Neoplasms of the Brain and Pituitary Gland

2016 ◽  
pp. 733-764
Keyword(s):  
Pituitary Gland ◽  
The Brain

ADRENOCORTICAL FUNCTION IN PATIENTS WITH ACUTE SEVERE BRAIN AND PITUITARY LESION

1962 ◽  
Vol 40 (2) ◽  
pp. 254-262 ◽  
Author(s):  
H. H. Bassøe ◽  
R. Emberland ◽  
E. Glück ◽  
K. F. Støa
Keyword(s):  
Pituitary Gland ◽  
Adrenal Cortex ◽  
Artificial Ventilation ◽  
Practical Significance ◽  
Adrenocortical Function ◽  
The Third ◽  
Low Levels ◽  
Pituitary Lesion ◽  
Steroid Excretion ◽  
The Brain

ABSTRACT The steroid excretion and the plasma corticosteroids were investigated in three patients with necrosis of the brain and of the pituitary gland. The patients were kept alive by artificial ventilation. In two of the patients the neutral 17-ketosteroids and the 17-hydrocorticosteroids fell to extremely low levels. At the same time, the number of eosinophil cells showed a tendency to increase. Corticotrophin administered intravenously twice to the third patient had a stimulating effect on the adrenal cortex. The theoretical and practical significance of these findings is discussed.

Distribution of lamprey gonadotropin-releasing hormone in the brain and pituitary gland of larval, metamorphic, and adult sea lampreys, Petromyzon marinus

1994 ◽  
Vol 72 (1) ◽  
pp. 48-53 ◽  
Author(s):  
Glenda M. Wright ◽  
Kim M. McBurney ◽  
John H. Youson ◽  
Stacia A. Sower
Keyword(s):  
Pituitary Gland ◽  
Preoptic Area ◽  
Petromyzon Marinus ◽  
Gonadotropin Releasing Hormone ◽  
Immunoperoxidase Technique ◽  
Dorsal Region ◽  
Releasing Hormone ◽  
Sea Lampreys ◽  
The Brain

Lamprey gonadotropin-releasing hormone was demonstrated in the brains of larval, metamorphic, and adult sea lampreys, Petromyzon marinus, using an immunoperoxidase technique. Gonadotropin-releasing hormone was observed in the neurohypophysis and preoptic area of the brain of larval, metamorphic, juvenile, and prespawning adults. The occurrence of immunoreactive cells and the intensity of the immunostaining was lowest in larvae, but by stage 5 of metamorphosis there was a marked increase in the prevalence and staining of these cells, which continued into adults. In larvae and lampreys in metamorphic stages 1–4, most immunoreactive fibres were confined to the dorsal region of the neurohypophysis. During stage 5 there was an expansion of immunopositive fibres into the ventral portion of the neurohypophysis. Prominent immunoreactivity was observed throughout the neurohypophysis from stage 5 onward through the adult stages. Changes in immunoreactivity of these cells and fibres in the brain and neurohypophysis correlate well with increased concentrations of hormone in the brain during development and with the timing of presumed changes in activity of cells in the adenohypophysis during metamorphosis.

Contribution from local conversion of thyroxine to 3,5,3'-triiodothyronine to intracellular 3,5,3'-triiodothyronine in several organs in hypothyroid rats at isotope equilibrium

1982 ◽  
Vol 101 (3) ◽  
pp. 386-396 ◽  
Author(s):  
J. van Doom ◽  
F. Roelfsema ◽  
D. van der Heide
Keyword(s):  
Cerebral Cortex ◽  
Pituitary Gland ◽  
Subcellular Fractions ◽  
Thigh Muscle ◽  
Intracellular Level ◽  
Carrier Free ◽  
Tissue Homogenates ◽  
Isotope Equilibrium ◽  
Layer Chromatography ◽  
The Brain

