Morphometric and Functional Changes of Rat Pituitary Somatotropes and Lactotropes after Central Administration of Somatostatin

Milošević, Verica; Brkić, Branislava; Velkovski, S.D.; Sekulić, Milka; Lovren, Mirjana; Starčević, Vesna; Severs, Walter B.

doi:10.1159/000028223

Cited by 17 publications

(20 citation statements)

References 18 publications

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“…Acute central SRIF administration directly into rat brain ventricles inhibits somatotroph, lactotroph [77], LH-secreting gonadotroph [78] and thyrotroph [79] proliferation. In adrenalectomized rats that have higher CRH levels due to lack of glucocorticoid negative feedback, both octreotide and pasireotide inhibited increased pituitary mitotic activity [80].…”

Section: Physiological Effects Of Srif Receptor Signalingmentioning

confidence: 99%

Pituitary somatostatin receptor signaling

Ben-Shlomo

Melmed

2010

Trends in Endocrinology & Metabolism

180

131

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Somatostatin (SRIF) is a major regulator of pituitary function, mostly inhibiting hormone secretion and to a lesser extent pituitary cell growth. Five SRIF receptor subtypes (SSTR1-5) are ubiquitously expressed G-protein coupled receptors. In the pituitary, SSTR1, SSTR2, SSTR3 and SSTR5 are expressed, with SSTR2 and SSTR5 predominating. As new SRIF-analogs have recently been introduced for treatment of pituitary disease, we evaluate the current knowledge of cell-specific pituitary SRIF receptor signaling and highlight areas of future research for comprehensive understanding of these mechanisms. Elucidating pituitary SRIF receptor signaling enables understanding of pituitary hormone secretion and cell growth, and also points to future therapeutic development for pituitary disorders. Keywords somatostatin receptors; pituitarySomatotropin-release inhibitory factors (SRIF) or somatostatins are cyclic peptides cleaved from a precursor pre-pro-somatostatin peptide to produce two bioactive products SRIF14 (14 amino acids) and SRIF28 which comprises an additional 14 N-terminal amino acids [1]. SRIFs are phylogenetically ancient, as SRIF-like immunoreactivity is found in protozoans, primitive intervertebrates and vertebrates [1,2]. SRIFs are produced from specialized cells in the brain, gastrointestinal tract (GIT), liver, pancreas, lungs, immune system, kidneys, adrenals and urogenital tracts [1]. SRIF exerts broad, mostly inhibitory effects on endocrine and exocrine secretions. Other than pituitary hormones discussed in this review, SRIF also inhibits secretion of gastro intestinal tract (GIT) hormones including insulin, glucagon, gastrin, cholecystokinin, vasoactive intestinal peptide and secretin. SRIF also inhibits exocrine gastric acid, pepsin, pancreatic enzymes, bile and intestinal fluids secretions [3]. SRIF inhibits gastric emptying, gallbladder contraction, and small intestine segmentation, but inducess migrating motor complex activity and splanchnic vasoconstriction [1]. Brain SRIF inhibits release of hypothalamic hormones including corticotropin releasing hormone (CRH), thyrotropin releasing hormone (TRH), and also dopamine and norepinephrine [1].Hypothalamic SRIF is a major regulator of pituitary gland hormone secretion and to a lesser extent, pituitary cell development and growth. The peptide is produced predominantly in the Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Released SRIF is rapidly inactivated by tissue and blood peptidases, and the very short halflife (~ 2 minutes) limits its therapeutic use. Octreotide and lanreotide are clinically approved ...

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Section: Physiological Effects Of Srif Receptor Signalingmentioning

confidence: 99%

Pituitary somatostatin receptor signaling

Ben-Shlomo

Melmed

2010

Trends in Endocrinology & Metabolism

180

131

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“…Both forms of SRIH are also found in nonneuronal tissues, including the gastrointestinal tract, endocrine pancreas, thyroid [4], adrenals [5,6], thymus [7], and ovaries [8]. Hypothalamic SRIH is known to inhibit growth hormone (GH), thyrotropin-stimulating hormone (TSH), and prolactin (PRL) secretion from the anterior pituitary [3,9,10]. Also, somatostatin inhibits secretion of several non-pituitary hormones such as insulin, glucagon, gastrin, secretin [11] and aldosterone [12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Effects of Centrally Applied Somatostatin on Pituitary Adrenocorticotropes in Female Rats

