Disease relevance of SST

• Here we use perforated-patch recordings to show that, in addition to this pathway, the peptide somatostatin inhibits the calcium current in chick ciliary ganglion neurons by a second soluble pathway involving a cyclic GMP-dependent protein kinase (cGMP-PK) [1].
• Preincubation of the excised choroid with pertussis toxin (200 ng/ml) reverses the inhibitory effects of both morphine and somatostatin [2].
• Somatostatin inhibits intestinal mucosal mast cell degranulation in normal conditions and during mast cell hyperplasia [3].
• Compared with results regarding the direction of the overgrowth in the neuronal maturation process in the previous study using the chick exencephaly model, the findings of overmatured blood vessels were compatible with NSE- and somatostatin-positive elements that appeared especially in the overgrowth foci [4].

High impact information on SST

• SOM (also coreleased from posthatch choroid terminals) can inhibit ACh release in both posthatch and St 40 choroids, suggesting that the SOM receptor interacts with both DHP-sensitive and -insensitive channels [5].
• The pharmacological specificity of Ca2+ channel-secretion coupling in acetylcholine (ACh) and somatostatin (SOM) release was studied in the chick eye choroid neuromuscular junctions and in dissociated ciliary ganglion (CG) neurons [5].
• Comparative genomics provides evidence for close evolutionary relationships between the urotensin II and somatostatin gene families [6].
• Because several peptides originally found in the pituitary as within the central nervous system have been localized in lymphoid tissues and because somatostatin (somatotropin-release-inhibiting hormone, SRIH) can act on cells of the immune system, we searched for this peptide in lymphoid organs [7].
• In sharp contrast to these findings for N-proCT, the other bioactive C-cell peptides, CT and somatostatin, showed no mitogenic effects in human or chicken osteoblast cultures [8].

Chemical compound and disease context of SST

• A somatostatin receptor inhibits noradrenaline release from chick sympathetic neurons through pertussis toxin-sensitive mechanisms: comparison with the action of alpha 2-adrenoceptors [9].

Biological context of SST

• Intense immunoreactivity for the polysialylated form of neural cell adhesion molecule (PSA-NCAM) on both the LHRH neurons and the SST-positive fibers during this period suggests that this less adhesive form of NCAM is involved in the migratory process [10].
• The tissue distribution of somatostatin (SST) immunoreactivity was studied in the nasal and forebrain region in the chick embryo [11].
• During prolonged applications of NE or SS the extent of inhibition decreases due to desensitization and reblock kinetics are significantly slowed (time constant increases from 60 msec to > 100 msec for both NE and SS) [12].
• To explore whether these sequences could enhance transactivation by other inducible transcription factors, they were examined for their ability to synergize with the chick vitellogenin estrogen response element and the rat somatostatin cAMP response element [13].
• Inhibition of growth hormone-stimulated lipolysis by somatostatin, insulin, and insulin-like growth factors (somatomedins) in vitro [14].

Anatomical context of SST

• In particular, the observation that PSS1 mRNA, but not PSS2 mRNA, occurs in the preoptic area and in the ventral hypothalamic nuclei suggests that, of the two somatostatin isoforms, only SS1 acts as a hypophysiotropic factor [15].
• The effect of PSA removal is more likely to involve changes in the interaction of the migrating neurons with a subset of the SST-positive olfactory fibers and/or other elements in the forebrain rather than an alteration in the pattern of their axonal substrate [10].
• By E6.5, the neurons and SST-positive medial branch of the olfactory nerve have proceeded toward the septal area [10].
• These results indicate that the expression of SST in the nasal and forebrain regions is transient in the chick embryo [11].
• The acid-extract from both splenic and ventral lobes of pancreas was fractionated by reverse-phase high-performance liquid chromatography, and the SST-like immunoreactivity was measured in the radioimmunoassay using anti-SST-14 serum [16].

Associations of SST with chemical compounds

• The classical neurotransmitter acetylcholine (ACh) and the potential modulatory peptide somatostatin are colocalized in terminals of avian choroid neurons [17].
• The same effect is seen with 100 nM somatostatin, 10 microM dynorphin, and 100 microM met-enkephalin arginine phenylalanine [2].
• Kinetic basis for the voltage-dependent inhibition of N-type calcium current by somatostatin and norepinephrine in chick sympathetic neurons [12].
• In both preparations, this demodulatory interaction occurred between voltage-independent (opioids) and voltage-dependent (Som, GABA, and NE) modulatory pathways [18].
• At early developmental stages somatostatin receptors coupled predominantly to the current that was sensitive to both omega-CgTX GVIA and nitrendipine [19].

Physical interactions of SST

• Inhibition of PTH receptor binding and PTH mediated adenylate cyclase activity by somatostatin [20].

Regulatory relationships of SST

• Insulin stimulates somatostatin and inhibits glucagon secretion from the perfused chicken pancreas-duodenum [21].

Other interactions of SST

• Involvement of thyrotropin-releasing hormone receptor, somatostatin receptor subtype 2 and corticotropin-releasing hormone receptor type 1 in the control of chicken thyrotropin secretion [22].
• Retinas were also examined using histofluorescence for dopamine histochemistry, for AChE, and immunohistochemistry with antibodies to CAT, tyrosine hydroxylase, GABA, 5-HT, Leu-enkephalin, and somatostatin [23].
• Extracts of discrete lobes of chicken pancreas were assayed for somatostatin (SRIF), insulin and glucagon immunoreactivity [24].
• These were localized in enteric ganglia and contained neurofilament immunoreactivity, vasoactive intestinal peptide immunoreactivity, and somatostatin immunoreactivity [25].
• Bundles of nerve fibers showing somatostatin and choline acetyltransferase immunoreactivity were found in the choroid layers of the eye [26].

Analytical, diagnostic and therapeutic context of SST

• This somatostatin inhibition of Ca2+ current did not desensitize and was not characterized by the slowing of Ca(2+)-current activation (kinetic slowing) observed in whole-cell recordings [1].
• A discrete population of cells of the endocrine pancreas contains immunoreactive somatostatin as shown by immunofluorescence [27].
• The identities of somatostatin- and enkephalin-immunoreactive materials were confirmed by high pressure liquid chromatography [28].
• In the present investigation, the chicken neural retina was studied for the presence of structures exhibiting somatostatin-like immunoreactivity by utilizing an indirect immunofluorescence technique [29].
• Immunohistochemical characterization of monolayer cell cultures of embryonic chicken pancreas and measurement of somatostatin release [30].

References