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Normal pituitary gland: changes in shape, size, and signal intensity during the 1st year of life at MR imaging.

Magnetic resonance images of the pituitary glands in 48 endocrinologically normal neonates and infants were analyzed to determine the changes in pituitary gland size, shape, and signal intensity that occur during the 1st year of life. A progressive increase in the length--but not height--of the gland was seen throughout the 1st year. When corrections for total brain size were made, the pituitary gland was found to diminish in relative cross-sectional area throughout infancy. Upward convexity of the gland was seen in 63% of neonates less than 1 month of age, but in only 4% of infants older than 2 months. Hyperintensity of the adenohypophysis relative to the brain stem was visualized on T1-weighted images in 18 of the 24 (75%) neonates and infants less than 2 months old; this appearance was never seen in older infants. An area of high signal intensity was visualized in the posterior pituitary in 32 of 48 cases (67%), and its visualization was unrelated to age. The neonatal and young infant pituitary gland is thus significantly rounder, brighter, and relatively larger during the first 2 months of life than in later infancy.

Humans↗

Intake of monosaccharides or amino acids induces pituitary gland synthesis of proteins regulating intestinal fluid transport.

In cholera diarrhoea, the pituitary gland produces a 60-kDa protein known as antisecretory factor (ASF) which reverses intestinal secretion induced by the cholera toxin. We show here that ASF-like proteins are produced in the rat during intestinal secretion triggered by intake of a 500 mg dose of mannose, sorbitol, glycine or alanine. All the ASF-like proteins reversed cholera secretion, and all were of a similar size. However, they differed in charge: mannose and sorbitol induced a protein with an isoelectric point of 4.5; glycine induced two proteins, one with a pI of 6.3, the other of 7.7; and alanine induced two proteins, one with a pI of 6.3, the other of 9.4. Antibodies against naturally occurring ASF from porcine pituitary gland neutralized ASF induced by cholera toxin and two of the amino acid-induced proteins, while the sugar-induced protein(s) did not cross-react. All the proteins showed affinity to agarose and were dissociated again with methyl alpha-D-glucoside. A single peroral dose of cholera toxin or sorbitol induced antisecretory proteins which persisted in the pituitary gland for only 1-3 days. Seven treatments gave a sustained response, the protein induced by cholera toxin persisting for over 2 months, and that induced by sorbitol about 1 month.

Amino Acids↗

Effects of acute ovariectomy on anterior pituitary gland follicle-stimulating hormone and luteinizing hormone secretion in the metestrous rat.

Changes at the anterior pituitary gland level which result in follicle-stimulating hormone (FSH) release after ovariectomy in metestrous rats were investigated. Experimental rats were ovariectomized at 0900 h of metestrus and decapitated at 1000, 1100, 1300, 1500, 1700 or 1900 h of metestrus. Controls consisted of untreated rats killed at 0900 or 1700 h and rats sham ovariectomized at 0900 h and killed at 1700 h. Trunk blood was collected and the serum assayed for FSH and luteinizing hormone (LH) concentrations. The anterior pituitary gland was bisected. One-half was used to assay for FSH concentration. The other half was placed in culture medium for a 30-min preincubation and then placed in fresh medium for a 2-h incubation (basal FSH and LH release rates). The basal FSH release rate and the serum FSH concentration rose significantly by 4 h postovariectomy and remained high for an additional 6 h. The basal FSH release rate and the serum FSH concentration correlated positively (r=0.71 with 72 degrees of freedom) and did not change between 0900 and 1700 h in untreated or sham-ovariectomized rats. In contrast, the serum LH concentration and the basal LH release rate did not increase after ovariectomy. Ovariectomy had no significant effect on anterior pituitary gland FSH concentration. The results suggest that the postovariectomy rise in serum FSH concentration is the result, at least in part, of changes which cause an increase in the basal FSH secretion rate (secretion independent of the immediate presence of any hormones of nonanterior pituitary gland origin). The similarities between the selective rises in the basal FSH release rate and the serum FSH concentration in the ovariectomized metestrous rat and in the cyclic rat during late proestrus and estrus raise the possibility that an increase in the basal FSH release rate may be involved in many or all situations in which serum FSH concentration rises independently of LH.

Animals↗

Beta-endorphin and methionine-enkephalin levels in discrete brain regions, spinal cord, pituitary gland and plasma of morphine tolerant-dependent and abstinent rats.

