Somatostatin

Vale, Wylie; Brazeau, Paul; Rivier, Catherine; Brown, Marvin; Boss, Barbara D.; Rivier, J.; Burgus, Roger; Ling, Nicholas; Guillemin, Roger

doi:10.1016/b978-0-12-571131-9.50014-1

Cited by 72 publications

(72 citation statements)

References 38 publications

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“…Alternatively one could postulate the converse-i.e., NE blocks the inhibitory effects of somatostatin on basal secretion which is itself unchanged. However, further studies on the interaction of somatostatin and NE and on the Somatostatin and TRF are both widely distributed throughout the central nervous system, often in similar locations (1,3,(31)(32)(33) 7-its responsiveness to levels of somatostatin of the order of 10-8 M-i.e., similar to or possibly somewhat less than those that we and others have found in the hypothalamus and median eminence (3). Nevertheless our in vitro observations clearly cannot be extrapolated to the in vivo situation without further studies.…”

Section: Discussionmentioning

confidence: 99%

Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus.

Hirooka¹,

Hollander²,

Suzuki³

et al. 1978

Proc. Natl. Acad. Sci. U.S.A.

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Somatostatin in concentrations of 10-6 to 10-8 M inhibited basal release of thyrotropin releasing factor in organ culture of rat hypothalamus. Norepinephrine in doses of 10-4-10-6 M induced release of thyrotropin releasing factor which increased progressively with time and was temperature and dose dependent. This enhanced thyrotropin-releasing-factor release was inhibited by somatostatin at 10-6-10-8 M. The tetradecapeptide somatostatin, which is extensively distributed throughout the central nervous system, gastrointestinal tract, and pancreas (1-3), inhibits release of various hormones including growth hormone (4), thyrotropin (5), glucagon (6) and insulin (4). Somatostatin infusion lowers circulating thyrotropin in man (7), and passive immunization of rats with specific somatostatin antiserum increases basal and thyrotropin releasing factor (TRF)-stimulated thyrotropin secretion (8). These experiments imply an interrelationship between TRF and somatostatin and pituitary thyrotropin secretion. Potential local effects of somatostatin within the hypothalamus itself, either directly on peptide hormone secretion or via an action upon neurotransmitters, are equally likely and have not been critically examined.Studies of the regulation of TRF synthesis and release are complicated by the fact that the hormone is widely distributed throughout the central nervous system so that measurements of the hormone in the peripheral blood, regardless of their accuracy, may not faithfully mirror concentrations of TRF actually delivered to the anterior pituitary (9). Moreover, measurements of hormone levels in the hypophyseal portal circulation require surgical cannulation under anesthesia which entails the administration of anesthetics, many of which affect hypothalamic hormone release (10), and in most instances measurements require prior hypophysectomy as well, to permit sampling of the entire hypothalamic outflow (11). Our own approach has been to utilize short-term organ culture of rat hypothalamus as a model for delineating factors modulating in vitro release of TRF. We have found that somatostatin at 10-6 M-10-8 M inhibits basal release of TRF. Moreover, norepinephrine (NE) in doses of 10-4-10-6 M increases release of TRF, an effect which is not seen in the presence of somatosta- were killed by decapitation at 10-11 a.m. After the brain was exposed by removal of the skull with sterile instruments, it was carefully placed in a sterile plastic petri dish which contained Ca2+, Mg2+-free Hanks' balanced salt solution, bacitracin (2.1 X 10-5 M), and glucose (6 mg/ml). Prior to use the dishes had been "gassed" with 5% C02/95% air. Dissection was performed in a laminar flow hood with sterile instruments at a plane 1 mm lateral to the midline and at a depth of 1 mm. The fragments were obtained from the area between the posterior margin of the optic chiasm and the anterior portion of the mammillary body. Microscopic examination (Fig. 2) demonstrated that the fragments included parts of the paraventricular, dorsomedial, vent...

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Section: Discussionmentioning

confidence: 99%

Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus.

Hirooka¹,

Hollander²,

Suzuki³

et al. 1978

Proc. Natl. Acad. Sci. U.S.A.

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“…The recent discovery that the hormone somatostatin (the somatotropin release inhibiting factor; SRIF) is present in a large number of locations in the central and peripheral nervous systems and in endocrine cells of the thyroid gland and the gastro-entero-pancreatic (GEP) endocrine system (see HoKFELT et al, 1975;VALE et al, 1975;PEARSE et al, 1977) has been followed only to a limited extent by phylogenetical studies. As usual when a new hormone is being discovered, most of the original investigations were made in the conventional mammals and birds.…”

Section: Jan-bertil Siljevall6mentioning

confidence: 99%

Some Phylogenetical Aspects on the Occurrence of Somatostatin in the Gastro-Entero-Pancreatic Endocrine System

Falkmer

Elde

Hellerström

et al. 1977

Arch. Histol. Jap., Arch. Histol. Jpn

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“…SST is a regulatory peptide originally discovered as the hypothalamic factor inhibiting growth hormone release [16,107] and subsequently found to have wide distribution and multiple functions in the brain [34,112]. SST acts via six subtypes of G-protein-coupled receptors, of which SSTR2(a) is one of the most abundant in the brain [54,112,101].…”

Section: Introductionmentioning

confidence: 99%

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

et al. 2015

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Alzheimer's disease and other age-related neurodegenerative disorders are associated with deterioration of the noradrenergic locus coeruleus (LC), a probable trigger for mood and memory dysfunction. LC noradrenergic neurons exhibit particularly high levels of somatostatin binding sites. This is noteworthy since cortical and hypothalamic somatostatin content is reduced in neurodegenerative pathologies. Yet the role of a somatostatin signal-

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Somatostatin

Cited by 72 publications

References 38 publications

Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus.

Somatostatin inhibits release of thyrotropin releasing factor from organ cultures of rat hypothalamus.

Some Phylogenetical Aspects on the Occurrence of Somatostatin in the Gastro-Entero-Pancreatic Endocrine System

Critical role of somatostatin receptor 2 in the vulnerability of the central noradrenergic system: new aspects on Alzheimer’s disease

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