A Quantitative Study on Feedback Control of Lh by Testosterone in Young Adult and Old Male Rats

Pirke, Karl M.; Geiss, Michael; Sintermann, R.

doi:10.1530/acta.0.0890789

Cited by 43 publications

(16 citation statements)

References 8 publications

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“…As age advances, female rats show a de creased negative feedback response to estro gen [Shaar et al, 1975;Huang et al, 1976;McPherson et al, 1977], but male rats show an increased negative feedback response to testosterone [Shaar et al, 1975;Pirke et al, 1978]. The site of negative feedback action of sex steroids is located in the basomedial hy pothalamus (BMH) in male dogs [Davidson and Sawyer, 1961a], male rats [Lisk, 1962], female rabbits [Davidson and Sawyer, 1961b;Kanematsu and Sawyer, 1964] and female rats [Lisk, 1960;Chower and McCann, 1961;Ramirez et al, 1964] by implantation of es trogen or testosterone in the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

No Neuron Loss from Hypothalamic Nuclei of Old Male Rats

Peng¹,

Hsu²

1982

Gerontology

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Neuron density, volume of the area and total neuron number were measured in the medial preoptic area, supraoptic nucleus, paraventricular nucleus, anterior hypothalamic area, ventromedial nucleus, dorsomedial nucleus and arcuate nucleus of the hypothalamus in young adult male rats (3.5–5 months old) and in old male rats (26–27 months old) of the Sprague-Dawley strain. There is no neuron loss in all measured areas. The results correlate well with the sex difference in the functional changes of the feedback response to sex steroids in old rats.

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Section: Discussionmentioning

confidence: 99%

No Neuron Loss from Hypothalamic Nuclei of Old Male Rats

Peng¹,

Hsu²

1982

Gerontology

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“…In the testis of aging beagle dogs, it appears that both LC atrophy and hyperplasia occur and are associated with an elevation in circulating LH levels (Ewing et al, 1987). By contrast, the decline in circulating testosterone that occurs during senescence in rats occurs while LH levels are declining (Pirke, 1979) and appears to be related to a reduction in the capacity of the LC to respond to LH rather than to a decline in LC number (Chen et al, 1994).…”

Section: The Senescent Lcmentioning

confidence: 99%

“…Testosterone levels decline with age in most strains of rats (Chan et al, 1977) as well as in humans (Horton and Tait, 1967;Vermeulen et al, 1972). In rats, this decrease is probably secondary to declining LH levels (Pirke, 1979;Roberts et al, 1989;Prentice et al, 1992;Chen et al, 1994), although this is somewhat paradoxical because one would expect LH to increase in order to maintain testosterone levels. This is in contrast to the situation in man where LH levels tend to increase with age, presumably because of decreasing testosterone levels (Rubens et al, 1974;Vermeulen, 1978).…”

Section: B Comparative Biologymentioning

confidence: 99%

Rodent Leydig Cell Tumorigenesis: A Review of the Physiology, Pathology, Mechanisms, and Relevance to Humans