The effect of morphine tolerance-dependence, protracted and naloxone-precipitated abstinence on the levels of beta-endorphin and methionine-enkephalin in discrete brain regions, spinal cord, pituitary gland and plasma was determined in the male Sprague-Dawley rats. Among the brain regions examined, the levels of beta-endorphin in descending order were: hypothalamus, amygdala, midbrain, hippocampus corpus striatum, pons and medulla and cortex. The levels of beta-endorphin in midbrain, hypothalamus, and pituitary of morphine tolerant-dependent rats were decreased significantly. During protracted withdrawal beta-endorphin levels were decreased in amygdala, spinal cord and pituitary. During naloxone-precipitated abstinence beta-endorphin levels were increased in corpus striatum, midbrain and cortex. In addition, in naloxone-precipitated abstinence beta-endorphin levels were decreased in pituitary gland and hippocampus but increased in plasma. The levels of methionine-enkephalin in brain regions in decreasing order were: corpus striatum, pons and medulla, amygdala, hypothalamus, midbrain, hippocampus and cortex. The levels of methionine-enkephalin in pons and medulla, amygdala, hippocampus and pituitary gland were decreased in morphine tolerant-dependent rats. During protracted abstinence from morphine, methionine-enkephalin levels in spinal cord, amygdala, pons and medulla, midbrain, cortex, corpus striatum and pituitary gland were decreased. The levels of methionine-enkephalin in hypothalamus and corpus striatum of naloxone-precipitated abstinent rats were increased but were decreased in amygdala and pituitary gland. These results suggest that during morphine tolerance-dependence and during protracted abstinence beta-endorphin and methionine-enkephalin levels in discrete brain regions and pituitary gland are decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Immunohistochemical demonstration of tenascin in human pituitary glands and adenomas.

The expression of tenascin in 8 cases of normal fetal and adult human pituitary glands and in 51 cases of human pituitary adenomas was investigated immunohistochemically with the use of polyclonal antibodies against human tenascin. The immunohistochemical study demonstrated that tenascin is expressed in both fetal and adult normal epithelial cells of the anterior lobe of pituitary glands and in tumor cells of pituitary adenomas, which suggests that tenascin is synthesized by normal pituitary cells as well as by pituitary adenoma cells. Plurihormonal pituitary adenomas, especially those producing 4 or 5 different hormones, tended to show the highest incidence of positive immunoreactivity for tenascin, suggesting that tenascin may be involved in the aggressive behaviour of plurihormonal adenomas.

Adenoma↗

Early organization of the pituitary gland in Sparus aurata L. (Teleostei). An ultrastructural study.

The cell organization of the pituitary gland and the relationship between neurohypophysis and adenohypophysis in early developmental stages of the gilthead sea bream, Sparus aurata, were studied by electron microscopy. In newly hatched larvae, the pituitary gland was embedded in the ventral floor of the diencephalon and separated from the hypothalamus by a continuous basal lamina. Elongated mesenchymal cells next to the ventral surface were observed. At this stage, there was no neurohypophysis and the adenohypophysis consisted of undifferentiated endocrine cells with small scarce secretory granules and a few stellate cells, with no distinctive zonation. An incipient neurohypophysis was present in 1-day-old larvae. The first evagination of the neurohypophysis into the adenohypophysis were observed in 2-day-old larvae and developed progressively with age, being deeper in the caudal zone. Two regions in the adenohypophysis, one anterior--the presumptive pars distalis--and one posterior--the presumptive pars intermedia--were found in 2-day-old larvae. Three regions (rostral and proximal pars distalis and pars intermedia) were clearly distinguishable in 4-day-old larvae. The ultrastructural features of the pituitary endocrine cells varied during gland differentiation, with the secretory granules gradually increasing in number and size, accompanying organelle development. Nevertheless, even in the oldest larvae studied (65 days), undifferentiated cells similar to those in the earliest stages were observed. The first blood vessels appeared in the neurohypophysis around 16 days after hatching. During early development, the pituitary gland progressively emerged from the ventral floor of the brain. By 16 days, the principal pattern of the pituitary gland architecture appeared to be established.

Animals↗

Requirement of the pituitary gland for gonadal hormone effects on hepatic drug metabolism in rats.

