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R W Steger

Publications and source records attributed to R W Steger.

At least 37 records · Page 2Linked to original sources
PubMed1994

Growth hormone (GH) binding and effects of GH analogs in transgenic mice.

Overexpression of human (h) or bovine (b) growth hormone (GH) in transgenic mice is associated with marked (2- to 12-fold) and significant increase in hepatic binding of GH and prolactin (PRL). This is due to an increase in the number of GH and PRL receptors (GHR, PRLR) per mg of microsomal protein without changes in binding affinity. Comparison of results obtained in transgenic animals expressing bGH with a mouse metallothionein (MT) or a rat phosphoenolpyruvate carboxykinase (PEPCK) promoter suggests that effects of bGH on hepatic GHR and PRLR do not require GH overexpression during fetal life and, within the dose range tested, the effects on PRLR are not dose dependent. The increase in hepatic GHR was accompanied by significant increases in plasma GH-binding protein (GHBP) and in mean residence time of injected GH. Thus, life-long elevation of peripheral GH levels alters the availability of both free GH and GHR. Site-directed in vitro mutagenesis was used to produce hGH and bGH analogs mutated within one of the sites involved in binding to GHR and PRLR. Mutating hGH to produce amino acid identity with bGH at Position 11, 18 (within Helix 1), 57, or 60 (within the loop between Helix 1 and 2) did not affect binding to GHR in vitro, or somatotropic activity in transgenic mice in vivo but reduced lactogenic activity in Nb2 cells by 22%-45%. Mutations of bGH designed to produce amino acid identity with hGH at one to four of the corresponding positions in the bGH molecule did not interfere with binding to GHR or somatotropic activity in vivo, and failed to produce significant binding to PRLR but resulted in alterations in the effects on the hypothalamic and anterior pituitary function in transgenic mice. Apparently region(s) outside the domains examined are essential for lactogenic activity of hGH, and different portions of the GH molecule are responsible for its diverse actions in vivo.

Animals↗
PubMed1994

Neuroendocrine and reproductive consequences of overexpression of growth hormone in transgenic mice.

Availability of recombinant growth hormone (GH) and development of long-acting formulations of this material will undoubtedly lead to widespread use of GH in animal industry and in medicine. GH can act, directly or indirectly, on multiple targets, but its influence on the reproductive system and on the hormonal control of reproduction is poorly understood. Overexpression of GH genes in transgenic animals provides a unique opportunity to study the effects of long-term GH excess. Transgenic mice overexpressing bovine, ovine, or rat GH (hormones with actions closely resembling, if not identical to, those of endogenous [mouse] GH), exhibit enhancement of growth, increased adult body size, and reduced life-span as well as a number of endocrine and reproductive abnormalities. Ectopic overexpression of bovine GH (bGH) driven by metallothionein or phosphoenolpyruvate carboxykinase promoters is associated with altered activity of hypothalamic neurons which produce somatostatin, loss of adenohypophyseal GH releasing hormone (GHRH) receptors, and suppression of endogenous (mouse) GH release. Elevation of plasma levels of GH (primarily bGH) and insulin-like growth factor (IGF-I) in these transgenic mice leads to increases in the number of hepatic GH and prolactin (PRL) receptors, in the serum levels of GH-binding protein (GHBP), in the percent of GHBP complexed with GH, and in the circulating insulin levels. In addition, plasma adrenocorticotropic hormone (ACTH) and corticosterone levels are elevated. Plasma levels of luteinizing hormone (LH), as well as its synthesis and release, are not consistently affected, but follicle-stimulating hormone (FSH) levels are suppressed, apparently due to pre- and post-translational effects. Pituitary lactotrophs exhibit characteristics of chronic enhancement of secretory activity, and plasma PRL levels are elevated. Prolactin responses to mating or to pharmacological blockade of dopamine synthesis are abnormal. Reproductive life span and efficiency are reduced in both sexes, with the severity and frequency of reproductive deficits being related to plasma bGH levels. Most transgenic females expressing high levels of bGH are sterile due to luteal failure. Overexpression of human GH which, in the mouse, interacts with both GH and PRL receptors leads to additional endocrine and reproductive abnormalities including stimulation of LH beta mRNA levels and LH secretion, loss of responsiveness to testosterone feedback, overstimulation of mammary glands, enhanced mammary tumorigenesis, and hypertrophy of accessory reproductive glands in males.

