A role for 5-hydroxytryptamine in descending inhibition of spinal sexual reflexes

Marson, Lesley; McKenna, Kevin E.

doi:10.1007/bf02259106

Cited by 178 publications

(85 citation statements)

References 33 publications

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“…The serotoninergic system has been involved in the control in the sexual behavior in mice and humans (17,23). Serotonin acts as an inhibitor of the ejaculation (17,23,24). Because a decrease in tryptophan hydroxylase (the enzyme catalyzing the rate-limiting step in the synthesis of serotonin) mRNA in the dorsal raphe has been reported in ERβKO KI mice (25), our present behavioral results are not in keeping with this molecular data.…”

Section: Discussioncontrasting

confidence: 61%

Estrogen dependent activation function of ERβ is essential for the sexual behavior of mouse females

Antal

Petit-Demoulière

Méziane

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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We previously generated and characterized a genuine estrogen receptor (ER) β-null mouse line (named ERβ ST L−/L− ) and showed that ERβ ST L−/L− mice were sterile, due to an ovulation impairment in females and to an unknown reason in males, as their reproductive organs and spermatozoid motility appeared normal. We report here an assessment of the sexual behavior of ERβ ST L−/L− null mice. We found that ERβ ST L−/L− males display mildly impaired sexual behavior and that ERβ ST L−/L− females are significantly less receptive and less attractive than wild-type (WT) females. Decreased attractivity is also exhibited by ERβAF2 0 but not by ERβAF1 0 mutant females (females devoid of either AF2 or AF1 activation function of ERβ). Interestingly, by using an odor preference test, we have determined that the low attractiveness of ERβ ST L−/L− and ERβAF2 0 females is related to a deficiency of a volatile chemosignal.T he role of estradiol (E2) and estrogen receptor α (ERα) on the sexual behavior of the mouse is well known (1). ERα-null females do not display sexual receptivity, although they are as sexually attractive as wild-type (WT) controls. ERα-null males exhibit severely reduced numbers of mounts, thrusts and intromissions, and very few ejaculate (2). In contrast, ERβ has not yet been reported to play an important role in mouse sexual behavior (3). Several mouse lines bearing partial null mutations of ERβ have been generated and named according to the laboratory of origin (4, 5): ERβKO CH originated from a Chapel Hill laboratory (6), ERβKO ST from a Strasbourg laboratory (7), and ERβKO WY from Wyeth (8). The ERβKO CH line has been duplicated and a second colony, named ERβKO KI , has been established at the Karolinska Institut (9). A study performed on ERβKO CH males and females showed that they performed normally in sexual behavior tests. Nevertheless, a delay in the age of the first ejaculation was reported in these mice, without further consequences in adults (10), as adults ERβKO CH males were fertile and sired litters with the same efficiency as their WT counterparts (3). Contrasting with an apparent minor role in sexual behavior, ERβ appeared to be a major determinant of antianxiety behaviors in female mice (11,12), and, in a transient manner, of aggressive behaviors in male mice (13). ERβ was also reported to be involved in male mouse brain defeminization (14).We recently reported the generation and characterization of a complete ERβ-null mouse, the ERβ ST L−/L− mouse, of which the morphological phenotype contrasts in many aspects with that of the described ERβKO KI mutant (5). ERβ ST L−/L− females were sterile, due to ovulation impairment, and males exhibited infertility from an unknown reason because their internal and external reproductive organs appeared morphologically normal. Because ERβ ST L−/L− mice of both sexes displayed reproductive anomalies, we performed sex behavioral tests to evaluate the extent of ERβ involvement in mouse reproductive functions. We found that ERβ is required for a normal sexual beh...

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Section: Discussioncontrasting

confidence: 61%

Estrogen dependent activation function of ERβ is essential for the sexual behavior of mouse females

Antal

Petit-Demoulière

Méziane

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…The effects also seem to be species-specific (Paredes et al, 2000). Intrathecal injection of 5-HT in the spinalized anesthetized male rat blocked the appearance of the coitus reflex, suggesting that endogenous 5-HT may act in the descending input to the lumbar spinal cord that inhibits sexual reflexes (Marson and McKenna, 1992). A similar procedure in other experiments also inhibited ejaculation as well as penile intromission in rats, suggesting an alternative role of 5-HT in the transmission of sensory feedback information necessary for sexual responses (Svensson and Hansen, 1984).…”

Section: A 5-hydroxytryptaminementioning

confidence: 91%

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

Andersson

2011

Pharmacological Reviews

315

326

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“…In the third test vehicle-treated rats were still improving their ejaculation frequency, whereas paroxetine-and fluvoxamine-treated rats remained on the level of the second test, resulting in a significant difference. In general, serotonin inhibits sexual behavior and ejaculation (Hull et al, 2004;Marson and McKenna, 1992), and the reduced ejaculation frequency and trend to increased ejaculation latency could reflect increased serotonergic neurotransmission. Another possibility is that the SSRItreated rats experience increased anxiety to approach the female.…”

Section: Sexual Behaviormentioning

confidence: 99%

“…In particular behavior in which serotonergic neurotransmission plays a crucial role, including sexual behavior (Ahlenius and Larsson, 1997;Hull et al, 2004;Marson and McKenna, 1992), anxiety (Bagdy, 1998;Graeff, 2002), depression (Berendsen, 1995;Nutt et al, 1999) and schizophrenia (Kusljic et al, 2003), can be expected to be vulnerable to SSRI-treatment during adolescence.…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic treatment with fluvoxamine and paroxetine during adolescence on serotonin-related behavior in adult male rats

Jong

Snaphaan

Pattij

et al. 2006

European Neuropsychopharmacology

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Selective Serotonin Reuptake Inhibitors (SSRIs) are designed to treat adults, but are increasingly prescribed for adolescents. SSRIs might cause permanent changes in serotonin-related behavior in adolescents, since their serotonergic system is still developing.Male Wistar rats were treated with paroxetine (15 mg/kg p.o.) or fluvoxamine (30 mg/kg p.o.) throughout adolescence. After a washout period their behavior in the elevated plusmaze, prepulse inhibition test, Forced swimming test and elevated T-maze were studied. In addition, the effects of the 5-HT 1A receptor agonist 8-OH-DPAT on sexual behavior and lower lip retraction were measured. Paroxetine mildly inhibited weight gain during treatment. Both SSRIs caused a reduction in ejaculation frequency and in time spent on the open arm of the elevated plus-maze in adult rats. avoidance latency in the elevated T-maze compared to paroxetine. No differences between the groups were found in the other tests. Apparently, chronic treatment with SSRIs during adolescence may cause mild changes in adult behavior.

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A role for 5-hydroxytryptamine in descending inhibition of spinal sexual reflexes

Cited by 178 publications

References 33 publications

Estrogen dependent activation function of ERβ is essential for the sexual behavior of mouse females

Estrogen dependent activation function of ERβ is essential for the sexual behavior of mouse females

Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction

Effects of chronic treatment with fluvoxamine and paroxetine during adolescence on serotonin-related behavior in adult male rats

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