Previous studies have demonstrated an important role for the pituitary gland in the regulation of hepatic drug and steroid metabolism. The present studies were carried out to determine the relationship between the pituitary gland and the actions of gonadal hormones on hepatic drug metabolism in rats. Testosterone administration to castrated male rats increased hepatic microsomal cytochrome P-450 concentrations and enhanced the rates of ethylmorphine demethylation and benzo(a)pyrene hydroxylation. Estradiol treatment, on the other hand, lowered cytochrome P-450 levels and decreased the rates of aniline, ethylmorphine and benzo(a)pyrene metabolism in orchiectomized rats. However, when given to hypophysectomized male rats, neither testosterone nor estradiol affected cytochrome P-450 levels or enzyme activities. Similarly, 5alpha-dihydrotestosterone administration increased hepatic drug metabolism only in the presence of the pituitary gland. The effects of both testosterone and estradiol were fully demonstrable in the absence of the thyroid or adrenal glands, excluding the need for either organ. The results indicate an absolute dependence on the pituitary gland for gonadal hormone (testosterone and estradiol) actions on hepatic mixed-function oxidases.

Adrenalectomy↗

Ornithine decarboxylase activity and polyamines in the anterior pituitary gland during the rat oestrous cycle.

The biosynthesis of polyamines, an ubiquitous group of amines shown to be essential for normal cellular growth and differentiation, was studied in the rat anterior pituitary gland during the different stages of the oestrous cycle. The activity of ornithine decarboxylase (ODC), which catalyses the rate-limiting step in the biosynthesis of polyamines, was low during oestrus, metoestrus and dioestrus. However, a marked transitory rise in ODC activity was found in the pituitary gland on the evening of pro-oestrus. The rise in ODC activity was accompanied by an increase in the pituitary content of the polyamines putrescine and spermidine. Ovariectomy did not significantly change the basal ODC activity in the pituitary gland. Oestrogen treatment of ovariectomized rats resulted in a marked stimulation of pituitary polyamine biosynthesis. The largest effects were observed when oestrogen was given as two injections 72 h apart, which gave rise to levels of ODC activity comparable to those observed on the evening of pro-oestrus. The increase in polyamine synthesis in the anterior pituitary gland during pro-oestrus appeared not to be related to the preovulatory secretion of LH or prolactin, since neither LH-releasing hormone nor thyrotrophin-releasing hormone (which induces a secretion of prolactin) affected pituitary ODC activity. The observed biosynthesis of polyamines may be associated with the cellular proliferation which occurs in the anterior pituitary gland at oestrus.

Animals↗

Localization, transport, and uptake of D-aspartate in the rat adrenal and pituitary glands.

Large amounts of D-aspartate (D-Asp) are present in the rat adrenal and pituitary glands. D-Asp is thought to be synthesized in the mammalian body and also accumulates in various tissues following intraperitoneal or intravenous administration. This report examines the origins of D-Asp in the adrenal and pituitary glands. We administered D-Asp to male rats intraperitoneally and immunolocalized this exogenous D-Asp in adrenal and pituitary tissue, using an anti-D-Asp antiserum which was previously developed in our laboratory. D-Asp levels in the rat adrenal gland have been shown to undergo a transient increase at 3 weeks of age and to decrease rapidly thereafter. We found that in the adrenal gland, exogenous D-Asp administered intraperitoneally was incorporated into the same region of the adrenal cortex in which endogenous D-Asp was present. By Northern and Western blot analysis and immunohistochemistry of glutamate (Glu) transporter, we also found that expression of the Glu transporter (GLAST), which has an affinity for D-Asp, transiently increased at 3 weeks of age and that localization patterns of the Glu transporter within the tissue were almost coincident with those of endogenous D-Asp. These observations suggest that D-Asp in the adrenal cortex of 3-week-old male rats is primarily acquired by uptake from the vascular system. We have previously shown that D-Asp is specifically localized in prolactin (PRL)-containing cells in the anterior lobe of the adult rat pituitary gland. Here we report that in the pituitary gland, exogenous D-Asp accumulated in endothelial cells, but not in PRL-containing cells. Northern and Western blot analysis and immunohistochemistry of Glu transporter revealed that developmental changes in the Glu transporter (GLAST) expression did not correlate with tissue levels of D-Asp and that the Glu transporter was not expressed in PRL-containing cells. These observations suggest that, in contrast to the adrenal gland, most of the D-Asp in the pituitary gland of adult male rats originates inside the gland itself.

Adrenal Glands↗

[Growth factors in the pituitary gland].