Animals↗
PubMed1993

Diabetes disrupts copulatory behavior and neuroendocrine responses of male rats to female conspecifics.

Streptozotocin-induced diabetes disrupts copulatory behavior in the male rat. The increase in serum luteinizing hormone (LH) that occurs in the male rat in response to the presence of a receptive female is absent in most diabetic rats. A female-induced testosterone rise is not seen in diabetic male rats, including those showing an increase in LH. The female-induced LH rise appears to be secondary to increased hypothalamic norepinephrine metabolism, which is severely attenuated in diabetic rats not exhibiting an LH rise in response to a female.

Animals↗
PubMed1993

Streptozotocin-induced diabetes blocks the positive feedback release of luteinizing hormone in the female rat.

The effects of streptozotocin-induced (STZ) diabetes on the release of gonadotropins was studied in female rats. In the first experiment, rats were ovariectomized and 2 days later were injected with STZ. Three weeks later rats were treated with estrogen and progesterone and blood samples were taken via intraatrial cannulae for luteinizing hormone (LH) assay. Afternoon surges of LH were seen in 4/5 control but 0/8 STZ rats. Pituitary responses to LH-releasing hormone in vitro did not differ. In the 2nd experiment, ovariectomized estrogen-primed rats were killed prior to and during a progesterone-induced LH surge. As in Experiment 1, STZ-treatment inhibited the LH surge but did not effect the afternoon rise in median eminence norepinephrine turnover which has previously been shown to be important in stimulating LH release. Turnover of norepinephrine in the anterior hypothalamus was depressed in the diabetic rats both prior to and during the expected time of the LH surge. Dopamine turnover was depressed in all three brain regions studied. It can be concluded that the positive feedback control of LH release is severely attenuated in diabetic rats but the mechanism explaining the loss is not clear. Diabetes-induced alterations in hypothalamic catecholamine metabolism may be involved but further work is needed to more carefully define these relationships.

Animals↗
PubMed1993

Plasma microdialysis. A technique for continuous plasma sampling in freely moving rats.

Microdialysis provides a means of continuous plasma sampling without repeated blood drawing. We report here the use of a specially designed and constructed microdialysis probe to sample plasma glucose, protein, and luteinizing hormone from the right atrium of a freely moving rat. Our probe has a unique side-arm tubing, which can be used to draw blood for in vivo probe calibration and infuse heparin continuously to prevent blood clotting. Glucose recovery rate (18%) of the probe remained relatively stable in continuously heparinized rats over 24 hr, but it dropped rapidly to 1% in nonheparinized rats. The concentration of plasma glucose was significantly underestimated, when it was converted from the perfusate concentration based on the in vitro, but not in the in vivo, recovery rate of the probe. The recovery of plasma protein was only 0.07% initially and rapidly declined to about 0.03%. Luteinizing hormone was not detected in the perfusates from either normal or luteinizing hormone-releasing hormone-stimulated rats. These results indicate that continuous heparinization and in vivo probe calibration are essential for successful plasma microdialysis, and our current dialysis membrane can be used to sample non-protein-bound molecules in the plasma.

Animals↗
PubMed1993

Effects of streptozotocin-induced diabetes on neuroendocrine responses to ovariectomy and estrogen replacement in female rats.

