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F H Bronson

Publications and source records attributed to F H Bronson.

At least 73 records · Page 4Linked to original sources

Deterioration of the capacity for sexual arousal in aged male mice.

This experiment queried the frequency with which sexual inactivity in aged male mice is caused by a specific failure to arouse. Level of arousal was assessed in 30-month-old CB6F1 males by measuring each individual's willingness to walk on a treadmill in order to stay close to a receptive female and, in a separate test, by determining the amount of corticosterone secreted in response to a female. Sexual capacity was examined in a third test by challenging each male with a series of receptive females. Absolute time spent near a female on a treadmill, a measure of both endurance and arousal, correlated strongly (0.82) with the frequency with which an old male achieved ejaculation in its test of sexual capacity. Another treadmill measure, the proportion of a male's time spent near a female, correlated less well with ejaculation frequency (0.45) but this measure probably underestimated the importance of arousal. The magnitude of the corticosterone response to a test female also correlated significantly with ejaculation frequency (0.44). When viewed in toto, these results suggest that specific variation in the capacity of aged male mice to experience arousal accounts for 20% to 67% of the variation in their total sexual performance.

Aging↗

Endocrine responses to sexual arousal in male mice.

The endocrine correlates of sexual arousal were explored in male mice. Using indwelling atrial cannulae, temporal changes in the blood levels of six hormones were monitored in sexually rested vs. sexually sated males before and during their exposure to receptive females. The vaginae of some test females were artificially occluded to assess separately the impact of intromission on hormone levels. Sexually rested males responded to receptive females with dramatic increases in their blood levels of corticosterone, epinephrine, and norepinephrine. These changes occurred independently of intromission. Blood titers of these three hormones did not change in sexually sated males when they encountered a receptive female. Both sexually sated and sexually rested males discharged LH in a reflex-like manner immediately upon perceiving a test female. PRL was released only in response to ejaculation, and FSH titers were unaffected by the presence of a female. In general, a receptive female elicits a variety of hormonal responses in a male mouse. Some hormones seem to be discharged in response to sexual arousal per se, whereas others are released with varying degrees of independence of this process. Viewed from another perspective, the present results allow the presentation of a relatively detailed scheme that temporally relates sensory input to hormonal response during the sexual interactions of male mice.

Animals↗

The regulation of luteinizing hormone secretion by estrogen: relationships among negative feedback, surge potential, and male stimulation in juvenile, peripubertal, and adult female mice.

These experiments queried the potential for developmental change in the positive and negative feedback sensitivities of LH secretion to estradiol. Serum LH levels were compared in juvenile, peripubertal, and adult female mice after ovariectomy and challenge with a variety of 4-day steroid treatments. Since male stimuli accelerate the attainment of puberty in this species, comparisons also were made between age- and weight-matched groups of pre- vs. postpubertal females, obtained by housing them in either the presence or absence of males. The following conclusions were derived from eight experiments. 1) Progressively more estradiol is required to suppress the postovariectomy rise in serum LH as the female mouse develops the juvenile stage to full adulthood. 2) This slow, progressive change is due in part to a steadily increasing capacity to secrete LH when unhindered by any negative feedback regulation by the ovary; it is not due to developmental changes in estradiol metabolism. 3) The LH surging mechanism is functional and already coupled to its circadian oscillator in the juvenile mouse, but surges of adult magnitude could not be induced with exogenous steroid until the peripubertal period. 4) The estradiol requirements for preovulatory LH surging change markedly after the peripubertal stage of development; a wide range of temporal changes in blood estradiol levels will elicit LH surging in the adult mouse, but the immature female requires a rigid pattern of change involving only a narrow range of blood levels of this steroid. 5) Exposure of peripubertal females to male stimuli alters neither their negative feedback sensitivity to estradiol nor their estrogen requirements for LH surging. These conclusions are integrated into two working models that focus first on the estrogen requirements for LH surging in the adult mouse, and second on the maturation of this process and the attainment of pubertal ovulation. (Endocrinology 108: 506, 1981)

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Episodic release of luteinizing hormone in male mice: antagonism by a neural refractory period.