There are increasing numbers of evidence that many factors, such as growth factors and cytokines, exist in the pituitary gland, and modulate the release of pituitary hormone both in vivo and in vitro. They indicate the importance of autocrine and paracrine control system within the pituitary gland. For instance, activin, a compound whose existence and nature (in contrast to the related protein inhibin) was not contemplated before its discovery in 1986, has been shown to be synthesized in gonadotrophs and to produce diverse effects on the anterior pituitary. We would like to introduce some recent studies on growth factors in the pituitary gland.

Activins↗

Characteristics of corticosteroid inhibition of adrenocorticotrophin release from the anterior pituitary gland of the rat.

The occurrence and nature of corticosteroid inhibition of ACTH secretion at the rat anterior pituitary gland was investigated using three experimental models: animals bearing lesions of the basal hypothalamus, and two preparations of the gland incubated in vitro; these were tissue segments and collagenase-dispersed cells. Release of ACTH in the experiments was provoked using one of three distinct stimuli: acid extracts of whole hypothalami, corticotrophin releasing activity released by serotonin from hypothalami incubated in vitro and synthetic ovine corticotrophin releasing factor. Irrespective of whether ACTH was measured directly by radioimmunoassay (in the experiments in vitro) or indirectly in terms of corticosterone production (in the lesioned animals), its stimulated release from the anterior pituitary gland was inhibited by corticosterone. Two phases of inhibition were observed; these had some of the characteristics inferred previously from experiments with intact animals and designated fast feedback and delayed feedback. However, the fast feedback demonstrable in lesioned animals did not show the rate-sensitivity shown previously in intact animals. 11-Deoxycortisol (or 11-deoxycorticosterone) and prednisolone proved to be agonists of corticosterone in provoking fast feedback in lesioned animals, whereas they had been shown respectively to act as an antagonist or to have no effect in intact rats. Several steroids were able to cause delayed feedback in lesioned rats, but beclomethasone dipropionate (shown to be an agonist of corticosterone in intact rats) proved to have no inhibitory effect at the anterior pituitary gland of lesioned animals. It is concluded that the dynamics of corticosteroid feedback mechanisms at the anterior pituitary gland, as indicated by experiments in lesioned animals, differ from those operative in the intact animals. Other work suggests that a more important site for such inhibitory mechanisms in vivo is the hypothalamus.

Adrenocorticotropic Hormone↗

Minor interference of low-dose pulses of GnRH with the positive effect of oestradiol on the pituitary gland.

In the ovariectomized rat we investigated the effects of prolonged treatment with oestradiol and 'physiological' pulses of exogenous GnRH on the GnRH-responsiveness of the pituitary gland. Rats were for 20 h pre-treated with either GnRH (3-ng pulses of 3 min duration every 20 min) or saline and for 19 h with either oestradiolbenzoate (OB; 3 micrograms/sc injection) or oil. Then LH and FSH responses were evoked by continuous test infusions of GnRH at the rates of either 60, 100, 150 or 1000 ng/h, lasting 10 h. It appeared that, irrespective of pre-treatment with either GnRH or saline, OB caused an increase of the maximal LH and FSH responses (that is the responses to the maximal stimulus of 1000 ng GnRH/h), and an increase of the GnRH-sensitivity of the pituitary gland, as far as the FSH secretion is concerned. GnRH pulses caused, irrespective of pre-treatment with OB or oil, a decrease of the GnRH-sensitivity of the pituitary gland, as well as a decrease of the maximal FSH response and of the pituitary FSH content. It was concluded that low-dose pulses of exogenous GnRH desensitize the pituitary gland and deplete the pituitary FSH stores, but do not change the positive effect of oestradiol on the maximal gonadotropin response.

Animals↗

Identification of a new growth hormone family protein, somatolactin-like protein, in the rainbow trout (Oncorhyncus mykiss) pituitary gland.

A cDNA encoding a new GH family protein expressed in the rainbow trout (Oncorhyncus mykiss) pituitary gland was identified. Because the deduced amino acid sequence of this cDNA shares 56% homology with rainbow trout (rt) somatolactin (rtSL), we named it as rtSL-like protein (rtSLP). Comparison of the amino acid sequences of rtGH, rainbow trout prolactin (rtPRL), and rtSLP revealed that rtSLP shares 26% and 21% identity with that of rtGH and rtPRL, respectively. Trout SLP contains not only the known GH family protein conserved domains but also all of the four cysteine residues that are responsible for the formation of two disulfide linkages in GH, PRL, and SL. Immunoblot analysis revealed that rtSLP is secreted from the pituitary gland once it is synthesized. Unlike rtSL, rtSLP mRNA was readily detectable in pituitary glands of 2-yr fish (30-34 cm in length) but not in embryos or 1-yr fish (17-25 cm in length). Furthermore, the level of rtSLP mRNA in male fish is 2-fold higher than that in female fish. These results suggest that rtSLP might play a role in regulating the reproductive maturation in rainbow trout.

