摘要:

This paper presents the first detailed localization of luteinizing hormone (LH)-containing cells and fibers in the rat central nervous system. These immunoreactive elements were identified by four LH antisera, two directed against the intact LH molecule and two against LHb. Cell bodies, immunoreactive for LH were found throughout the rostral-caudal extent of the hypothalamic arcuate and ventromedial nuclei, the periarcuate area ventral to the ventromedial nucleus, and the retrochiasmatic area. Immunopositive fibers were traced to numerous structures within the brain including discrete regions of the hypothalamus, septal area, nucleus of the diagonal band, bed nucleus of stria terminalis, amygdala, thalamus, periaqueductal gray, raphe nuclei, brainstem reticular nuclei, locus ceruleus, parabrachial nucleus, dorsal motor nucleus of vagus, and the nucleus of the solitary tract, with a few fibers extending into spinal cord central gray. This pattern of fiber distribution corresponds closely with those described for fibers containing several other anterior pituitary hormones. The extensive projection for LH may provide neuroanatomical substrate mediating reproductive events as it does in the pituitary, or it may serve some modulatory function in brain which is independent of its role in reproduction.

ISSN:0028-3835    

DOI:10.1159/000124818

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In order to evaluate thyrotropin function in the genetically hypoprolactinemic rat, (IPL nude), we measured by radioimmunoassay TRH hypothalamic content, pituitary TSH content and serum TSH, T3, T4, both in IPL nude and control rats at various times over the 24-hour period. Compared to normal rats, the hypothalamic TRH content in the IPL nude rat showed similar variations during the day, whereas a slight increase was observed during the night characterized by a significant difference at 20.00 h. Pituitary weight and TSH content were doubled in IPL nude rats; however, when expressed as µg TSH/µg protein or DNA, a significant increase was found only at 17.00 and 20.00 h. Serum TSH and total serum T3, T4 depicted similar variations although they were minute but nonetheless significant modifications, i.e. an increase of TSH at 17.00 and 23.00 h and a decrease of T4 at 11.00 h. However, only FT4 concentrations (and not-FT3) were slightly but significantly decreased in IPL rats over the experimental times. In conclusion, the slight increase in hypothalamic TRH and pituitary TSH contents and the absence of main associated variations of serum TSH, T3 and T4 do not lend support to the hypothesis that TRH could be the cause of the hypoprolactinemia of these rats. On the contrary, the observed thyrotropin axis variations might be rather interpreted as the consequence of i

ISSN:0028-3835    

DOI:10.1159/000124819

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The effects of morphine and naloxone on hypothalamo-pituitary-adrenocortical (HPA) activity and blood pressure were studied in rats in which adrenergic transmission had been impaired pharmacologically. The αi-adrenoceptor antagonist, prazosin and the tyrosine hydroxylase inhibitor, α-methyl-para-tyrosine (α-MPT), increased the hypothalamic corticotrophin releasing factor (CRF) content and the plasma corticotrophin (ACTH) concentration and exaggerated the HPA response to stress. In addition, the spontaneous secretion of CRF by hypothalami in vitro was increased by α-MPT-treatment. Morphine enhanced the basal and stress-induced activity of the HPA system in vivo. It also stimulated the secretion of CRF by hypothalami in vitro. Naloxone did not affect resting HPA activity but reduced markedly the stress-induced release of corticotrophin. The effects of morphine and naloxone on the HPA axis, in vivo, were reduced by pretreatment with α-MPT and prazosin, respectively. The HPA responses could not be correlated with the changes in blood pressure which the drugs caused. The results suggest that opioid substances stimulate HPA activity by depressing the activity of the adrenergic pathways which inhibit the secretion of

