and ejaculation. The modalities of action of DA are however unclear, although the various DA receptors may differentially mediate the activity of DA

Preliminary Evidence for an Association Between Variants of the Catechol-O-Methyltransferase (COMT) Gene and Premature Ejaculation.

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Studies have suggested that dopamine plays a role in the neurobiological mechanism that triggers ejaculation, leading scientists to hypothesize that dopamine-related genetic polymorphisms could contribute to symptoms of premature ejaculation (PE). To investigate associations between dopamine

Emerging and investigational drugs for premature ejaculation.

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Over the past 20-30 years, the premature ejaculation (PE) treatment paradigm, previously limited to behavioural psychotherapy, has expanded to include drug treatment. Pharmacotherapy for PE predominantly targets the multiple neurotransmitters and receptors involved in the control of ejaculation

Therapeutic targets for premature ejaculation.

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Premature ejaculation (PE) is the most common male sexual complaint, and may exert a profound negative impact on the man's life and partnership. Using currently available treatment alternatives (e.g., selective serotonin uptake inhibitor, agents acting locally on the penis), PE can be treated in

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