Amino Acid Sequence↗

Drug metabolizing enzymes in the rat pituitary gland.

Brain protection against chemicals is mainly provided by the specific properties of cerebral microvessels forming the blood-brain barrier. In addition, several drug metabolizing enzymes have been evidenced both in brain tissue and in cerebral capillaries, suggesting their participation in the enzymatic protection of this organ. The pituitary gland, like true circumventricular organs, lacks a tight vascular endothelium and therefore is especially sensitive to blood-native toxic or pharmacologically active molecules. We report here the presence of cytochrome P-450 in the pituitary gland and its main mitochondrial localization. The O-dealkylase activity measured towards 7-benzoxyresorufin, a substrate for the main cytochrome P-450 isoforms involved in the metabolism of xenobiotics, was 5 times higher in the pituitary gland than in the brain cortex. Similarly, microsomal epoxide hydrolase, which inactivates reactive epoxides to trans diol molecules, and two conjugating enzymes, 1-naphthol UDP-glucuronosyltransferase and glutathione-S-transferase, display respectively 6, 4 and 7 times higher activities in the pituitary gland. 7-Benzoxyresorufin-O-dealkylase, 1-naphthol UDP-glucuronosyltransferase and membrane-bound epoxide hydrolase activities were significantly increased in the pituitary gland as an adaptive response to an in vivo treatment by an exogenous inducer, 3-methylcholanthrene. These results suggest that these enzymatic systems play a role in the protection of the pituitary gland towards drugs or toxic substances.

Animals↗

Dexamethasone induces advanced growth hormone expression in the fetal rat pituitary gland in vivo.

The effects of dexamethasone (DEX) on the onset of GH expression in the fetal rat pituitary gland were studied. Pregnant rats received oral administration of DEX dissolved in drinking water (25 mg/liter) for 40 h before killing on days 16-19 of pregnancy. The number of immunoreactive GH cells in the control fetus on day 18 was very small, whereas it was remarkably increased by DEX to a compatible value obtained from control fetuses on day 19. The effect of DEX on the induction of immunoreactive GH cells was found to be less potent on day 17 and not evident on day 16. The population of GH cells on day 19 was doubled, and they stained more intensely by GH antiserum after DEX treatment. In situ hybridization revealed that there were many GH messenger RNA (mRNA)-positive cells in the pituitary gland of a DEX-treated fetus at day 18, whereas they were negligible in number in the age-matched control. Northern blot analysis revealed that DEX induced accumulation of small amounts of GH mRNA in the fetal pituitary gland on day 17, whereas it induced a marked elevation of GH mRNA level on day 18. Reducing the levels of endogenous glucocorticoids by the administration of metyrapone (0.5 mg/ml in drinking water) to the pregnant rats from day 17-19 resulted in the significant reduction in the number of GH cells at day 19. Short-term treatment of DEX (duplicate sc injections at 18 h and 6 h before killing) also induced immunoreactive GH cells on day-18 fetuses but not on day-17 fetuses. Immunoreactive GH cells appeared on day 17 only after quadruplicate injections of DEX during last 40 h, suggesting that there is a difference in fetal sensitivity to DEX between days 17 and 18. These results indicate that immunoreactive GH cells and GH mRNA are inducible by DEX at an earlier stage of the fetal life than they normally appear. It is suggested that glucocorticoids play an important role in the development of GH cells in the fetal pituitary gland in vivo.

Animals↗

Immunocytochemical detection of parathyroid hormone-like substance in the goldfish brain and pituitary gland.

Parathyroid hormone (PTH)-like substance was immunocytochemically detected in the goldfish brain and pituitary gland using the peroxidase-antiperoxidase method with an antiserum raised against bovine PTH1(-84). Immunoreactive cell bodies were found in the nucleus preopticus in the preoptic area, and immunoreactive fibers could be traced from these cell bodies to the pituitary, in which immunoreactivity was detected in the neurohypophysis. These findings suggest that PTH-like substance is biosynthesized in the neuroendocrine cells in the brain and released in the neurohypophysis in the pituitary gland. Our results are discussed in relation to the hypercalcemic regulation of the pituitary gland in teleosts.

Animals↗