Sexual behavior in male rodents

Hull, Elaine M.; Domínguez, Juan M.

doi:10.1016/j.yhbeh.2007.03.030

Cited by 386 publications

(267 citation statements)

References 171 publications

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“…Because injection of µ receptor agonists into the MPOA deteriorates male sexual behavior [5,20], the target of opioid peptides might be the MPOA. In addition, because stimulation of the MPOA activates neurons projecting to the nPGi in the PAG [29], opioid stimulation on the MPOA might be sent through the PAG to the nPGi, which is known to be the primary source of tonic descending inhibition of erections and ejaculatory reflexes [2,6,9].…”

Section: Discussionmentioning

confidence: 99%

Naloxone Blocks the Deterioration of Male Sexual Behavior Induced by Alarm Pheromone in Rats

Kobayashi

Kiyokawa

Arata

et al. 2013

The Journal of Veterinary Medical Science

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ABSTRACT. Previously, we have demonstrated that the alarm pheromone deteriorates sexual behavior in male rats, which was blocked by pretreatment with a corticotrophin-releasing hormone (CRH) antagonist. Studies have shown that an opioid antagonist blocked the deterioration of male sexual behavior following intracerebroventricular administration of CRH. Therefore, possibly, the pheromone effects could also be mediated by the opioid system. In this study, we pretreated rats with naloxone, an opioid receptor antagonist, and examined the following sexual behavior modulations in male rats that were exposed to the alarm pheromone. Naloxone blocked the deterioration of sexual behavior in a dose-dependent manner. On the basis of these data and the results of the previous study, we conclude that the alarm pheromone activates the CRH system, which then activates the opioid system, to deteriorate male sexual behavior. KEY WORDS: alarm pheromone, naloxone, opioid, rat, sexual behavior.doi: 10.1292/jvms.12-0454; J. Vet. Med. Sci. 75(6): 761-765, 2013 Sexual behavior is one of the most important activities for organisms and has been studied for many years. In addition to sexual behavior itself, it also has been demonstrated that various types of stressors can deteriorate male sexual behavior. For example, 2 hr of immobilization elongated intromission latency, increased number of mounts needed for an ejaculation and decreased hit rate (number of intromissions/sum of mounts and intromissions) in male rat [27]. Similarly, water immersion elongated mount, intromission and ejaculation latency, and post ejaculation interval (PEI), and it increased the number of mounts and intromissions, and decreased the hit rate [27]. In addition, we have shown that sexual behavior was also deteriorated by the alarm pheromone [16].We previously showed that foot-shocked male Wistar rats release an alarm pheromone, which aggravates stressinduced hyperthermia (SIH) in pheromone-exposed rats [10] via the vomeronasal system [14]. We can induce the release of this pheromone by electrical stimulation to the perianal region of the anesthetized donor rat [14]. In addition, this alarm pheromone was shown to be water-soluble, because exposure to water droplets collected from the ceiling of the box in which the alarm pheromone was released produced all responses that are observed in recipients directly exposed to the pheromone [12]. This pheromone solution allows us to observe pheromone effects in different experimental paradigms; it can evoke several responses, such as aggravated SIH in the home cage [12,14], increased defensive and risk assessment behaviors in a modified open-field test [15] and enhanced acoustic startle reflex (ASR) [7,8]. In addition to its effects on individual animals, the effects of the alarm pheromone on social behavior have been analyzed [16]. When we presented the alarm pheromone during sexual behavior, male sexual behavior was deteriorated as indicated by the increasing number of mounts and decreasing hit rate, whereas female se...

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Section: Discussionmentioning

confidence: 99%

Naloxone Blocks the Deterioration of Male Sexual Behavior Induced by Alarm Pheromone in Rats

Kobayashi

Kiyokawa

Arata

et al. 2013

The Journal of Veterinary Medical Science

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“…The regulation of these phases is mediated by various central nervous systems structures. The medial preoptic area of the hypothalamus is involved in the control of libido and ejaculation, the locus coeruleus in the mediation of sexual arousal, and the nucleus paragigantocellularis and the paraventricular nucleus of hypothalamus in ejaculation control (17)(18)(19)(20). Interestingly, the ERβ protein is detectable in the preoptic area, the paraventricular nucleus of the hypothalamus, the dorsal raphe, and locus coeruleus (21,22).…”

Section: Discussionmentioning

confidence: 99%

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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“…Male mating is coordinated by gonadal steroid hormones including estrogen and testosterone, which signal through their receptors including estrogen receptors a and b (ERa and ERb), and androgen receptor (AR), respectively. ERa and AR are analogous to fru M in that they control all aspects of male courtship in mammals [13]. Male mice mutated for AR are feminized externally and engage in no sexual behaviors.…”

Section: Separable Genes Control Distinct Behavioral Parametersmentioning

confidence: 99%

Modular genetic control of innate behaviors

Xu¹

2013

BioEssays

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Many complex behaviors are genetically hardwired. Based on previous findings on genetic control of mating and other behaviors in invertebrate and mammalian systems, I suggest that genetic control of complex behaviors is modular: first, dedicated genes specify different behavioral patterns; secondly, separable genetic networks govern distinct behavioral components. I speculate that modular genetic encoding of complex behaviors may in part reflect modularity in brain development and function.

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Sexual behavior in male rodents

Cited by 386 publications

References 171 publications

Naloxone Blocks the Deterioration of Male Sexual Behavior Induced by Alarm Pheromone in Rats

Naloxone Blocks the Deterioration of Male Sexual Behavior Induced by Alarm Pheromone in Rats

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

Modular genetic control of innate behaviors

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