A refractory period of LH secretion follows both an internally generated and a female-induced, episodic release of LH in male mice. These experiments examined the duration of the refractory period and investigated its physiological basis. Plasma LH was measured in sequential blood samples that were withdrawn from chronically cannulated male mice. The males were exposed to two successive stimuli that were presented at 10-, 25-, or 45-min intervals; the two stimuli were a female both times, LHRH both times, or LHRH first and a female second. Males that were exposed to two successive females released LH in response to the second female only if 45 min had elapsed between exposures. All males in the LHRH-LHRH treatment group released LH after both injections of LHRH at all three stimulus intervals. The female stimulus evoked LH secretion in the LHRH-female treatment group at all three times after LHRH administration. In a second set of experiments, testosterone capsules that maintained the seminal vesicle weights of castrated males at well above normal levels did not block their LH responses to a female stimulus. When taken together, these results indicate that a refractory period lasting between 25 and 45 min follows episodes of LH release that are socially generated, that this refractory period has its basis in altered neural rather than pituitary activity and, finally, that this neurally based refractory period is not a result of inhibitory hormonal feedback.

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Effects of prior intrauterine position and housing on oestrous cycle length in adolescent mice.

Female mice that had developed in utero between 2 male (2M females) or 2 female (0M females) fetuses were housed individually at 32 days of age in the presence of a male. The 0M females had a significantly shorter cycle. When the females were housed in groups of 5 in the presence of a male, cycle length in 0M females was significantly longer than that of 2M females for the first cycle recorded, but this relationship reversed completely by the third and fourth cycles. These results are compatible with a hypothesis that former intrauterine proximity to male fetuses affects the intrinsic timing of the oestrous cycle and the capacity to emit oestrus-suppressing cues and/or the sensitivity to such cues.

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Sexual characteristics of adult female mice are correlated with their blood testosterone levels during prenatal development.

Mice produce litters containing many pups, and the female fetuses that develop between male fetuses have significantly higher concentrations of the male sex steroid testosterone in both their blood and amniotic fluid than do females that develop between other female fetuses. These two types of females differ during later life in many sexually related characteristics. Thus, individual variation in sexual characteristics of adult female mice may be traceable to differential exposure to testosterone during prenatal development because of intrauterine proximity to male fetuses.

Age Factors↗

Recovery of sexual activity with experience in aged male mice.

Aged CBF1 male mice that have been housed in isolation for prolonged periods of time often fail to show any sexual behavior when exposed acutely to receptive females. To separate the potential effects of social isolation from those of aging, the sexual responsiveness of aged males was tested both before and after a series of five-day pairings with young females. About one-half of the old males showed a complete recovery of their sexual responsiveness following these repeated pairings. Other aged males showed only a partial recovery and still others remained totally unresponsive. Changes in physical endurance, testicular steroid titer and arousability are posed as possible bases for those instances of sexual recovery that were observed.

Aging↗

Release of luteinizing hormone in male mice during exposure to females: habituation of the response.

Male mice release luteinizing hormone when exposed for a short time to a female. In this experiment, multiple blood samples were withdrawn by atrial cannulas from tethered males during either continuous or intermittent exposure to nonreceptive females. After an immediate, transient release of luteinizing hormone, continuous exposure to the same female was accompanied by only random, spontaneous elevations in plasma levels of this hormone. Successive presentations of the same female at 2-hour intervals elicited gradually diminishing luteinizing hormone responses. Exposing such unresponsive males to novel, diestrous females, however, dramatically stimulated their release of the hormone. These results demonstrate habituation of a socially induced, neuroendocrine response involving reproductive hormones.

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Rapid deposition of subcutaneous areolar tissue in response to sexual stimulation in mice.

