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13. Secretion of luteinizing hormone-releasing factor (LRF), luteinizing hormone (LH) and follicle stimulating hormone (FSH) as a motor pattern of female sex motivational system and exploration/marking motivational system; facilitated by estrogen and androgen and suppressed by ACTH and progestin. The hormonal control of the gonads is organized in two steps. A luteinizing hormone-releasing factor (LRF) is released from neurons in the arcuate nucleus and median eminence of the hypothalamus (Arimura, 1977). The LRF is then transported to the anterior pituitary in the hypothysial portal system where it stimulates the production of luteinizing hormone (LH) and follicle stimulating hormone (FSH) (Schally et al, 1971). The LH and FSH, in turn, are responsible for stimulation of the gonads. The secretion of luteinizing hormone-releasing factor (LRF) may be stimulated by coitus in both male and female muroid rodents. In females of the microtine rodents (voles and their relatives), ovulation normally occurs only in response to coitus (Dewsbury, 1977). Virtually all other muroid rodents whose cycles have been described have spontaneous ovulation on a regular cycle that is usually between four and seven days in length (Dewsbury, 1977). Some of these spontaneous ovulators may also release LRF and ovulate in response to coitus under special circumstances, and they have been called "facultative reflex ovulators" (Joch1e, 1975). The critical stimuli of coitus in the female rat for the release of LRF apparently include both the stimulation of the genital tract caused by the male's intromission and other stimuli, especially olfactory, associated with the mating. The LRF release is greatest if intromission takes place and less if intromission is blocked (Moss, 1974). It can be obtained from cervical stimulation alone (Takahashi et al, 1975) but still occurs during coitus despite cutting of the pelvic nerves that transmit the effects of cervical stimulation (Spies and Niswander, 1971). In the male rat there are increases in luteinizing hormone in the serum, presumably reflecting LRF secretion, as a result of coitus or as a result of exposure to female odors that may be associated with coitus (Kamel et al, 1977). Similar results have been obtained in other muroid rodents including the vole (Richmond and Stehn, 1976), hamster (Macrides et a1, 1974), and mouse (Macrides et a1, 1975). The stimuli of coitus are complex and it is likely that more than one motivational mechanism is activated during this process; therefore, it is difficult to know if the release of LRF is equivalent to a motor pattern activated by one or another motivational mechanism. The maximal release of LRF in the female following vaginal or cervical stimulation suggests that it may be a motor pattern of the female sex motivational mechanism that can be activated by such stimulation. Consistent with this hypothesis is the fact that the stimulus is not effective unless the animal has been primed with estrogen and progestin (Moss, 1974) which is also the case with the female sex motivational mechanism. The release of LRF in females after cutting of the pelvic nerve and in males by odors alone suggests that the exploration/marking motivational mechanism might also activate the release of LRF. This would also be consistent with the dependence of the effect in females upon priming with estrogen and progestin. The possibility that LRF is a motor pattern of the exploration/marking motivational mechanism is supported by abundant indirect data. As mentioned above the LH (and LRF) secretion of male rats is stimulated by female odors (Kamel et 81, 1977), and the greatest response is made to odors of estrous females; this parallels exploration/marking responses to estrogen-dependent pheromones (site 8). The estrous cycles of females may be initiated and accelerated by androgen-dependent pheromones from the male, as demonstrated in mice (Whitten, 1956; Bronson and Whitten, 1.968) and deermice (Bronson and Marsden, 1964). Since androgen-dependent pheromones also induce exploration/marking in females (site 9), the effects may be due to the same mechanism. There has been speculation that the same process could be involved (Whitten, 1966) in another effect that has been found to occur in most muroid rodent species that have been investigated; implantation from a previous mating is blocked if the female encounters another, strange male (Bruce, 1959; Kenney et al, 1977 Other studies indicate that male odors may trigger the initial onset of puberty in mice (Vanderbergh, 1969; Bronson and Desjardins, 1974) and voles (Richmond and Stehn, 1976) which is probably due to a surge in LRF secretion. In the vole, the odors must come from a strange male which would be expected if the exploration/marking motivational mechanism were involved; low estrogen levels would be expected to preclude the operation of a filter for androgen-dependent pheromones, leaving only one remaining motivating input, that from unfamiliar conspecific odors. Olfactory bulbectomy, as would be predicted from the preceding analysis, can disrupt normal ovulatory cycling in mice (Vandenbergh, 1973) and hamsters (Carter, 1973). Negative data have been obtained from the rat, however (Moss, 1971). Since the stimuli that activate exploration/marking in the male are also present during copulation and fighting encounters, this could also be responsible for observations that androgen production, presumably reflecting LRF and 1H secretion, is elevated in male muroid rodents following copulation (Purvis and Haynes, 1914; Taleisnik et a1, 1966) and fighting (Bronson and Marsden, 1973). Stimulation or lesions of the preoptic region and ventromedial hypothalamus evoke or block, respectively, the secretion of LRF {McCann, 1974). Since these are the proposed locations of the motivational mechanisms of exploration/marking and female sex motivational mechanisms, the data are consistent with the proposal that LRF release is a motor pattern activated by these motivational mechanisms. On the other hand, contrary to what I would predict, lesions of the medial preoptic area do not abolish the release of luteinizing hormones in response to coitus in male rats (Kamel and Frankel, 1978). As in the case of other types of' motor patterns, the release of LRF and LH may also require specific releasing inputs. However, unlike motor patterns that are released by exteroceptive stimuli, the LRF secretion is released by internal stimuli generated by an internal clock that occur at one particular time of the animal's diurnal cycle {Alleva et al, 1971). Estrogen facilitates both the release of LRF and the secretion of LH by the anterior pituitary that occurs in response to the LRF (Arimura, 1977; Brown-Grant, 1977). It is often considered that this is responsible for the periodicity of the estrous cycle; rising levels of estrogen during the follicular phase of the cycle triggers the releasing of' LRF and LH and the consequent ovulation in spontaneously ovulating muroid rodents such as the rat. Since LRF and LH, in turn, stimulate the production of estrogen from the ovary, this creates a positive feedback cycle that may be part of the determining factors for the four day estrous cycle of the rat. It should be noted that in addition to this long-duration positive feedback cycle, there is also a much shorter duration negative feedback; the initial effect of an estrogen injection is to reduce the secretion of LH (Arimura, 1977). A similar process may occur with androgen in the male. Although the short-term effect of androgen is to reduce LH secretions the long-term effect is apparently facilitative, since castration abolishes the secretion of the gonadotropic hormones (Arimura, 1977), and androgen administration restores it (Kamel and Frankel, 1979). Progestins inhibit the secretion of luteinizing hormone in response to the releasing factor (Arimura, 1911). This may be the basis for the fact that the estrous cycle is suppressed during pregnancy or pseudopregnancy at which time the corpus luteum releases a large amount of progestin into the general circulation. ACTH also inhibits the release of luteinizing hormone, either by blocking the responsiveness of the anterior pituitary cells that secrete the hormone, or else by blocking the release of the releasing hormone from the hypothalamus (Ogle, 1977). The effect is not due to ACTH stimulation of adrenal corticosteroids, since it is present after adrenalectomy.
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