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The relationship between the pineal gland and the pituitary gland was investigated in male rats. The results indicate that the hypothalamo-adenohypophysial-gonadal axis is affected by the pineal gland, but the appearance of castration cells following gonad ablation may be only slightly modified by alterations in pineal gland function.
Treatment of orchidectomized rats with LH, FSH or prolactin decreased the tubulin content of the medial basal hypothalamus (MBH), whereas FSH or prolactin augmented it in the adenohypophysis (AH). After castration, negative correlations existed between serum LH and total or polymerized MBH tubulin, whereas in the AH positive correlations were found. After estradiol-progesterone treatment of spayed rats a significant correlation was found between serum LH and the percentage of AH tubulin in the polymerized form.
The mechanism by which high doses of estrogen influences lipid metabolism was studied with a microtubular blocking agent. Castrated male rats received oral injection daily for 14 days of 3 mg hexestrol in olive oil, or oil alone as controls. About half of the animals in each group were injected intraperitoneally with 4 mg/100 g body weight colchicine 3 hr before they were killed. Hexestrol treatment caused an accumulation of esterified cholesterol in the liver while it decreased those in serum. Triglyceride concentrations slightly decreased in the liver but were unaffected in serum. On polyacrylamide-gel disc electrophoresis, the peaks of high density lipoproteins (HDL) and low density lipoproteins (LDL) were decreased remarkably. Electron microscopic examination of hepatocytes revealed electron-lucent lipid droplets in the cytoplasm. After a colchicine treatment of the control animals, concentrations of esterified cholesterol and triglycerides markedly increased in the liver, while those in serum decreased. Electron microscopic examination of hepatocytes revealed numerous secretory vesicles filled with nascent VLDL. In hexestrol-treated animals, the colchicine treatment was associated with marked decreases in serum-esterified cholesterol and triglyceride as seen in the controls. However, there were no further increases of esterified cholesterol in the liver, and the increase of triglycerides was slight. Electron microscopic examination showed less secretory droplets than in the controls. These data suggest that very low density lipoproteins (VLDL) synthesis in the liver of hexestrol treated rats was inhibited. An accumulation of esterified cholesterol with a marked decrease in serum could not be accounted for by the inhibition of lipoproteins secretion, but rather by their enhanced entry into the liver.
The sensitivity of resting and proliferating cells of the seminal vesicle to X-irradiation and adriamycin has been investigated. Stimulation with testosterone propionate (250 micrograms/day) was started 11 days after castration in BALB/c mice. X-rays (2.5-7.5 Gy total body irradiation) and intraperitoneal injections of adriamycin (4-16 mg/kg body weight) were administered at various times before or after induction of proliferation by testosterone injection. The DNA contents and the weights of the seminal vesicles were determined at 4 days after the start of stimulation. A Do for X-rays of about 10 Gy was found for the seminal vesicle epithelium. For both X-irradiation and adriamycin no significant differences in sensitivity were observed between quiescent (Go) and proliferating (G1; S) seminal vesicle cells.
In the open-field test, male rats usually defecate more and ambulate less than females. A strain was studied in which the males defecate less than females, while still ambulating less. Infants of this strain were castrated (males) or injected with testosterone propionate (females) and tested in the open field as adults. There were significant effects of these neonatal treatments on ambulation, but not on defecation, in contrast to previous reports for the latter measure in rats showing a sex difference in defecation taking the usual direction. It is suggested that absence of the usual direction of a sex difference normally under the developmental control of androgen may indicate a genotype which has escaped from such control. Finally, a number of 'sibling' effects' were observed, i.e. effects on the adult behaviour of the members of one sex in a litter produced by treatments administered in infancy to members of the other sex.
The aggressive behaviour of female hamsters was studied while they were housed in large enclosures with males and in brief tests with males or females. Some females are not aggressive with any male, whereas others are very aggressive toward all males in both testing conditions. Females that are not aggressive toward intact males may be very aggressive toward castrated males or females. When the animals are housed together for long periods of time, males dominate only if they are much heavier. Male dominance takes a relatively long time to establish and often there is an equivocal period characterized by reversals of dominance. Female dominance is rapidly established. Unless the male is much heavier, the female determines the presence or absence of agonistic behaviour.