Abstract. The intracellular conversion of T4 to T3 was investigated in various tissues of hypothyroid rats after continuous iv infusion of radiolabelled T3 and T4. Two groups of 4 thyroidectomized rats were infused with carrier-free 125I-labelled T4 as well as 131I-labelled T3 until isotope equilibrium was achieved. Plasma, various tissue homogenates (liver, kidney, pituitary, thigh muscle, cerebral cortex and cerebellum) and subcellular fractions (nuclei, mitochondria, microsomes, cytoplasm) from liver, kidney and the pituitary gland were extracted for thin layer chromatography. The [125I]T3/[131I]T3 ratios were determined and the extra contribution of [125I]T3 derived from local conversion of [125I]T4 to the total [125I]T3 was calculated in percent. In addition to the [125I]T3 derived from plasma, [125I]T3 derived from locally converted [125I]T4 was present in all tissues investigated. There was substantially more, although in varying quantities, in the cerebral cortex (79 ± 2%), the cerebellum (68 ± 4%) and the pituitary gland (53 ± 1%) than in the liver (10 ± 6%), the kidney (11 ± 5%) and thigh muscle (17 ± 6%); in the latter tissues most of the 125I-labelled T3 is derived directly from plasma. These results indicate that in the brain of severe hypothyroid rats there is pronounced conversion of T4 to T3 and effective binding of the T3 produced whereas the T3 in the liver, kidney, and muscle is predominantly derived from plasma. At the intracellular level, within the investigated tissues, the locally formed T3 was distributed equally over the subcellular fractions.

Regulation of Gonadotropins

2019 ◽  
Author(s):  
Daniel J. Bernard ◽  
Yining Li ◽  
Chirine Toufaily ◽  
Gauthier Schang
Keyword(s):  
Pituitary Gland ◽  
Granulosa Cells ◽  
Positive Feedback ◽  
Sex Steroids ◽  
Somatic Cells ◽  
Inhibin B ◽  
Dependent Manner ◽  
Α Subunit ◽  
Theca Cells ◽  
The Brain

The gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), are glycoproteins produced by gonadotrope cells of the anterior pituitary gland. The two hormones act on somatic cells of the gonads in both males and females to regulate fundamental aspects of reproductive physiology, including gametogenesis and steroidogenesis. In males, LH stimulates testosterone production and sperm maturation. FSH also regulates spermatogenesis, though the importance of the hormone in this process differs across species. In females, FSH stimulates ovarian follicle maturation. Follicles are structures composed of oocytes surrounded by two types of somatic cells, granulosa and theca cells. FSH stimulates granulosa cells to proliferate and to increase their production of the aromatase enzyme. LH stimulates theca cells to make androgens, which are converted into estrogens by aromatase in granulosa cells. A surge of LH also stimulates ovulation of mature follicles. Gonadotropin-releasing hormone (GnRH) from the brain is the principal stimulator of gonadotropin synthesis and secretion from the pituitary. The sex steroids (androgens and estrogens) that are produced by the gonads in response to the gonadotropins feedback to the brain and pituitary gland. In the brain, these hormones usually slow the release of GnRH through a process called negative feedback, which in turn leads to decreases in FSH and LH. The steroids also modulate the sensitivity of the pituitary to GnRH in addition to directly regulating expression of the genes that encode the gonadotropin subunits. These effects are gene- and species-specific. In females, estrogens also have positive feedback actions in the brain and pituitary in a reproductive cycle stage-dependent manner. This positive feedback promotes GnRH and LH release, leading to the surge of LH that triggers ovulation. The gonadotropins are dimeric proteins. FSH and LH share a common α-subunit but have hormone-specific subunits, FSHβ and LHβ. The β subunits provide a means for differential regulation and action of the two hormones. In the case of FSH, there is a second gonadal feedback system that specifically regulates the FSHβ subunit. The gonads produce proteins in the transforming growth factor β (TGFβ) family called inhibins, which come in two forms (inhibin A and inhibin B). The ovary produces both inhibins whereas the testes make inhibin B alone. Inhibins selectively suppress FSH synthesis and secretion, without affecting LH. The pituitary produces additional TGFβ proteins called activins, which are structurally related to inhibins. Activins, however, stimulate FSH synthesis by promoting transcription of the FSHβ subunit gene. Inhibins act as competitive receptor antagonists, binding to activin receptors and blocking activin action, and thereby leading to decreases in FSH. Together, GnRH, sex steroids, activins, and inhibins modulate and coordinate gonadotropin production and action to promote proper gonadal function and fertility.

Sign in / Sign up

Export Citation Format

Share Document