Many of the reproductive processes of house mice are regulated exteroceptively by social cues. Puberty in a female mouse, for example, is a labile event that can be accelerated markedly if the young female is housed with an adult male. The relevant male stimuli in this case are a combination of pheromonal and tactile cues. The female's responses to these cues include an immediate, sequential release of gonadotropic and ovarian hormones, which in turn evoke a series of predictable changes in most of the female's reproductive tissues and culminate in the pubertal ovulation. I report here an unexpected consequence of exposing a young female mouse to a male, namely an intense response of a non-reproductive tissue. Specifically, young female mice experience a rapid thickening of their subcutaneous areolar tissue when they are exposed to males. The proximal cause of this response seems to be largely, but not exclusively, an enhanced secretion of ovarian oestrogen.

Animals↗

The reproductive ecology of the house mouse.

This paper attempts to integrate the physiological and ecological perspectives of the reproductive biology of the house mouse (Mus musculus). The endeavor is made within a larger context to provide a prototype for mammalian reproductive ecology in general. Specifically, the environmental regulation of the reproduction of Mus musculus is examined in relation to its ecological opportunism and, in particular, in relation to its history of global colonization. House mice can live as commensals of man or under totally feral conditions. Stable, high density, commensal populations are characterized by an insular division of the living space into demeterritories, each dominated by a single male. Feral populations typically are characterized by temporal, spatial, and social instability. Territoriality is improbable under such conditions, particularly given the necessity for large home ranges in most feral habitats. In both feral and commensal populations, however, male aggressiveness promotes the large-scale dispersal of young, all of which are potential colonizers. Of the ten or so environmental factors known to influence reproduction in house mice, seven probably are of routine importance in natural populations: diurnal modulation by daily light:dark cycles; caloric intake; nutrition; extreme temperature; agaonistic stimuli; socio-tactile cues; and priming pheronomes. The last two factors named operate directly on the secretion of luteinizing hormone or prolactin; the others act at many points in the reproductive system. Reproduction in the house mouse seems divorced from photoperiodically induced seasonality; indeed, this species breeds well even in constant darkness. Seasonal breeding may or may not then occur, depending upon dietary considerations, with or without a secondary interaction with variation in ambient temperature. There is no evidence for a dependence upon secondary plant compounds. Some of the effects of priming pheromones that have been observed previously in laboratory mice probably play no meaningful role in wild populations. The remaining pheromonal phenomena can be conceptualized as a single cueing system that has three components: (a) urinary cues of socially dominant males can accelerate ovulation in females, adult or prepubertal; (b) female urinary cues may elevate pheromonal potency in adult males, thereby forming a feedback loop by which the females elicit their own ovulation; and (c) the male's action on prepubertal females can be blocked by urinary cues emanating from other females. When all of the above is viewed in toto, the reproductive biology of the house mouse seems uniquely suited to support ecological opportunism. The relatively few environmental inhibitors of reproduction in this species should enhance the ability of dispersing young to colonize an exceptionally wide variety of habitats and climates...

Animals↗

Control of the preovulatory release of luteinizing hormone by steroids in the mouse.

The regulation of the preovulatory release of LH by steroids was examined in the mouse, a species in which ovulation is strongly influenced by priming pheromones. Ovariectomized mice were implanted with estradiol in Silastic capsules to involve negative feedback. Preovulatory-like LH surges then were induced by injections of either estradiol benzoate (EB) or progesterone. LH surges were not observed in the absence of steroid injection. LH surges always occurred at lights out on a 14-h light, 10-h dark cycle on the day after EB injection but occurred on the same day as progesterone injection. The amount of EB or progesterone injected seemed unimportant but, in either case, had to be given within a limited diurnal period of sensitivity. LH surges comparable to those of intact proestrous females were produced either by injecting both EB and progesterone or by manipulating the background dose of encapsulated estradiol. In the latter regard, when ovariectomized females were implanted with a wide range of doses of estradiol (0.1--1000 microgram/capsule), a decided window phenomenon became apparent. That is, LH surging could be induced by steroid injections only within a limited range of background doses of encapsulated estradiol. The relationship of the above findings to the pheromonal control of LH secretion and ovulation in mice is as yet unclear.

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