et al. 2000

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Effects of intracerebroventricular (i.c.v.) application of somatostatin (SRIH-14 or SRIH-28) on growth and function of pituitary adrenocorticotropes (ACTH cells) were examined in adult female Wistar rats. Animals were subjected to i.c.v. administration of three 1-μg doses of SRIH-14 or SRIH-28 dissolved in 5 μl saline every second day. Controls were treated in the same way with the same volume of saline only. ACTH-producing cells were studied using the peroxidase-antiperoxidase (PAP) immunohistochemical procedure; blood samples were collected for hormone analyses 5 days after the last injection. SRIH-28 treatment decreased (p < 0.05) all morphometric parameters compared to control rats. Volume of ACTH cells decreased by 10%, nuclei by 36% and volume density by 13%. No significant changes (p > 0.05) in these parameters occurred after SRIH-14 treatment. Plasma concentration of ACTH in SRIH-28-treated rats was significantly lower (p < 0.05) than in control rats by 35%. In SRIH-14-treated rats, plasma concentration of ACTH was slightly, but not significantly (p > 0.05) increased by 13% compared to saline treatment. These observations suggest that centrally administered somatostatin-28, but not somatostatin-14, is specifically involved in the control of growth and secretory activity of ACTH cells in female rats. Thus, selective pharmacological manipulation of SRIH-28 receptors reached from CSF may affect ACTH activity without altering actions usually attributed to receptors sensitive to SRIF-14.

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“…The number of nuclei in immunoreactive ACTH-cells per mm 3 was estimated using the formula of Weibel and Gomez [19] according to Weibel [18]. Since rat ACTH cells are mononuclear, the numerical density of the nuclei (N V ) corresponds to the number of cells per mm 3 .…”

Section: Methodsmentioning

confidence: 99%

“…In the pituitary, SRIH also blocks the release of other hormones, such as thyrotrophin (TSH) [2] prolactin (PRL) [3] and gonadotrophins [4,5]. At the periphery, SRIH is a modulator of endocrine and exocrine functions and regulates differentiation and proliferation of normal and tumor cells [6,7].…”

Section: Introductionmentioning

confidence: 99%

Pituitary ACTH cells in female rats after neonatal treatment with SRIH-14.

Milošević

Nestorović²,

Terzić³

et al. 2010

Folia Histochem Cytobiol.

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Abstract:The prolonged effects of neonatal SRIH-14 treatment on pituitary ACTH cells were investigated. Neonatal female rats were injected subcutaneously with SRIH (20 μg/100g b.w.) every 12 hours for five consecutive days (3 rd -7 th day of life). Groups of rats were then killed at the juvenile (16 th day), peripubertal (38 th day) or adult (80 th day) stage. ACTH cells were visualized using the peroxidase-antiperoxidase immunocytochemical procedure. Morphometry and stereology were used to evaluate the ACTH-immunoreactive cell volume and volume density. The histological and immunocytochemical characteristics of ACTH cells in neonatally treated females were changed in all examined periods. Thus, SRIH-14 induced significant (p<0.05) decreases of ACTH cell volume in juvenile, peripubertal and adult rats by 26%, 39% and 14%, respectively, in comparison to the corresponding controls. The volume density of ACTH cells was also diminished (by 31%; p<0.05) at the juvenile stage in comparison with the corresponding controls. In peripubertal and adult rats, the volume densities of ACTH cells were somewhat lower (17% and 14%, respectively), but the decreases did not reach statistical significance. These findings suggest that neonatal treatment with SRIH-14 exerts a marked prolonged inhibitory effect on ACTH cell morphology extending to the adult period of life.

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Morphometric and Functional Changes of Rat Pituitary Somatotropes and Lactotropes after Central Administration of Somatostatin

Cited by 17 publications

References 18 publications

Pituitary somatostatin receptor signaling

Pituitary somatostatin receptor signaling

Effects of Centrally Applied Somatostatin on Pituitary Adrenocorticotropes in Female Rats

Pituitary ACTH cells in female rats after neonatal treatment with SRIH-14.

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