3-Methylcholanthrene treatment induced large increases in high-spin P-450 form(s) in intact microsomal membranes from New Zealand White rabbit or C57BL/6N mouse liver but not in rabbit lung, kidney or intestine. Testosterone enhanced the high-spin/low-spin ratio of P-450 in female C57BL/6N liver to the same degree as 3-methylcholanthrene treatment; there was no additive increase in the ratio with treatment of testosterone plus 3-methylcholanthrene. The same effect was seen in ovariectomized females. In the liver of normal or castrated C57BL/6N mice, estradiol-17 beta pretreatment caused no significant change in the high-spin/low-spin ratio. Vigorous homogenization of the microsomes can decrease the high-spin/low-spin ratio, more so in control than in 3-methylcholanthrene-induced C57BL/6N microsomes. Vigorous exercise (20-min swim) and fasting for 2 days significantly enhanced the high-spin/low-spin ratio in C57BL/6N liver. Temperature studies showed that the low-spin electron paramagnetic resonance signal intensity, as a function of absolute temperature in the range of 16 to 70 degrees K, was consistent with a simple Boltzmann dependence within the Kramers doublet giving rise to the microwave transition. We conclude that, within the limits of measurement, the low-spin state acts like an isolated state and is not in thermal equilibrium with the high-spin form of P-450.
A karyometric study of the spontaneous development of four topographic subdivisions in the paraventricular nucleus was made in male albino mice from the 5th to the 190th day of postnatal life. Another 25 animals were castrated at 20 days and examined at 25, 35, 45, 55 and 85 days of life. A comparison was established between both groups of mice.
Time-response curves for barium chloride and noradrenaline were obtained in the isolated vas deferens of 30-day castrated rats. The contractions induced by a maximal dose of barium chloride reached a peak after about 20-30 sec and then decreased to a lower level (fade). 5 min after drug addition the response had faded to about 20% of the peak contraction while in normal preparations it decreased to about 55%. When calcium was removed from the nutrient solution, both peak and 5-min effects of sequential doses were reduced, and fell progressively at a faster rate than in normal preparations. When Ca2+ concentration was increased from 1.8 mM up to 36.0 mM, fading was abolished. The data were analyzed on the basis of receptor changes involving the translocation of calcium in smooth muscle.
The influence of different experimental and physiological conditions on sex steroid binding protein (SBP) concentrations in the blood (and in hepatic and testicular cytosols) has been studied on male rainbow trout. SBP was measured with a specific binding assay. The aim was to further understanding of regulation of the SBP and in particular to determine the respective influences of reproductive and metabolic status. Twelve days after hypophysectomy, pituitary and steroid hormones were dramatically decreased and SBP concentrations were significantly lowered in blood (-32%) and in hepatic cytosol (-46%) while the binding protein concentration remained constant in testicular cytosol. Castration of maturing animals did not influence SBP concentration in blood and liver cytosol. Toward the end of the reproductive cycle, a dramatic decrease (-80%) of plasma SBP concentration occurred that appears independent of androgen changes that take place during this period, but is concomitant with a rapid increase of plasma growth hormone (GH) levels (and possibly secondary to a natural arrest of food intake). Long-term fasting that increases endogenous GH but decreases plasma IGFs (insulin-like growth factors) concentrations also induces a limited but significant decrease in SBP concentration. Treatment of intact control trout with recombinant bovine GH (1 microgram/g wt, twice a week, for 6 weeks) increased plasma IGF concentrations but did not significantly increase SBP levels. These results suggest that in mature male trout, testicular androgens have little or no influence on SBP regulation. GH levels or liver GH responsiveness and IGF might be involved in SBP regulation. This would, in part, explain the large decrease in SBP around spermiation in trout.
Sexual behavior of long-term castrated rhesus males was not increased by administration of the hydroxylated metabolite of testosterone (T), 17 beta, 19-dihydroxy-5 alpha-androstan-3-one diacetate (19-OH-DHTA) at a dose of 1 mg/kg/day. Simultaneous administration of 19-OH-DHTA and estradiol benzoate (EB) also failed to increase the level of sexual performance, but daily injection (1 mg/kg/day) of testosterone propionate (TP) was very effective in effective in activating sexual behavior.