The effects of streptozotocin-induced (STZ) diabetes on the negative feedback regulation of LH and FSH were evaluated in adult female rats. Rats were injected with STZ (50 mg/kg) or vehicle and ovariectomized 10 days later. Estrogen (EB; 100 micrograms/kg) or oil injections were given on alternate days, starting on the day of ovariectomy. Blood samples for LH, FSH and PRL assay were taken on days 10, 13, 15 and 17. The rats were decapitated on day 17. One hour prior to sacrifice, one half of the animals were injected with alpha-methyl-p-tyrosine for determination of catecholamine turnover rates. Pituitaries were incubated to determine basal secretion rates. Rats treated with STZ exhibited the expected weight loss and elevation of plasma glucose levels. At the time of ovariectomy, FSH, but not LH or PRL, was depressed in the diabetic rats. The postovariectomy rise in LH and FSH was severely attenuated in the diabetic rats. EB treatment was more effective in lowering LH and FSH levels in the diabetic as compared to the control rats. Median eminence (ME) norepinephrine (NE) and dopamine (DA) turnover was higher in the oil-treated diabetic rats than oil-treated controls. EB also caused a greater decrease in ME NE and DA turnover in the diabetic rats. EB was more effective in decreasing in vitro LH secretion and increasing in vitro PRL secretion from pituitaries of control as compared to STZ-treated animals. These results demonstrated that STZ-induced diabetes leads to an attenuation of LH and FSH release after ovariectomy and potentiates the negative feedback effects of EB.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Premature ageing in transgenic mice expressing different growth hormone genes.

Transgenic mice expressing various growth hormone genes have markedly reduced life spans, with few animals surviving beyond 12 months in some of the lines. Except for an increased incidence of mammary tumours in female mice expressing human growth hormones, pathological findings in debilitated or moribund transgenic mice resemble the well-documented degenerative changes that occur at a much greater chronological age in normal rodents. This study demonstrates that 10-month-old male transgenic mice expressing bovine growth hormone (known as 25-copy PEPCK. bGH transgenic mice) also show age-related changes in hypothalamic and striatal neurotransmitter metabolism that are not seen in normal litter mate controls until at least 24 months of age. Female mice and male mice with a lower circulating concentration of bGH (known as 5-copy PEPCK. bGH transgenic mice) live longer and fail to show the same magnitude of change in neurotransmitter synthesis and release. Although more work needs to be done to determine the physiological significance of these changes and to determine their relationship to the general effects of ageing on the CNS, transgenic mice expressing various growth hormone genes may provide an interesting and valuable model with which to study the ageing process.

Aging↗
PubMed1992

Effects of treatment of normal and hyperprolactinemic rats with cyclosporine in vivo on the release of gonadotropins and prolactin from their pituitaries in vitro.

Cyclosporine (CyA) is extremely useful as an immunosuppressant and it is believed that at least some of its actions are due to antagonizing PRL effects. To determine whether the reported ability of CyA to inhibit gonadotropin release can be modified by PRL, we have examined the effects of treatment of normal and hyperprolactinemic rats with CyA in vivo on the release of LH, FSH and PRL from their pituitaries in vitro. Hyperprolactinemia was induced by implantation of capsules containing diethylstilbestrol (DES) and the animals were examined while the capsules were still in place (DES-IN) or after they had been removed (DES-OUT). Treatment with CyA significantly reduced plasma LH levels in control DES-IN rats without reducing basal LH release from the pituitaries of these animals in vitro. In the DES-IN rats, CyA exposure in vivo did not modify plasma PRL levels, but reduced PRL release in vitro, and interfered with the inhibitory action of dopamine (DA) on PRL release. The effect of DA on gonadotropin release in vitro was modified by CyA treatment. Administration of CyA failed to antagonize the suppressive effects of hyperprolactinemia on plasma LH and FSH levels or on the basal rates of gonadotropin release by incubated pituitaries. We conclude that CyA can reduce PRL release but does not interfere with the actions of PRL on anterior pituitary function.

Animals↗
PubMed1992

Acute effects of delta-9-tetrahydrocannabinol on dopaminergic activity in several rat brain areas.