ISSN:0028-3835    

DOI:10.1159/000124820

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The effects of ovariectomy and of 17β-estradiol (estradiol) treatment in vivo and in vitro on the ability of melatonin to inhibit dopamine release from the female rat hypothalamus and on [125I]-iodomelatonin binding sites in the brains and hypothalami of female rats were investigated. In long-term (2–4 weeks) ovariectomized (OVX) female rats, the inhibitory effect of melatonin in vitro on dopamine release from the hypothalami was abolished. After implantation of estradiol capsules, the ability of melatonin to inhibit dopamine release from the hypothalamus was reinstated and resembled that observed in intact female rats at estrus and in females exhibiting spontaneous persisting estrus. Similar reinstatement of the responsiveness to melatonin was observed in hypothalami of OVX rats shortly (2 h) after a single subcutaneous injection of estradiol (200 µg/animal). Incubation of hypothalami of OVX rats in vitro for 50–90 min with estradiol (0.1–1 nM) resulted in a partial (up to 50%), time and steroid concentration-dependent reinstatement of the ability of melatonin to inhibit the induced dopamine release. Conversely, incubations with estradiol in vitro reduced the ability of melatonin to inhibit dopamine release from the hypothalami of intact rats at proestrus. Such incubations had no effect on the release of dopamine from hypothalami of rats at estrus or of short-term OVX (3 days) rats. The changes in the responsiveness of the hypothalamus to melatonin were accompanied by profound changes in the binding of [125I]-iodomelatonin, to synaptosomes isolated from whole brains and from hypothalami of the OVX female rats. In OVX rats, the densities of the binding sites in the brains and particularly in the hypothalami decreased to 18 and 24% respectively, of the values observed in control females at estrus. The apparent dissociation constant of the remaining sites was significantly lower (ca. 90 nM) than that observed in the intact controls (ca. 300 nM). An almost complete reinstatement of the [125I]-iodomelatonin binding sites was observed in synaptosomes prepared from the hypothalami of OVX rats shortly (2 h) after a single subcutaneous injection of estradiol, or after incubation with estradiol in vitro. The estradiol-mediated reinstatement of [125I]-iodomelatonin binding sites was less pronounced in synaptosomes prepared from whole brains. The results clearly show that estradiol directly modulates the responses of the dopaminergic neurosecretory system in the hypothalamus to melatonin. This phenomenon may be primarily associated with the estradiol-induced changes in the density and function of melatonin receptors in the hypothalamus. In addition, the data point to the existence of extrahypothalamic melatonin binding sites, whose function may be indirectly regulated by ovarian h

ISSN:0028-3835    

DOI:10.1159/000124821

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Studies were conducted to determine if the hypothermic effects of barbiturates were responsible for their ability to suppress luteinizing hormone (LH) secretion in rats following ovariectomy or treatment with gonadal steroids. In both ovariectomized rats and rats treated with estradiol and progesterone, pentobarbital caused a marked hypothermia and blocked LH hypersecretion. In ovariectomized rats, the LH-suppressing effects of pentobarbital could be prevented by maintaining normal core body temperature. However, in steroid-treated rats, the maintenance of normal core body temperature did not prevent the pentobarbital-induced blockade of the steroid-induced LH surge. These data indicate that the pentobarbital-induced reduction of LH secretion in ovariectomized rats is temperature-dependent, while its blockade of the steroid-induced LH surge is not. Additionally, this study provides further evidence for the differential neuronal regulation of LH secretion following ovariectomy and during the steroid-induced surge in LH.

ISSN:0028-3835    

DOI:10.1159/000124822

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Acute exposure to footshock stress increased the pituitary level of cyclic adenosine monophosphate (AMP) in vivo and sharply increased plasma levels of adrenocorticotropic hormone, β-endorphin and β-lipotrophic hormone, as well as prolactin. Seven days after bilateral lesions of the paraventricular nucleus of the hypothalamus, the pituitary cyclic AMP response to stress was totally eliminated and the increases in plasma levels of these pituitary hormones were blunted. We conclude that while the pituitary hormonal responses to stress might be mediated by several neurohumoral factors, the stress-induced increases in pituitary levels of cyclic AMP in vivo are mediated largely via corticotropin-releasing factor, released from neurons which project from the paraventricular nucleus to the median eminenc

ISSN:0028-3835    

DOI:10.1159/000124823

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

To investigate the site at which angiotensin II (AII) acts to increase adrenocorticotrophic hormone (ACTH) secretion, the effects of intraventricular (IVT) or intravenous (IV) injection of the AII antagonist saralasin on the ACTH responses to IVT or IV injection of AII were examined in conscious male rats. AII does not cross the blood-brain barrier, but IVT as well as IV saralasin are known to prevent the binding of circulating AII to circumventricular organs. IV AII (0.2–200 ng) induced dose-related increases in ACTH secretion and a transient increase in the corticotrophin-releasing hormone (CRH) content of the median eminence. IVT injection of saralasin (10 µg) blocked the ACTH responses to IV AIL The same dose of saralasin given intravenously did not produce a comparable decrease in the ACTH response to IV AIL IVT injection of 1 and 10 ng AII increased plasma ACTH in a dose-related manner. The increase in plasma ACTH induced by IVT administration of angiotensin was not inhibited by IV infusion of saralasin (12 µg/kg/min). On the other hand IV infusion of this dose of saralasin abolished or reduced the ACTH response to IV injection of larger doses of AII. These data support the conclusion that circulating AII stimulates ACTH secretion by acting on the circumventricular organs to increase CRH secretion. They also suggest that AII receptors inside the blood-brain barrier as well as AII receptors in the circumventricular organs trigger increases in ACTH secret