Having previously found that King-Holtzman rats respond behaviorally to dihydrotestosterone (DHT), this strain was used to compare the effectiveness of DHT and dihydrotestosterone propionate (DHTP) in maintaining and reinstating copulatory behavior. The 5 alpha-reduced androgens were capable of stimulating mating behavior in these castrated male rats. DHT and DHTP were equally effective in maintaining ejaculatory behavior, whereas DHT was slightly more potent behaviorally than DHTP in restoring mating responses. It was found that as little as 200 micrograms hormone/day restored ejaculatory behavior in 78% of the DHT-treated and 50% of the DHTP-treated rats. In both the maintenance and restoration paradigms, the mating performance of the DHT(P) treated males declined over time. The present data suggest that the conversion of androgen to estrogen may not be critical for the activation of male mating behavior.
To determine the lowest doses of testosterone propionate (TP) that cause clearcut behavioral changes in castrated male rhesus monkeys (behavioral thresholds), observations were made on eight males during successive 4-week treatment periods while they received daily doses of TP ranging from 25 micrograms to 12.8 mg subcutaneously. Males were tested with each of the same four ovariectomized females (32 pairs, 1408 one-hour behavior tests). Two females were untreated and the other two received either 5 or 15 micrograms estradiol benzoate sc per day. TP injections were given at 1600 hr, and plasma samples were obtained at 0800 hr (352 samples). Individual males had widely different behavioral thresholds from 50 micrograms up to 3.2 mg TP per day. Males showed two types of response: A, a graded increase in ejaculatory activity as plasma testosterone values increased, and B, an all-or-none type of response in which there were no further increases in ejaculation with increasing plasma levels once the behavioral threshold had been reached. At levels below the physiological range, small changes in plasma testosterone were associated with marked changes in behavior. The female partner exerted a pronounced effect upon the responses of males to TP treatment.
Sex differences in aortic cholesterol esterase activity and changes in the activity following castration and gonadal hormone treatment were investigated in rats. Differences in the enzyme activity were apparent after 2.5 months and became most significant after 6 months. The activity in the aorta and the liver was significantly higher in female rats. Prepubertal orchiectomy increased the aortic activity, feminizing the type of metabolism, whereas postpubertal orchiectomy, and both pre- and postpubertal ovariectomy induced no change in the activity. The administration of testosterone to female rats significantly decreased the aortic activity, masculinizing the type of metabolism. However, the administration of testosterone or of 17 beta-estradiol to male rats had no effect. These results suggest (1) that there are clear sex differences in aortic cholesterol esterase activity, (2) that prepubertal exposure to androgens plays a critical role in the sexual differentiation in aortic and hepatic cholesterol ester metabolism, and (3) that the administration of testosterone can temporarily masculinize the type of metabolism. These results partly explain the sexual differences in susceptibility to atherosclerosis.
Female rats of the Wistar strain were rendered hyperprolactinemic by grafting one additional pituitary gland under the right kidney capsule at various ages (5 days group A; 30 days group B and 90 days group C). Age matched animals were sham operated to serve as controls. Plasma levels of PRL and LH were measured by specific double antibody RIA. Basal preoperative PRL levels were increased rapidly after grafting, reaching values over 100 ng/ml, in front of the 20 ng/ml showed by sham operated controls. Plasma LH levels were significantly decreased in all hyperprolactinemic groups as compared to controls. After Estradiol Benzoate (EB) administration all control rats showed an increase in PRL levels in a pulsatile manner with higher values found in the afternoon. PRL response in transplanted rats was less evident and with absence of pulsatility. LH responses to EB in control animals showed a biphasic pattern, with a negative feed-back in the first hours followed by a positive effect at 31 or 55 h after the injection. This pattern of response started in the control rats from group A at 19 days of age. Before that, only the negative feed-back effect was present. In grafted animals from the same group no positive feed-back effect could be detected at any time studied. In group B, a reduction in the positive feed-back effect, more evident after 90 days of hyperprolactinemia was detected. Animals of group C on the contrary showed an increased positive feed-back effect 40 days after grafting. Eight days after castration a reduction in PRL levels was detected in all groups, together with an increase in LH values. PRL values after ovariectomy were less reduced in grafted animals, and these rats also showed a less marked LH increase. This effect is more evident in group B. All these data seem to point out that hyperprolactinemia is capable of modifying the feed-back system between E2 and LH, and that the age at which hyperprolactinemia starts has a profound effect.