In this work, we examined the acute effects of two doses of delta-9-tetrahydrocannabinol (THC) on several pre- and postsynaptic biochemical measures of dopaminergic activity in the striatum, limbic forebrain, and hypothalamic-anterior pituitary area of adult male rats. The exposure to a low dose of THC (0.5 mg/kg bw) decreased the number of striatal D2 dopaminergic binding sites, but did not affect their affinity. Treatment with a higher dose of THC was ineffective. In addition, both doses decreased the number of D1 dopaminergic binding sites in the limbic forebrain without changing their affinity. We did not find any changes in the dopamine (DA) or L-3,4-dihydroxyphenylacetic acid (DOPAC) content, or in the DOPAC/DA ratio, in either the striatum or limbic forebrain. THC treatment produced a dose-related decline in plasma prolactin (PRL) levels. Furthermore, both the basal and DA-inhibited in vitro release of PRL were reduced in animals exposed to THC in a dose-dependent manner. This inhibitory effect of THC on PRL release was accompanied by a decreased DOPAC/DA ratio in medial basal hypothalamus that, in turn, may be a result of the fall in PRL levels rather than a direct action of the drug. These data show that acute exposure to THC can alter brain dopaminergic neurotransmission. Our results suggest that the reduction of PRL release following THC exposure, both in vivo and in vitro, might be elicited by a direct action of THC on the pituitary.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Catecholamines stimulate testicular testosterone release of the immature golden hamster via interaction with alpha- and beta-adrenergic receptors.

Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.

Animals↗
PubMed1991

delta 9-Tetrahydrocannabinol antagonism of the anterior pituitary response to estradiol in immature female rats.

The potential estrogenicity or antiestrogenicity of delta 9-tetrahydrocannabinol (THC), the chief psychoactive constituent of marijuana, was evaluated in immature female rats treated for 3 days with estradiol (E2; 1 microgram/kg), THC (10 mg/kg body weight), or E2 + THC. Estradiol treatment significantly increased anterior pituitary, uterine, and oviduct weights. When THC was administered with E2, it prevented the E2-induced increase in pituitary weight, but had no effect on either the uterine or oviduct weight response to E2. In the E2 treatment group, basal prolactin levels were increased and a prolactin surge occurred on the afternoon of the 26th day of age. However, E2-stimulated basal and surge levels of prolactin were significantly attenuated by concomitant THC treatment. Moreover, pituitary prolactin concentrations, which were elevated in E2-treated rats, did not differ from control values in E2 + THC-treated animals. The E2-induced decrease in dopamine turnover rates in the medial basal hypothalamus and increase in the number of anterior pituitary dopamine D2-binding sites (Bmax) were not affected by concomitant THC treatment. Thus, THC antagonizes E2 action on the anterior pituitary via yet to be elucidated mechanism(s).

Animals↗
PubMed1991

Effects of delta-9-tetrahydrocannabinol exposure on adrenal medullary function: evidence of an acute effect and development of tolerance in chronic treatments.

Previous studies have shown that the secretion of several stress-related hormones can be altered by exposure to marihuana or its purified constituents. The purpose of this study was to examine changes in adrenal medullary function caused by acute, subchronic and chronic treatments with two different doses of delta-9-tetrahydrocannabinol (THC). Acute exposure to THC caused a significant decrease in the adrenal medulla contents of both norepinephrine (NE) and epinephrine (E) and a significant increase in the E/NE ratio. These effects were mainly observed with the highest dose of THC, but they were not accompanied by a statistically significant decrease in adrenal medulla tyrosine hydroxylase activity, the rate-limiting enzyme in the catecholamine (CA) synthesis. These effects disappeared after seven or fourteen days of a daily THC treatment, which suggests the development of tolerance to this drug. Analysis of plasma PRL, ACTH and corticosterone levels showed some THC-related changes in these hormones. THC-induced modifications in ACTH and corticosterone were not in parallel to the changes in the adrenal medulla function, whereas those effects of acute THC on PRL release were statistically correlated with decreases of CA contents following acute THC. In conclusion, acute exposure to THC caused an alteration in the adrenal medullary function, reflected by a fall in endogenous stores of both CAs which could influence the adrenal medullary response to stress situations. This acute effect of THC could be mediated by the pituitary secretion of PRL, although the possibility of an effect directly exerted on the adrenal medulla chromaffin cells should be also considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1991

Entrainment of Syrian hamsters to short photoperiod T-cycles does not reverse the inhibitory nature of feedback lighting on the photoperiodic response.

