Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunocytochemical staining after controlled proteolytic treatment of the sections with pronase revealed widespread distribution of neuronal cell bodies with somatostatin-like immunoreactivity (SLI) in the rat forebrain. SLI-positive neurons were found in regions of the neocortex, the pyriform cortex, the cingulate cortex, the striatum, the olfactory tract and tubercle, the nucleus accumbens, the septum, and the hypothalamus. These results are consistent with previous radioimmunoassay findings and suggest the presence of large somatostatin-like (possibly precursor) molecules in the neurons stained for SLI after pronase treatment.
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PMID:Somatostatin-containing neurons in the rat brain: widespread distribution revealed by immunocytochemistry after pretreatment with pronase. 36 Aug 18

The gene encoding a novel mouse somatostatin receptor termed mSSTR3 was isolated and characterized. The sequence of mSSTR3 shows 46 and 47% identity with mSSTR1 and mSSTR2, respectively. mSSTR3 binds somatostatin-14 and somatostatin-28 with high affinity, but shows very low affinity for the somatostatin analogs MK-678 and SMS-201-995. In addition, mSSTR3 is coupled to pertussis toxin-sensitive G proteins and mediates somatostatin inhibition of forskolin-stimulated and dopamine D1 receptor-stimulated cAMP formation, indicating that it is coupled to adenylylcyclase. The pharmacological properties of mSSTR3 and its ability to couple with adenylylcyclase distinguish SSTR3 from the other cloned somatostatin receptors and indicates that it mediates biological functions different from SSTR1 or SSTR2. In situ hybridization indicates that SSTR3 mRNA is widely distributed in the mouse brain, and its expression in the nucleus of the lateral olfactory tract and in the piriform cortex, the primary olfactory cortex in the rodent brain, suggests that SSTR3 may participate in the processing and modulation of primary sensory information.
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PMID:Cloning of a novel somatostatin receptor, SSTR3, coupled to adenylylcyclase. 132 99

The distribution of somatostatin immunoreactivity in the basal ganglia and amygdala of the squirrel monkey (Saimiri sciureus) was studied with specific polyclonal antibodies directed against somatostatin-28 and somatostatin-28(1-12). Both antibodies gave similar results with regard to the distribution of somatostatin-immunoreactive neuronal profiles. A moderately dense and highly heterogeneous network of somatostatin-positive fibers was observed throughout the striatum. A dorsoventral gradient of increasing immunoreactivity was noted in the striatum and the caudate nucleus was found to strain generally less intensely than the putamen. The immunoreactive fibers within the striatum were mostly thin and varicose and formed patches corresponding to the striosomes, as visualized on adjacent sections immunostained for calbindin. Although some somatostatin cell bodies rimmed the striosomes, most of the positive cells were rather uniformly scattered in the striatum. These medium-sized cells were significantly smaller in the caudate nucleus (93 microns2, S.D. = 26 microns2) than in the putamen (122 microns2, S.D. = 39 microns2), but their density was significantly higher in the caudate nucleus (29.7 cells/mm2, S.D. = 8.8 cells/mm2) than in the putamen (20.5 cells/mm2, S.D. = 7.0 cells/mm2). The nucleus accumbens stained moderately and positive cell bodies were evenly dispersed throughout this structure. In contrast, the olfactory tubercle displayed a heavily stained neuropil but positive neurons were encountered only in its polymorph layer. In the sublenticular region, dense fiber plexuses appeared in register with nonreactive cell clusters of the nucleus basalis of Meynert and of the nucleus of the anterior commissure. More caudally, a dense bundle of positive fibers was observed at the level of the ansa lenticularis, the inferior thalamic peduncle, and the adjoining bed nucleus of the stria terminalis. Several fibers contributing to this bundle were of the woolly type. Woolly fibers also coursed in the substantia innominata between the ventral aspect of the globus pallidus and the optic tract, and ascended in the internal medullary lamina separating the internal and external segments of the globus pallidus. Somatostatin-immunoreactive cell bodies were uniformly scattered throughout the substantia innominata. The various nuclei of the amygdala showed a wide range of immunoreactivity. The central nucleus was lightly reactive, whereas the intercalated masses displayed a moderate staining. A dorsoventral gradient of immunostaining was noted in the ventrolateral portion of the amygdala, the lateral nucleus being moderately to densely stained and the basal nucleus very lightly to lightly immunoreactive.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Distribution of somatostatin immunoreactivity in the forebrain of the squirrel monkey: basal ganglia and amygdala. 134 31