Cook

Klinefelter

Hardisty

et al. 1999

Critical Reviews in Toxicology

175

122

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Leydig cells (LCs) are the cells of the testis that have as their primary function the production of testosterone. LCs are a common target of compounds tested in rodent carcinogenicity bioassays. The number of reviews on Leydig cell tumors (LCTs) has increased in recent years because of its common occurrence in rodent bioassays and the importance in assessing the relevance of this tumor type to humans. To date, there have been no comprehensive reviews to identify all the compounds that have been shown to induce LCTs in rodents or has any review systematically evaluated the epidemiology data to determine whether humans were at increased risk for developing LCTs from exposure to these agents. This review attempts to fill these deficiencies in the literature by comparing the cytology and ontogeny of the LC, as well as the endocrine and paracrine regulation of both normal and tumorigenic LCs. In addition, the pathology of LCTs in rodents and humans is compared, compounds that induce LC hyperplasia or tumors are enumerated, and the human relevance of chemical-induced LCTs is discussed. There are plausible mechanisms for the chemical induction of LCTs, as typified by agonists of estrogen, gonadotropin releasing hormone (GnRH), and dopamine receptors, androgen receptor antagonists, and inhibitors of 5alpha-reductase, testosterone biosynthesis, and aromatase. Most of these ultimately involve elevation in serum luteinizing hormone (LH) and/or LC responsiveness to LH as proximate mediators. It is expected that further work will uncover additional mechanisms by which LCTs may arise, especially the role of growth factors in modulating LC tumorigenesis. Regarding human relevance, the pathways for regulation of the hypothalamo-pituitary-testis (HPT) axis of rats and humans are similar, such that compounds that either decrease testosterone or estradiol levels or their recognition will increase LH levels. Hence, compounds that induce LCTs in rats by disruption of the HPT axis pose a risk to human health, except for possibly two classes of compounds (GnRH and dopamine agonists). Because GnRH and prolactin receptors are either not expressed or are expressed at very low levels in the testes in humans, the induction of LCTs in rats by GnRH and dopamine agonists would appear not to be relevant to humans; however, the potential relevance to humans of the remaining five pathways of LCT induction cannot be ruled out. Therefore, the central issue becomes what is the relative sensitivity between rat and human LCs in their response to increased LH levels; specifically, is the proliferative stimulus initiated by increased levels of LH attenuated, similar, or enhanced in human vs. rat LCs? There are several lines of evidence that suggest that human LCs are quantitatively less sensitive than rats in their proliferative response to LH, and hence in their sensitivity to chemically induced LCTs. This evidence includes the following: (1) the human incidence of LCTs is much lower than in rodents even when corrected for detection bias; (2) several ...

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“…Mich.) or testosterone propionate (20 mm exposed length of 0.062 in internal diameter, 0.175 in outer diameter silastic tu bing: Dow-Coming). The capsules were constructed as previously described [11,21] and were implanted subcutaneously in animals lightly anesthetized with ethyl ether. Empty capsules were im planted in control rats.…”

mentioning

confidence: 99%

Acute Restraint Stress Decreases Tuberoinfundibular Dopaminergic Neuronal Activity: Evidence for a Differential Response in Male versus Female Rats

Demarest¹,

Moore²,

Riegle³

1985

Neuroendocrinology

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The basal activity of tuberoinfundibular dopaminergic (TIDA) neurons is higher and the response of these neurons to the stimulatory actions of prolactin is greater in the female than in the male rat. In the female rat, the restraint-stress-induced increase in serum prolactin concentrations is accompanied by a concurrent decrease in the activity of TIDA neurons. The purpose of the present study was to compare these effects of restraint in male and female rats. TIDA neuronal activity was estimated by measuring the rate of dopamine (DA) synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor, NSD 1015) and the rate of DA turnover (decline of DA after administration of atyrosine hydroxylase inhibitor; α-methyltyrosine) in the median eminence. Thirty minutes of restraint increased serum prolactin concentrations in both male and female rats, but a greater response was observed in the females. Restraint also decreased the rates of synthesis and turnover of DA in the median eminence of the female but not the male rat. The difference in the response of TIDA neurons in male and female rats to restraint is not the consequence of neuronal differentiation resulting from neonatal androgen exposure, because restraint also decreased the activity of TIDA neurons in androgen-sterilized female rats. The inability of restraint stress to reduce TIDA neuronal activity in the male rat appears to be the consequence of testosterone, since TIDA neurons were responsive to restraint following castration of the males. In addition, the ability of restraint stress to decrease TIDA neuronal activity was inhibited in castrated male rats by pretreatment with testosterone, and was facilitate in intact male rats by estradiol pretreatment. Neither castration nor pretreatment with estradiol or testosterone altered the responsiveness of TIDA neurons to restraint in the female rat. These results suggest that male-female differences in the response of TIDA neurons to restraint stress is a consequence of the actions of testosterone in the male rat.

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A Quantitative Study on Feedback Control of Lh by Testosterone in Young Adult and Old Male Rats

Cited by 43 publications

References 8 publications

No Neuron Loss from Hypothalamic Nuclei of Old Male Rats

No Neuron Loss from Hypothalamic Nuclei of Old Male Rats

Rodent Leydig Cell Tumorigenesis: A Review of the Physiology, Pathology, Mechanisms, and Relevance to Humans

Acute Restraint Stress Decreases Tuberoinfundibular Dopaminergic Neuronal Activity: Evidence for a Differential Response in Male versus Female Rats

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