The effect of intraventricular administration of dynorphin-(1-13) on luteinizing hormone (LH) release was studied in castrated conscious rats. The administration of 5 micrograms of dynorphin-(1-13) into the lateral ventricle inhibited LH secretion. Intravenous administration of naloxone blocked this suppressive effect of dynorphin on LH release. These results suggest a possible role of dynorphin, in addition to beta-endorphin and Met5-enkephalin, in the control of LH release in male rats.
Estradiol benzoate (E2) increases plasma lipids in hypothalamic obese, functionally castrated (OFC), obese laying (OL), and control laying hens (CONT). However, E2 reduces fattiness in OFC but not in OL or CONT hens. Antiestrogen, such as tamoxifen (TAM), reduces plasma lipids in OL and CONT, but not in OFC, hens and has no effect on fattiness in any of them. Apolipoprotein VLDL-II (apo-VLDL-II), lipoprotein lipase (LPL), and rate of lipolysis may mediate these estrogenic effects. In the present study, effects of E2 and TAM on fattiness, plasma apo-VLDL-II, in vitro lipolysis, and LPL activity in postheparin plasma and abdominal adipose tissue (AAT) were determined in OFC, OL, and CONT hens. Basomedial hypothalamic lesions were performed in 3-month-old White Leghorn hens. At the static phase, 10 months later, OFC OL, and CONT hens were divided into three subgroups and injected IM on alternate days, with either 2 mg E2/kg b.wt., 10 mg TAM/kg, or vehicle corn oil, for 5 weeks. In OL and OFC hens, body and AAT weights were higher than in CONT poullets. Food intake and ovarian weight were similar in OL and CONT, higher than in OFC hens. Plasma LPL activity was higher, whereas plasma apo-VLDL-II and stimulated lipolysis were lower in OFC than in OL and CONT hens. In OFC hens LPL activity per unit of AAT was half than in OL and CONT. Total LPL activity in AAT was similar in OFC and CONT and higher in OL hens. Levels of basal lipolysis were similar in all experimental hens. TAM did not affect any of the measured parameters in OFC hens. In OL and CONT hens, TAM depressed apo-VLDL-II, increased plasma LPL activity, but had no effects on AAT LPL activity, on stimulated lipolysis, or fattiness. E2 increased apo-VLDL-II to similar levels in all groups and reduced LPL activity in plasma and AAT of obese hens. Only in OFC hens did E2 enhance basal and stimulate lipolysis and reduce FI and fattiness. We conclude that in adult laying hens, unlike in cockerels and juvenile hens, estrogen reduces lipid incorporation in fat depots by enhancing apo-VLDL-II production that reduces plasma and AAT LPL activity. This may increase lipoprotein available for incorporation into developing yolks. The lack of estrogen in OFC hens reduces circulating apo-VLDL-II and thus increases LPL activity and amount of fat depots.
To examine estrogen-stimulated uterine growth we have monitored changes in uterine DNA synthesis, ornithine decarboxylase (ODC) activity and protein content as well as luminal epithelial (LE) cell mitotic index and ultrastructural changes. We have utilized this model to examine castrate mature rat uterine growth as a function of time between 18 and 40 hours following a single injection of 25.0 ug of estradiol-17B. LE cell mitotic index and protein content increases were maximally elevated as early as 18 hours postinjection while uterine ODC activity was maximal at 28 hours; uterine DNA synthesis increases continued throughout the experiment. In addition, the infusion of either 1 or 2 ug E2 plus progesterone over a 24 hour period, stimulated elevated ODC activity under both treatment regimens and LE cell mitotic index which was inversely related to E2 dose.