The effects of chronic prenatal and/or postnatal exposure to cocaine on somatostatin concentration and receptors were studied in the olfactory bulbs of rat pups at birth and at 15 days old. Wistar rats were injected subcutaneously with single daily doses of 40 mg cocaine hydrochloride/kg from days 7 to 19 of gestation, from day 7 of gestation to day 15 postpartum or from parturation to day 15 postpartum. Fetal exposure to cocaine decreased SS concentrations in the olfactory bulb of the newborn pups while prenatal-plus-postnatal exposure increased this parameter. Administration of cocaine only during lactation did not induce any change. Exposure during gestation or during nursing induced an increase in the total number of somatostatin receptors and a decrease in the affinity constant in the olfactory bulb of newborn and 15-day-old pups. These results suggest that the development of somatostatin receptors in the olfactory bulb can be altered by prenatal and/or nursing period exposure to cocaine.
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PMID:Somatostatin receptors increase in the olfactory bulb of developing pups after perinatal exposure to cocaine. 135 5

The distribution of somatostatin mRNA in the rat brain has been examined by in situ hybridization using 32P-labelled oligonucleotide probes. Numerous telencephalic and diencephalic areas contained labelled cells with the largest numbers of cells occurring in the anterior olfactory nucleus, olfactory and entorhinal cortices, hippocampus, neocortex, caudate nucleus, accumbens, septum, amygdala and periventricular nucleus. Fewer labelled cells occurred in the mesencephalon and rhombencephalon but groups were seen in the region of the central grey, lateral lemniscus, parabrachial and tegmental nuclei, medial longitudinal fasciculus and nucleus of the solitary tract. This distribution closely matches published maps of the distribution of somatostatin-immunoreactive cell bodies. The intensity of individual cell labelling has also been quantified using image analysis and compared with the intensity of somatostatin immunocytochemical cell staining. In situ hybridization cell labelling varied both within different regions and from region to region. Highest labelling was seen in the periventricular nucleus of the hypothalamus followed by telencephalic regions such as cortex, hippocampus and the medial nucleus of the amygdala. In contrast all brainstem areas had low levels of labelling with the lowest levels of the brain occurring in the dorsolateral tegmental nucleus. Somatostatin immunocytochemistry showed similar variations such that the intensity of cell immunostaining broadly paralleled the intensity of cell in situ hybridization labelling. Thus both peptide and mRNA levels were much lower in brainstem cells than in forebrain, although a close correlation between immunocytochemistry and in situ hybridization was not seen in all brain regions.
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PMID:Semi-quantitative analysis of somatostatin mRNA distribution in the rat central nervous system using in situ hybridization. 167 71

