摘要:

The effect of long-term decreases in circulating concentrations of prolactin was determined on the responsiveness of tuberoinfundibular dopamine (DA) neurons to this hormone. The activity of these neurons in ovariectomized rats was estimated by measuring the rate of DA synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor) in the median eminence at various times after serum concentrations of prolactin had been reduced by hypophysectomy or the chronic administration of a DA agonist (bromocriptine, 3 mg/kg/day). The concentration of DA in the median eminence, but not in striatum, declined progressively up to 12 days after hypophysectomy, but did not change at any time during bromocriptine treatment. On the other hand, norepinephrine concentrations in the median eminence were increased 12 days after both treatments. Within 24 h after hypophysectomy or the first injection of bromocriptine the rate of DA synthesis in the median eminence was decreased; this decrease was maintained for at least 12 days suggesting that tuberoinfundibular DA neuronal activity is normally maintained by endogenous prolactin. Intracerebroventricular (ICV) injections of prolactin (10 µg, 12 h prior to sacrifice) increased the rate of DA synthesis in the median eminence of control, 24-hour hypophysectomized and 24-hour bromocriptine-treated rats. After longer periods (6–12 days) of bromocriptine treatment or after hypophysectomy the responsiveness of tuberoinfundibular DA neurons to prolactin was reduced. Dose-response studies revealed that the sensitivity and magnitude of response to ICV prolactin was markedly reduced in 12-day hypophysectomized rats. The decreased responsiveness of tuberoinfundibular DA neurons to the actions of prolactin following long-term bromocriptine treatment and hypophysectomy is most likely due to the prolonged decrease in circulating prolactin, since the concurrent daily administration of bromocriptine and ICV prolactin for 12 days maintained the ability of tuberoinfundibular DA neurons to respond to prolactin. The decreased basal activity and responsiveness of tuberoinfundibular DA neurons to prolactin induced by hypoprolactinemia is reversible; 12 days after terminating chronic bromocriptine treatment basal activity and the responsiveness of tuberoinfundibular DA neurons to prolactin return to control values. These results suggest that the response of tuberoinfundibular DA neurons to prolactin is determined, in part, by the preceding circulating levels of this hormo

ISSN:0028-3835    

DOI:10.1159/000124100

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

To study the maturation of inhibitory influences on growth hormone (GH) secretion the effect of ether stress on plasma GH levels was studied during postnatal ontogenesis in female rats. Ether stress did not affect plasma GH levels in 1-day-old pups. A distinct decrease of plasma GH was found in 3- and 9-day-old pups, and the response was prevented by treatment of 3-day-old animals with somatostatin antiserum. No effect of ether stress on plasma GH was noted in 12-, 15-, 18- and 21-day-old rats. Treatment of intact 12-day-old pups with the somatostatin antiserum increased plasma GH level under basal conditions. The inhibitory effect of ether stress on plasma GH was noted again at the age 30 days and in adult animals. It is concluded that the hypothalamus of 3-day-old rats is able to release enough somatostatin to inhibit GH secretion after stress. At the period 12–18 days a phase of pituitary refractoriness was noted: ether stress as well as TRH injection (our previous observation) fail to affect plasma GH in female pups, probably due to high somatostatin secretion under basal conditions and (or) low capacity of pituitary to release GH. It is suggested that regulation of GH secretion is not mature until after the 21st day of lif

ISSN:0028-3835    

DOI:10.1159/000124101

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Neuroendocrine effects of the antiestrogen LYl 17018 were investigated in C57BL/6J mice. A series of subcutaneous injections of 17β-estradiol (E2) into ovariectomized mice increased pituitary glucose-6-phosphate dehydrogenase (G6PDH) specific activity, increased uterine wet weight, and suppressed the postovariectomy rise in serum LH. Simultaneous administration of LYl 17018 completely reversed the effects of E2 on G6PDH activity and uterine weight, and partially reversed the negative feedback of E2 on luteinizing hormone (LH). When administered in the absence of E2, LY117018 had no effect on G6PDH activity or serum LH, but increased uterine weight by 70%. Thus, LYl 17018 effectively antagonizes the effects of E2 at both uterine and pituitary levels, but acts as a partial agonist only in the uterus

ISSN:0028-3835    

DOI:10.1159/000124102

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The relationship between the steroid hormone 17β-estradiol and the muscarinic cholinergic receptors present in the preoptic area (POA), median hypothalamus and posterior hypothalamus of female rats was examined in vitro at various stages of the estrous cycle. Muscarinic receptors varied in a cyclic manner, specifically in the POA, as shown by an increase in the proportion of high-affinity agonist binding sites (RH) to 60% during the proestrus, as compared to (RH) proportion observed during diestrus-2 and during the afternoon of proestrus (35%). Exposure of POA homogenates to 17β-estradiol resulted in conversion of (RH) to low-affinity agonist binding sites (RL) This effect of the hormone was also restricted to the POA taken from rats during the morning of proestrus. It was blocked by the antiestrogenic drug, clomi-phene, and could be prevented by preoccupation of the muscarinic receptors by their own ligands prior to the addition of hormone. It follows that significant changes in POA muscarinic receptors in situ exactly coincided with the known critical time period characterized by high estrogen levels and high levels of estrogen receptors in the POA. These changes in muscarinic receptors might thus conceivably reflect variations in cholinergic activity in the POA during the estrous cycl