Experiments examining the photoperiodic effects of various light-dark cycles unexpectedly demonstrated that light during the subjective night is not necessarily photoinductive to the reproductive system of long day breeders. Feedback lighting (illumination in response to locomotor activity) and a high-frequency light-dark cycle with 1 minute (m) of light followed with 1 minute of dark (LD1m:1m) failed to maintain reproductive function in Syrian hamsters despite exposing the animal to 5-6 hours of light per cycle during the subjective night. In an effort to determine why feedback lighting and LD1m:1m do not maintain reproductive function, male Syrian hamsters were exposed to one of the following lighting conditions for ten weeks: a light-dark cycle with 14 hours of light followed by a 10 hour light-dark cycle of 1 minute of light followed by 1 minute of dark ¿LD14:10(1m:1m)¿; a cycle of a 14 hour light-dark cycle of 1 minute of light followed by 1 minute of dark, followed by 10 hours of dark ¿LD14(1m:1m):10)¿; a light-dark cycle of 2 hours of light and 21 hours of dark (LD2:21); a light-dark cycle of 2 hours of light and 22 hours of dark (LD2:22); LD2:21 in conjunction with feedback lighting (LD2:21/FB); LD2:22 in conjunction with feedback lighting (LD2:22/FB); constant dark (DD) or constant light (LL). All hamsters exposed to LD14(1m:1m):10 entrained. Only 7 of 12 hamsters exposed to LD14:10(1m:1m) entrained. This supports previous findings, which suggest that the circadian system has difficulty differentiating between LD1m:1m and LL. Exposure to LD2:22 and DD induced testicular regression, while LL, LD2:21 and LD14(1m:1m):10 maintained reproductive function, as expected. The addition of approximately 5 hours of nocturnal illumination by feedback lighting, however, not only failed to prevent reproductive regression in LD2:22, but attenuated the stimulatory nature of LD2:21. This suggests that feedback lighting is not only not stimulatory, but may be actively inhibitory. Perhaps this is due to a photoinhibitory effect of multitransitional nocturnal illumination. This hypothesis is supported by the finding that LD14:10(1m:1m) allows regression, while LD14(1m:1m):10 is stimulatory. These findings also imply that the state of the circadian system is instrumental in the reproductive system's interpretation of a light signal.

Activity Cycles↗
PubMed1991

Temporal sequence of neuroendocrine events associated with the transfer of male golden hamsters from a stimulatory to a nonstimulatory photoperiod.

The transfer of male golden hamsters from long day (LD) to short day (SD) conditions results in gonadal atrophy within 8 weeks and significant reductions in LH, FSH, and prolactin (Prl) secretion as early as 4 weeks. Changes in hypothalamic neurotransmitter metabolism precede these changes in pituitary hormone secretion. Thus median eminence norepinephrine (NE) turnover declines steadily after SD exposure, although the differences as compared to turnover in LD hamsters are not significant until Week 4. Median eminence dopamine (DA) turnover is reduced significantly within 1 week. Turnover of NE and DA in the medial basal hypothalamus also changes significantly within 1 or 2 weeks of SD exposure, but the changes are not maintained through Week 8, despite continued reductions in levels of circulating LH, FSH, and Prl. Reductions in median eminence NE metabolism appear to be responsible for the decrease in LH and FSH release. Initial decreases in Prl release appear to be hypothalamic in origin, but the hypothalamic factor(s) responsible for this change is not evident. An increase in inhibitory input from tuberoinfundibular dopaminergic neurons is clearly not involved.

Animals↗
PubMed1991

Possible involvement of hypothalamic monoamines in mediating the action of alpha-2u-globulin on the pituitary-testicular axis in rats.

