Somatostatin receptors in the central nervous system

Schindler, Marcus; Humphrey, P. P. A.; Emson, Piers C.

doi:10.1016/0301-0082(96)00030-5

Cited by 140 publications

(24 citation statements)

References 206 publications

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“…Somatostatin acts via a family of G-protein-coupled receptors known as somatostatin receptors 1-5 (SST1 - SST5), which are differentially distributed throughout the CNS [2]. Signaling through somatostatin receptors is complex and involves auto-, para-, or endocrine mechanisms [3-8]. Binding of somatostatin to its receptors induces G-protein activation through various pathways, resulting in the activation of several key enzymes, including adenylyl cyclase, phosphothyrosine phosphatase (PTPase) and mitogen activated protein kinase (MAPK) are modulated, along with changes in the intracellular levels of calcium and potassium ions [9].…”

Section: Introductionmentioning

confidence: 99%

The somatostatinergic system in the mammalian cochlea

et al. 2011

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BackgroundLittle is known about expression and function of the somatostatinergic system in the mammalian cochlea. We have previously shown that somatostatin administration may have a protective effect on gentamicin-induced hair cell loss. In this study, we have analyzed the cochlear expression of somatostatin receptor 1 (SST1) and somatostatin receptor 2 (SST2) at both the mRNA and the protein level in wild-type mice, as well as in SST1 and SST2 knock-out (KO) mice and in cultivated neurosensory cells.ResultsWe demonstrate that the somatostatin receptors SST1 and SST2 are specifically expressed in outer and inner hair cells (HCs) of the organ of Corti (OC), as well as in defined supporting cells. The expression of SST1 and SST2 receptors in cultivated P5 mouse OC explants was similar to their expression in inner and outer hair cells. Somatostatin itself was not expressed in the mammalian cochlea, suggesting that somatostatin reaches its receptors either through the blood-labyrinthine barrier from the systemic circulation or via the endolymphatic duct from the endolymphatic sac. We used mice with a deletion of either SST1 or SST2 to learn more about the regulation of SST1 and SST2 receptor expression. We demonstrate that in SST1 KO mice, SST2 was expressed in outer HCs and Deiters' cells, but not in pillar cells or inner HCs, as compared with wild-type mice. In contrast, in SST2 KO mice, the expression pattern of the SST1 receptor was not altered relative to wild-type mice.ConclusionsThese findings reveal that somatostatin receptors demonstrate specific expression in HCs and supporting cells of the mouse cochlea, and that absence of SST1 alters the expression of SST2. This specific expression pattern suggests that somatostatin receptors may have important functional roles in the inner ear.

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Section: Introductionmentioning

confidence: 99%

The somatostatinergic system in the mammalian cochlea

et al. 2011

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“…Tissue localization studies on SRIH receptor subtypes have shown a broad and overlapping receptor distribution [6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16]. Although the individual receptors possess distinctive expression patterns, assigning a functional response to an individual SRIH receptor subtype remains difficult, since a mixed receptor subtype population is present in almost all tissues studied.…”

Section: Introductionmentioning

confidence: 99%

Somatostatin Receptor Subtypes 2 and 5 Inhibit Corticotropin-Releasing Hormone-Stimulated Adrenocorticotropin Secretion from AtT-20 Cells

et al. 2002

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Somatostatin (SRIH) regulates pituitary adrenocorticotropin (ACTH) secretion by interacting with a family of homologous G protein-coupled membrane receptors. The SRIH receptor subtypes (sst₁–sst₅) that control ACTH release remain unknown. Using novel, subtype-selective SRIH analogs, we have identified the SRIH receptor subtypes involved in regulating ACTH release from AtT-20 cells, a model for cell line pituitary corticotropes. Radioligand-binding studies with ¹²⁵I-SRIH-14 and ¹²⁵I-SRIH-28 showed that SRIH-14 and SRIH-28 recognized specific, high-affinity and saturable membrane-binding sites. Nonpeptidyl agonists with selectivity for the sst₂ (L-779,976; compound 2) or sst₁/sst₅) (L-817,818; compound 5) receptor subtypes potently displaced ¹²⁵I-SRIH-28 from AtT-20 cell membranes, while agonists selective for the sst₁ (L-779,591; compound 1), sst₃ (L-796,778; compound 3) or sst₄ (L-803,087; compound 4) subtypes were inactive. Tyr¹¹-SRIH-14, compound 2 (sst₂) or compound 5 (sst₅) inhibited forskolin and corticotropin-releasing hormone (CRH)-induced increases in intracellular cAMP. Furthermore, the sst₂ and sst₅ agonists potently inhibited CRH-induced ACTH release from AtT-20 cells. These results provide the first evidence that sst₂ and sst₅ receptor subtypes, but not sst₁, sst₃ or sst₄, inhibit cAMP accumulation and regulate ACTH secretion in the AtT-20 cell model of the rodent corticotrope.

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“…In addition to its neuroendocrine role, SRIH has several neurophysiological actions [for reviews, see 1, 3, 4, 5]. SRIH has also been implicated in a variety of neurological diseases such as Alzheimer’s, Huntington’s, and epilepsy [6, 7], and has applications in cancer therapy [8]. …”

Section: Introductionmentioning

confidence: 99%

Effects of Sex Steroid Hormones on the Expression of Somatostatin Receptors sst1 and sst5 in Goldfish Pituitary and Forebrain

Canosa

Lin

Peter³

2003

Neuroendocrinology

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In the present paper the effects of estradiol and testosterone on the expression of the types 1 and 5 somatostatin receptors (sst1 and sst5) in the goldfish forebrain and pituitary were investigated. Estradiol increased the sst1 expression in both the forebrain and pituitary in a dose- and time-dependent manner. In addition, estradiol also increased the pituitary expression of sst5. On the other hand, testosterone had no effects on the expression of these receptor subtypes. Mature female goldfish were found to have higher sst1 and sst5 expression in the pituitary, as well as a higher expression of sst1 in the forebrain compared to sexually regressed animals. As estradiol treatment increases serum growth hormone levels in goldfish, these data suggest that sst1 and sst5 receptors are likely not directly involved in this aspect of growth hormone release.

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Somatostatin receptors in the central nervous system

Cited by 140 publications

References 206 publications

The somatostatinergic system in the mammalian cochlea

The somatostatinergic system in the mammalian cochlea

Somatostatin Receptor Subtypes 2 and 5 Inhibit Corticotropin-Releasing Hormone-Stimulated Adrenocorticotropin Secretion from AtT-20 Cells

Effects of Sex Steroid Hormones on the Expression of Somatostatin Receptors sst1 and sst5 in Goldfish Pituitary and Forebrain

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