Abstract:The present study was undertaken to determine if the diminished release of LH in male rats with age in response to castration or LHRH injection is due to alternations in the number or affinity of LHRH receptors in the pituitary. Young (3-4 months old) and old (18-20 months) male Sprague-Dawley rats were killed 0, 2, 4, and 8 days after castration. Serum was collected for determination of LH concentrations, and anterior pituitaries were removed for analysis of LHRH receptors. The numbers and affinity constants … Show more
“…Previous studies have found that LH levels increase after gonadectomy and the increase is greater in young than in old males. Moreover, LH is suppressed by T treatment in both young and old males, but old males are more sensitive to low doses of T than young males (Karpas, Bremner, Clifton, Steiner, & Dorsa, 1983; Pirke, Geiss, & Sintermann, 1978; Sartin & Lamperti, 1984; Shaar, Euker, Riegle, & Meites, 1975; Sonntag, Forman, Fiori, Hylka, & Meites, 1984). Although the mean levels of LH were higher in the young GX males than in the old GX males, in this study this difference did not achieve significance.…”
Neural estrogen receptors (ER), serum testosterone (T), estradiol (E2) and luteinizing hormone (LH), and masculine sexual behavior were measured in young (5 months) and old (24 1/2 months) Fischer 344 male rats. We found that old intact males, which displayed significantly lower levels of sexual behavior, T, and LH than young intact males, also had lower levels of nuclear ER (ERn) in the amygdala (AMG). The age difference in ER binding did not appear to be a consequence of altered blood E2 levels because circulating E2 did not differ between the two age groups. Gonadectomy eliminated ejaculatory behavior and significantly reduced ERn in young males. When we administered exogenous T to gonadectomized males in doses that approximated levels found in young intact males, we found that sexual performance of old males was stimulated to precastration levels but not to levels found in young males. Moreover, such treatment failed to increase ERn in the AMG of old males to the levels measured in the AMG of young males. These results suggest that there is an association between the inability of T to increase ERn concentration in the AMG and the deficits in sexual performance that are characteristic of old males. Thus, the capacity of neural tissue to bind estrogen, presumably derived from circulating T, may be a limiting factor in the determination of androgen responsiveness in aging males.
“…Previous studies have found that LH levels increase after gonadectomy and the increase is greater in young than in old males. Moreover, LH is suppressed by T treatment in both young and old males, but old males are more sensitive to low doses of T than young males (Karpas, Bremner, Clifton, Steiner, & Dorsa, 1983; Pirke, Geiss, & Sintermann, 1978; Sartin & Lamperti, 1984; Shaar, Euker, Riegle, & Meites, 1975; Sonntag, Forman, Fiori, Hylka, & Meites, 1984). Although the mean levels of LH were higher in the young GX males than in the old GX males, in this study this difference did not achieve significance.…”
Neural estrogen receptors (ER), serum testosterone (T), estradiol (E2) and luteinizing hormone (LH), and masculine sexual behavior were measured in young (5 months) and old (24 1/2 months) Fischer 344 male rats. We found that old intact males, which displayed significantly lower levels of sexual behavior, T, and LH than young intact males, also had lower levels of nuclear ER (ERn) in the amygdala (AMG). The age difference in ER binding did not appear to be a consequence of altered blood E2 levels because circulating E2 did not differ between the two age groups. Gonadectomy eliminated ejaculatory behavior and significantly reduced ERn in young males. When we administered exogenous T to gonadectomized males in doses that approximated levels found in young intact males, we found that sexual performance of old males was stimulated to precastration levels but not to levels found in young males. Moreover, such treatment failed to increase ERn in the AMG of old males to the levels measured in the AMG of young males. These results suggest that there is an association between the inability of T to increase ERn concentration in the AMG and the deficits in sexual performance that are characteristic of old males. Thus, the capacity of neural tissue to bind estrogen, presumably derived from circulating T, may be a limiting factor in the determination of androgen responsiveness in aging males.
“…As matured rats are reported to be stable at the level of estrogen in an ovariectomized animal model [16, 17], relatively young rats (10-week old, approximately 230 g) in the growth stage were used in this study to examine the SMF effects on the concentration change of estrogen.…”
The effects of a moderate-intensity static magnetic field (SMF) on osteoporosis of the lumbar vertebrae were studied in ovariectomized rats. A small disc magnet (maximum magnetic flux density 180 mT) was implanted to the right side of spinous process of the third lumbar vertebra. Female rats in the growth stage (10 weeks old) were randomly divided into 4 groups: (i) ovariectomized and implanted with a disc magnet (SMF); (ii) ovariectomized and implanted with a nonmagnetized disc (sham); (iii) ovariectomized alone (OVX) and (vi) intact, nonoperated cage control (CTL). The blood serum 17-β-estradiol (E2) concentrations were measured by radioimmunoassay, and the bone mineral density (BMD) values of the femurs and the lumbar vertebrae were assessed by dual energy X-ray absorptiometry. The E2 concentrations were statistically significantly lower for all three operated groups than those of the CTL group at the 6th week. Although there was no statistical significant difference in the E2 concentrations between the SMF-exposed and sham-exposed groups, the BMD values of the lumbar vertebrae proximal to the SMF-exposed area statistically significantly increased in the SMF-exposed group than in the sham-exposed group. These results suggest that the SMF increased the BMD values of osteoporotic lumbar vertebrae in the ovariectomized rats.
“…At the pituitary level, the impaired gonadotrophin response to LHRH observed in old rats [7] is not associ ated with changes in the number of LHRH receptors [44], but no data are presently available pertaining to LHRH accumulation and processing in the adenohypo physis of old rats. Moreover, variant forms of gonadotro phins have been detected in the pituitary gland of old rats, suggestive of changes with age in the biological activity of the hormones [45],…”
Section: Aging and Reproductive Functionmentioning
Aging is characterized by changes in neuroendocrine/endocrine functions which are manifest in female reproductive physiology and less perceptible in other functions such as thyroid, adrenal or growth/metabolic functions. The contribution of each level of the axis – hypothalamus, adenohypophysis or peripheral tissues – is not clearly established. Functional impairments with age are recognized in the peripheral glands (gonad, thyroid, adrenal) as well as in the pituitary, but increasing evidence is accumulating for a marked contribution of the hypothalamus in the age-associated endocrine changes observed in animals and humans. In old rats, multineuronal dysfunctions are demonstrated in the hypothalamus, with a documented decline in the activity of the neurons producing dopamine and thyrotropin-releasing hormone, and to a lesser extent luteinizing hormone- and growth hormone-releasing hormones, and alterations in regulatory mechanisms of these neurons are disclosed. Moreover, impairments are observed in the processing – binding, accumulation and intracellular distribution – of hypothalamic hormones in the adenohypophysis of old rats. Taken together, these observations are supportive of the view that the neuroendocrine/endocrine changes appearing with age result from a complex balance of functional alterations occurring at each level – central and peripheral – of the axis.
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