Neuropeptide-Y (NPY) and glucocorticoid receptors are coexpressed in many neurons in the brain. We addressed the question: Do glucocorticoids regulate the accumulation and/or secretion of immunoreactive (IR) NPY by fetal rat brain cells in culture, and if so, is the effect developmental stage dependent? Aggregates, formed from dissociated cells obtained from the hypothalamus-olfactory tubercle of 17-day-old fetuses, were cultured in serum-free medium for 23 days. On day 23, the aggregate NPY content was 6 ng/flask, and secretion (last 2 days) was approximately 12 ng/24 h. Exposure to dexamethasone (Dex; 20 nM) between days 0-23 led to a 1.9-fold increase in the aggregate content of NPY, whereas NPY secretion was not altered. When Dex exposure was limited to days 12-23, 16-23, 19-23, or 21-23, only a 12- to 23-day exposure induced NPY accumulation, and it was as effective as a 0- to 23-day exposure. The Dex-induced increase in NPY content was evident after a lag period of 4 days or more. When Dex exposure occurred on days 0-12, the aggregate NPY content on day 12 or 23 was not altered. None of these treatments altered the aggregate/medium content of immunoreactive somatostatin (SRIF) or the response to a 48-h exposure to forskolin (10 microM). Dex induction of NPY accumulation was a saturable function of the Dex concentration (maximal at 20 nM), and it was completely inhibited by RU486, a glucocorticoid/progesterone receptor antagonist; neither progesterone, 17 beta-estradiol, nor testosterone altered aggregate/medium NPY contents. Protein/DNA contents of the aggregates were either unaffected or slightly reduced by Dex. Thus, 1) Dex stimulates the accumulation of immunoreactive NPY, but not SRIF, by cultured fetal brain cells; 2) this effect requires a continuous 8-12 days of exposure to Dex during a late developmental stage in culture; 3) Dex does not potentiate or attenuate forskolin action on the NPY neuron; and 4) Dex action appears to be mediated by the glucocorticoid receptor. These results are consistent with glucocorticoid induction of production and/or decreased intracellular degradation of NPY, and with glucocorticoids regulating the NPY neuron in the perinatal brain in a developmental age-dependent manner.
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PMID:Dexamethasone-induced accumulation of neuropeptide-Y by aggregating fetal brain cells in culture: a process dependent on the developmental age of the aggregates. 167 32

To determine the effect of thyroid status on proTRH-derived peptide processing and secretion, the content and release of TRH and prepro-TRH25-50 (PYE27), as well as somatostatin (SRIF) from median eminence (ME) or olfactory lobe (OL) tissue was studied in the rat. In hypothyroid animals treated by thyroidectomy (Tx), the ME content of TRH and PYE27 was reduced by more than 50%; further, when compared with euthyroid controls there was a significant 2-fold enhancement of the in vitro release of these peptides from ME fragments in response to depolarizing concentrations (60 mM) of potassium. Hyperthyroidism (T4 treatment) caused either no change or an increase in the ME content of these peptides and their response to K+ in vitro did not differ from control animals. The OL content of TRH and PYE27 was unaffected by thyroid status. SRIF levels in both ME and OL as well as in vitro secretion from the ME did not change with either Tx or T4 treatment. The ratio of TRH/PYE27 secretion throughout release and content studies remained stable at 3:1 to 4:1. These findings support the view that TRH in the hypothalamus but not OL is regulated by thyroid hormone. In this location hypothyroidism enhances not only pro TRH synthesis but also release of TRH and another proTRH-derived peptide. The consistent ratio of TRH/PYE27 suggests that regulation of TRH production by thyroid hormone occurs predominantly at the transcriptional level and not through posttranslation processing.
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PMID:Hypothyroidism reduces content and increases in vitro release of pro-thyrotropin-releasing hormone peptides from the median eminence. 167 96

Immunohistochemistry on tissues of larval lampreys, Petromyzon marinus L., was used to determine the distribution of invariant somatostatin-14 (SST-14) and lamprey somatostatin-34 (SST-34) in the brain while antisera against porcine peptide tyrosine tyrosine (PYY), human neuropeptide Y (NPY), anglerfish peptide YG (aPY), salmon glucagon-like peptide (GLP), SST-14, and SST-34 were used in studies of the pancreas and anterior intestine. In the brain, SST-14 is the major form of somatostatin. SST-14- and SST-34-immunoreactive nerve fibers are distributed throughout the telencephalon, diencephalon, and mesencephalon. In the latter region SST-14 immunoreactivity is concentrated in nerve tracts in the nucleus interpeduncularis. Nerve cells within the olfactory bulbs are immunoreactive only to anti-SST-34. Cells immunostained with anti-SST-14 were localized within the ependymal and subependymal layers of the pars ventralis hypothalami and the subependymal layers of the pars dorsalis thalami. SST-14-immunoreactive perikarya are also distributed within the tegmentum mesencephali. Nerve fibers and cells immunoreactive to anti-SST-34 are detected in the pars ventralis hypothalami but these cells do not colocalize SST-14. Pancreatic islets, distributed within the epithelium and in the submucosal connective tissue at the esophageal-intestinal junction, are only immunoreactive to anti-insulin. The antisera revealed three distinct cell types in the intestinal epithelium: type 1 colocalizes aPY, NPY, and PYY; type 2 colocalizes SST-14 and SST-34; and type 3 demonstrates immunoreactivity only to anti-SST-34. Immunoreactivity to anti-GLP is absent.
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PMID:Distribution of two forms of somatostatin and peptides belonging to the pancreatic polypeptide family in tissues of larval lampreys, Petromyzon marinus L.: an immunohistochemical study. 167 24