ISSN:0028-3835    

DOI:10.1159/000124824

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

The presence of a peptide resembling atrial natriuretic factor (ANF) was demonstrated in the peripheral sympathetic ganglia of the rat by a sensitive radioimmunoassay. Partially purified ANF-like compounds from the superior cervical ganglia exhibited biological activities which were similar to the synthetic peptide of cardiac origin; they inhibited ACTH-stimulated aldosterone release in vitro and displaced labelled [125I]-ANF from rat adrenocortical cell receptors. The exact source and role of ANF in peripheral nervous structures is not fully understood. We suggest that in sympathetic ganglia ANF may act as a neurotransmitter and/or neuromodulator in a manner similar to other neuropeptides.

ISSN:0028-3835    

DOI:10.1159/000124825

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In order to investigate the influence of dopamine (DA) in modulating prolactin (PRL) response to vasoactive intestinal polypeptide (VIP), VIP (75 µg i.v. over 12 min) was administered to normal women and patients with microprolactinomas during saline or DA (0.06 µg/kg BW/min) infusion. In 8 normal women VIP caused PRL to rise from 7.9 ± 0.8 (mean±SE)to 33.4+ 17.1 ng/ml(p< 0.01), the peak occurring at 15 min, while it did not elicit any significant modification in serum PRL levels in 18 patients with microprolactinomas. DA infusion lowered serum PRL by 67 and 58.2% at 120 min in normal women and in patients with microprolactinomas, respectively, and abolished VIP-induced PRL response in normal women without influencing PRL response in patients with microprolactinomas. PRL responsiveness to VIP was not restored by dopaminergic disinhibition (domperidone 10 mg i.v.) in 4 patients tested. Two previously unresponsive patients showed a VIP-induced PRL increase, superimposable on that recorded in normal women, after successful selective adenomectomy. These data suggest that DA, although able to suppress VIP-induced PRL response in normals, does not play any major role in causing unresponsiveness to VIP in prolactinomas. The lack of PRL responsiveness to VIP might be intrinsic to the adenoma or due to alterations of PRL secretion regulatory mechanisms other than DA secondary to the presence of the tumor, or to a depletion of the readily releasable pool of

ISSN:0028-3835    

DOI:10.1159/000124826

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Arachidonic acid is metabolized to three distinct classes of metabolites: cyclooxygenase produces prostaglandins, prostacyclins, and thromboxanes; lipoxygenase produces hydroperoxyeicosatetraenoic acids and, epoxygenase, a NADPH-dependent cytochrome P-450 enzyme, produces epoxyeicosatrienoic acids. Addition of 5,6-epoxyeicosatrienoic acid (5,6-EET) to GH3 cells, a rat anterior pituitary cell line, produces a rapid, dose-dependent stimulation of prolactin (PRL) release. Incubation with arachidonic acid (AA) was ineffective at increasing PRL release. The lipoxygenase metabolite 5-hydroxyeicosatetraenoic acid (5-HETE), however, increased PRL release from GH3 cells but with a much lower maximal response than 5,6-EET. We examined the role of metabolism inhibitors in 5,6-EET-mediated PRL release. Mi-crosomal and cytosolic epoxide hydrolase (EH) inhibitors do not alter 5,6-EET-induced PRL release, suggesting that EH does not play a significant role in 5,6-EET mediated PRL release from GH3 cells. A chemical analog of 5,6-EET wherein the epoxide oxygen is replaced with a sulfur to afford 5,6-thioepoxyeicosatrienoic acid was also tested and found to stimulate the release of PRL, although not to the same extent as 5,6-EET. Although 5-HETE tends to increase PRL release from GH3 cells, 5,6-EET is significantly more potent at the stimulation of PRL release from GH3 cells.

ISSN:0028-3835    

DOI:10.1159/000124827

出版商:S. Karger AG    

年代:1987

数据来源: Karger