A major androgen-dependent urinary protein of male rodents, alpha 2u-globulin, has been shown to influence adenohypophyseal hormone release. In an attempt to elucidate the mechanisms of its action, we have examined several parameters of hypothalamic and pituitary function in adult male rats treated for 2 weeks with two injections daily of 0.75 mg alpha 2u-globulin and sacrificed 16 h after the last injection. This treatment led to an increase in plasma luteinizing hormone levels, a decrease in plasma prolactin levels, an increase in testosterone concentrations in both plasma and testicular tissue, and increases in testicular weights. The norepinephrine turnover in median eminence and anterior hypothalamus was increased in alpha 2u-globulin-injected animals, while the norepinephrine turnover in the remaining medial basal hypothalamus was reduced. alpha 2u-Globulin-treated animals had a significantly decreased dopamine turnover in the anterior hypothalamus, while in the medial basal hypothalamus the dopamine metabolism was increased. These data suggest that alpha 2u-globulin-induced changes in gonadotropin and prolactin secretion are mediated by changes in catecholamine metabolism in several hypothalamic regions. Increased testosterone secretion appears to be due to increased secretion of gonadotropins from the pituitary.

Alpha-Globulins↗
PubMed1991

Effects of heterologous growth hormones on hypothalamic and pituitary function in transgenic mice.

The expression of the mouse metallothionein-I (mMT) promoter/human growth hormone (hGH) fusion gene in transgenic mice leads to female sterility and major alterations in the function of the hypothalamic-adenohypophyseal system. These alterations include increases in median-eminence norepinephrine turnover and plasma LH levels, and a decrease in plasma prolactin levels in intact males, and an increase in median-eminence dopamine turnover combined with the suppression of plasma prolactin levels in ovariectomized females. To further characterize these changes and to determine whether they are due to the lactogenic or somatotropic activity of hGH, we have studied hypothalamic and pituitary function in transgenic mice expressing mMT/hGH, mMT/hGH.B 'variant', or mMT/bGH fusion genes. In males, the expression of the hGH.B gene was associated with a reduction in pituitary prolactin release in vitro and an increase in LH response to LHRH stimulation, while the bGH transgene did not affect any of the examined parameters of LH and prolactin release. Median-eminence norepinephrine turnover was increased in each of the three lines of transgenic males, while median-eminence dopamine turnover was reduced only in animals expressing the hGH.B gene. In ovariectomized females, plasma LH was suppressed by hGH variant expression, while median-eminence norepinephrine turnover was suppressed in both hGH.B and bGH animals. The turnover of dopamine was increased in the median eminence of females expressing either of the human genes (hGH or gHG.B) and reduced in the median eminence of ovariectomized bGH females. We conclude that the hGH.B gene is weakly lactogenic in mice, and that the chronic stimulation of either GH receptors (by bGH) or both GH and prolactin receptors (by hGH or hGH.B) can lead to profound alterations in the metabolism of hypothalamic neurotransmitters and pituitary hormone release.

Animals↗
PubMed1991

Influence of diabetes on the gonadotropin response to the negative feedback effect of testosterone and hypothalamic neurotransmitter turnover in adult male rats.

The influence of diabetes on the gonadotropin response to the negative feedback effect of testosterone (T) and hypothalamic neurotransmitter turnover rates in adult male rats was evaluated. Adult male Sprague-Dawley rats were made diabetic by an intraperitoneal injection of streptozotocin (STZ; 5 mg/100 g body weight) in citrate buffer. Vehicle-injected rats served as controls. On day 9, all rats were bilaterally castrated and treated subcutaneously on alternate days with either peanut oil or T propionate (TP) in peanut oil (100 micrograms/rat). Plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), and T concentrations were measured by specific radioimmunoassays from blood samples collected on day 1 (before castration) and 2, 4, 6, and 7 days after castration. On day 7 after castration (day 15 after vehicle or STZ treatment), 1 h before autopsy, the rats were injected intraperitoneally with saline or a tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine (25 mg/100 g BW), for the measurement of norepinephrine (NE) and dopamine turnover in median eminence and medial basal hypothalamus (MBH). Circulating FSH, LH, PRL, and T levels were significantly lower (FSH and T: p less than 0.001; LH and PRL: p less than 0.05) in gonad-intact rats treated with STZ than in vehicle-injected animals. The castration-induced increase in plasma LH levels was attenuated in diabetic rats. The suppressive effect of T on LH secretion was significantly greater (p less than 0.001) in STZ-treated rats relative to TP-treated nondiabetic controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