ISSN:0028-3835    

DOI:10.1159/000124103

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Facilitatory and inhibitory neural mechanisms involved in the expression of female sexual behaviors in male rats were examined with a dual operation technique. Male rats were castrated and the preoptic area was dorsally deafferented (anterior roof deafferentation, ARD) in order to remove the forebrain lordosis-inhibitory system. Male rats with ARD displayed not only lordosis but also soliciting behaviors in response to 2 µg estradiol benzoate (EB) and 0.5 mg progesterone (P). The ARD male rat then received a second operation involving the hypothalamus or lower brain stem, i.e., the ventromedial nucleus and the adjacent area (ventromedial hypothalamus, VMH) were damaged by a radiofrequency lesion generator; the hypothalamus de-efferented anterolaterally by means of a Halász knife cut posterior to the suprachiasmatic nucleus (ADC) or lesions of the pontine periventricular gray and the adjacent area (dorsomedial tegmental lesion, DMTL). The DMTL effectively suppressed lordosis in EB-P-primed male rats with ARD. Only 1 of 14 ARD-DMTL males showed lordosis. In contrast, the VMH lesions or the ADC failed to interfere with the facilitatory effect of ARD on female sexual behaviors in male rats tested with the same dose of EB-P. Thus, the pontine periventricular gray plays a critical role for lordosis regulation in males. These results suggest that the male rat brain possesses the minimal neural mechanism for the expression of female sexual behaviors associated with the development of the strong forebrain lordosis-inhibiting syste

ISSN:0028-3835    

DOI:10.1159/000124104

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Using catecholamine (CA) fluorescence histochemistry in combination with quantitative microfluorimetry, it has been shown that chronic treatment with triiodothyronine (T3) and thyroxine (T4; 2 × 10 and 2 × 36 µg/kg i.p., respectively, twice daily for 10 days), but not acute treatment (1 and 3.6 mg/kg i.p., respectively, 2 h before killing), increases CA utilization in the medial and lateral palisade zones of the median eminence and reduces noradrenaline (NA) utilization in the parvocellular part and magnocellular part of the paraventricular hypothalamic nucleus of the hypophysectomized male rat. Following chronic T4 treatment it could also be shown that the CA levels in the medial and lateral palisade zones of the median eminence were increased, while the NA levels were reduced in the parvocellular part of the paraventricular hypothalamic nucleus. Chronic T3 treatment induced similar changes – increased CA levels in the medial palisade zone and reduced NA levels in the magnocellular part of the paraventricular hypothalamic nucleus. Within the telencephalon, chronic but not acute treatment with T3 or T4 selectively increased dopamine (DA) utilization within the diffuse type of DA nerve terminal systems of the nucleus accumbens. This action of chronic treatment of T3 or T4 was highly selective and no changes in DA levels could be demonstrated in any DA nerve terminals analyzed in the nucleus caudatus putamen, nucleus accumbens and tuberculum olfactorium. In all the experiments the TSH levels remained undetectable and the low basal serum prolactin levels were not modulated in any experimental group in spite of the treatment with a tyrosine hydroxylase inhibitor in the CA utilization experiments. Following 2–3 weeks after hypophysectomy, serum T3 and T4 were decreased by 30–50%. In the acute experiments with T3or T4, serum T3 levels and T3 as well as T4 levels were markedly elevated after the respective treatments. In the chronic experiments, the T4 treatment resulted in significant increases in the serum levels of both T3 and T4. The present results indicate that discrete DA and NA nerve terminal systems within the median eminence (DA), nucleus accumbens (DA) and paraventricular hypothalamic nucleus (NA) can slowly respond to chronic treatment with T3 or T4. This effect is the result of a direct action of the thyroid hormones on the brain since TSH is absent in the hypophysectomized rat. The results indicate that thyroid hormones interact with those DA and NA nerve terminal systems known to be involved in the inhibitory dopaminergic mechanism in the external layer of the median eminence and also interact with the facilitatory noradrenergic mechanism within the parvocellular part of the paraventricular hypothalamic nucleus regulating TSH secretion. In view of the selective increase in DA turnover in the nucleus accumbens it is speculated that chronic thyroid hormone treatment may modulate behaviors by a direct central action. The effects of thyroid hormones in the CNS may be mediated via nuclear receptors. However, this remains to be demo