Specific oligonucleotide probes and in situ hybridization histochemistry were used to study the ontogeny and regulation of the mRNAs for proenkephalin A and preprosomatostatin in rat brain. In adult brain the most intense hybridization signal for the proenkephalin A mRNA was in caudate putamen, nucleus accumbens and olfactory tubercle. By contrast, the hybridization signal for preprosomatostatin mRNA was more diffusely scattered throughout the brain, with high signals in the neocortex, olfactory bulb and hippocampal formation. Studies of the ontogeny of these mRNAs revealed a different pattern of ontogenetic expression and differential regulation by dopaminergic input. The mRNA for preposomatostatin reached the highest level within the first postnatal week, whereas proenkephalin A mRNA progressively increased throughout the entire period studied. In addition the proenkephalin A mRNA showed a medial to lateral gradient in 2-day-old rat striatum which disappeared with increasing age, whereas preprosomatostatin mRNA increased in most brain areas in fairly uniform fashion with increasing age. Treatment of newborn rats with 6-hydroxydopamine increased the expression of proenkephalin A mRNA by 1.6 fold but had no effect on the expression of preprosomatostatin mRNA. The 6-hydroxydopamine-induced change in proenkephalin A mRNA expression was not observed until postnatal day 32, indicating that enkephalin-containing neurons of the developing striatum are relatively insensitive to dopamine input and that they cannot compensate for the neonatal lesion, despite the fact that the insult was given in a period of high plasticity of the neural tissue.
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PMID:Differential ontogenetic expression and regulation of proenkephalin and preprosomatostatin mRNAs in rat caudate-putamen as studied by in situ hybridization histochemistry. 168 33

The first part of this article deals with several aspects of efferents and afferents of the rat basal forebrain cholinergic system (BFChS) studied with anterograde transport of Phaseolus vulgaris leucoagglutinin (PHA-L). PHA-L tracing of the BFChS efferents revealed topographically differentiated axonal trajectories and patterns of presynaptic endings to the neocortex, mesocortex, olfactory nuclei and hippocampus. Combining this method with second immunolabeling, we identified the muscarinic cholinoceptive neurons in the neocortex and the somatostatinergic neurons in the hippocampus as being directly innervated by the magnocellular basal nucleus and the medial septum, respectively. The prefrontal cortex was identified as a source of afferent input to the basal forebrain cholinergic neurons. This projection also exhibits a topographic organization, which shows a reciprocal relationship with the BFChS efferents to the cortex. The second part of this article describes the anatomical changes of cortical cholinergic and some other neurotransmitter systems after long-term cholinergic denervation in the aged rat cortex. The spared cholinergic projection in the largely denervated areas shows abundant malformations, which are similar in appearance to the anatomical alterations of the surviving cholinergic fibers in dementia of the Alzheimer type (AD). Hypertrophic changes also occur in the serotonergic system. The neuropeptide-Y- and somatostatin-containing cortical systems respond with an increment of their axonal densities, in contrast to the decline of these peptides in AD. Although transsynaptic effects are mediated by long-term cholinergic lesions, they do not support the hypothesis that the cholinergic deficiency is a primary event in the pathophysiology of AD.
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PMID:The basal forebrain cholinergic system: efferent and afferent connectivity and long-term effects of lesions. 168 Feb 68


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