ISSN:0028-3835    

DOI:10.1159/000124105

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Seasonal breeding in the ewe is regulated by photoperiod through a pineal-dependent mechanism. Changes in the ability of estradiol to inhibit tonic LH secretion are critical. During anestrus, this ovarian steroid gains the ability to slow the frequency of pulsatile LH secretion through an action on the brain. Exposure of ovariectomized, estradiol-implanted ewes to short photoperiods during summer anestrus revealed that daylength can control LH pulse frequency. After removal of estradiol, LH pulse frequency still differed between long- and short-day ewes, suggesting photoperiodic modulation of LH and presumably GnRH secretion independent of gonadal steroids. Significantly, the effects of daylength expressed both in the presence and the absence of estradiol failed to occur in pinealectomized ewes. Long-term infusions of melatonin, given in physiological patterns to pinealectomized ewes, mimicked the effects of photoperiod on pineal-intact ewes. Specifically, a pattern of melatonin characteristic of that in short days (16-hour night-time rise) led to an increase in LH pulse frequency to a breeding season rate. Conversely, melatonin infusions typifying a long-day pattern (8-hour night-time rise) produced an anestrous pulse pattern. Pituitary sensitivity to GnRH was not reduced in sheep which were reproductively suppressed by photoperiod or melatonin treatments. These observations support the conclusion that day-length acts through pineal melatonin secretion to regulate a neural LH pulse generator which, by changing the frequency of GnRH pulses, determines the ewe’s seasonal reproductive stat

ISSN:0028-3835    

DOI:10.1159/000124106

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Corticotropin-releasing factor (CRF) receptors were localized in the human pituitary gland by an in vitro labeling light microscopic autoradiographic technique using an 125I-labeled analog of ovine CRF substituted with norleucine and tyrosine at amino acid residues 21 and 32, respectively. Specific binding sites for CRF were observed in the anterior lobe while no specific binding sites for CRF were present in the posterior pituitary lobe. The CRF binding sites in the anterior lobe occurred in clusters which predominated in the anteromedial portion of the lobe. This pattern of localization of CRF binding sites resembles previously reported distributions of corticotrophs in anterior pituitary. These data support the physiological role of endogenous CRF in regulating hormone secretion from the anterior lobe of the human pituitary.

ISSN:0028-3835    

DOI:10.1159/000124107

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

A portion of medial basal hypothalamus containing the supraoptic nuclei with the neurohypophysis attached was organ cultured. Hypothalamus and neurohypophysis were maintained in separate compartments, and the intact infundibular stalk passed through a hole in a fluid-tight barrier which separated the two compartments. After 24, 48 and 72 h in culture, vasopressin (VP) release from the neurohypophysis was measured during a control hour and again during an immediately subsequent test hour. Test hour VP release was expressed as a percentage of control hour release. Test substances were added to either the pituitary or the hypothalamus compartment. Acetylcholine stimulated pituitary VP release both when added to hypothalamus (10–5M) and when added directly to neural lobe (10–6 M and above). Acetylcholine 10–5 M and no effect when isolated neural lobes (severed from hypothalamus to culture) were similarly tested. Hexamethonium blocked the stimulation of pituitary VP release evoked by addition of acetylcholine to hypothalamus. However, in pituitary, atropine prevented the stimulatory effect of acetylcholine. Atropine had no effect on VP release from severed neural lobes. These data show that high concentrations of acetylcholine can stimulate VP release from pituitary both by a hypothalamic action and also by a direct effect in neural lobe. Further, a nicotinic cholinergic receptor mediates the action of acetylcholine in hypothalamus whereas a muscarinic cholinergic receptor is involved in the direct pituitary response to acetylcholine. Intact axonal connections between hypothalamus and pituitary are required in order for acetylcholine to stimulate VP release in neurohypop

ISSN:0028-3835    

DOI:10.1159/000124108

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

We have previously shown that incubation of rat pituitary cells in the presence of LHRH results in specific enhancement of nuclear estrogen receptor (ER) binding which cannot be accounted for by simple intracellular translocation of cytoplasmic receptor. In the present study, the role of cAMP in this response has been examined. Suspended pituitary cells from adult ovariectomized rats primed with estradiol were incubated with varying concentrations of LHRH or a highly active LHRH analog (LHRH-A) for 30 min at 37 °C, and levels of cAMP were determined. Total cAMP levels changed only in response to a concentration of 100 pmol/pituitary of either peptide; the stimulation by LHRH was twice that by LHRH-A. When the priming dose level of estradiol was reduced from 1.0 to 0.5 µg/day, stimulation of cells by 100 pmol of LHRH caused a much greater increase in cAMP levels. Separate incubation of subcellular fractions with a wide dose range of dibutyryl-cAMP (DBcAMP) resulted in a progressive loss of cytosol receptor binding capacity (which was also observed in whole cultured or suspended cells), but no significant concomitant change in nuclear receptor binding; however, whole cells in suspension or culture did show an increase in nuclear ER activity in the presence of 100 nM DBcAMP. This response was qualitatively, but not quantitatively, similar to that elicited by LHRH. When the effects of whole cell incubation with LHRH and LHRH-A on nuclear ER were compared with their effects on total cAMP levels, no correlation was observed; rising levels of cAMP did, however, coincide with falling levels of cytosol ER. Integration of these observations with our previous quantitative assessment of LHRH effects on the ER populations indicates that cAMP may mediate the diminution of cytosol ER levels, but it does not appear to be involved to any appreciable degree in the enhancement of the nuclear ER bindin

ISSN:0028-3835    

DOI:10.1159/000124109

出版商:S. Karger AG    

年代:1985

数据来源: Karger