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

Excitatory amino acids have been implicated in ischemic neuronal injury. To test this hypothesis in neonatal hypoxia-ischemia, lesions of the cortex and striatum were induced in 7-day-old rats by unilaterally ligating their carotid arteries and subjecting them to hypoxic conditions for 2 hours. Brains examined 1 week later demonstrated, within the regions of ischemic damage, a striking preservation of neurons that stained histochemically for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity. Concentrations of the neuropeptides somatostatin and neuropeptide Y, which colocalize in neurons containing NADPH-d, were unaffected in the areas of ischemic damage. The same pattern of injury with sparing of NADPH-d-reactive neurons was reproduced by focal microinfusion of the excitotoxin quinolinic acid, an endogenous N-methyl-d-aspartate (NMDA) agonist, into the striatum. These results support the hypothesis that neonatal hypoxic-ischemic injury is mediated through excitatory transmitters acting at the NMDA receptor and that the NADPH-d-reactive neurons in the neonate are resistant to excitotoxic damage. This pattern of cell vulnerability is unique to the developing striatum and may relate to the distinct pathological appearance of the basal ganglia that follows neonatal asphyxia.
 ...
PMID:Selective sparing of NADPH-diaphorase neurons in neonatal hypoxia-ischemia. 290 92

A new modification of the nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase reaction was used to study the distribution of a specific subset of neurons in rat striatum. These neurons are known to also contain somatostatin-like immunoreactivity (SLI). We have previously found a heterogeneous distribution of SLI in rat striatum. In the present study, we found NADPH-diaphorase neurons to be evenly distributed throughout the striatum and nucleus accumbens. There was no increase in the number of NADPH-diaphorase neurons in ventromedial striatum or nucleus accumbens where concentrations of SLI are highest. This suggests that there may be somatostatin afferents to ventromedial striatum and nucleus accumbens. In addition, the NADPH-diaphorase reaction was stable for up to 24 h in an animal model stimulating human autopsy conditions.
 ...
PMID:Topography of nicotinamide adenine dinucleotide phosphate-diaphorase staining neurons in rat striatum. 293 30

We have previously found that a biochemically distinct subset of neurons, containing nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), is selectively resistant to the degenerative process that affects the striatum in Huntington's disease (HD). We report the morphologic and histochemical characteristics of these striatal neurons and their distribution with respect to the histochemical compartments as defined by acetylcholinesterase (AChE) activity. Sections of striatum were stained histochemically for NADPH-d and AChE and immunocytochemically for somatostatin and neuropeptide Y-like immunoreactivity. The diaphorase end-product was contained within medium-sized neurons which corresponded morphologically to a category of aspiny interneurons. Combined techniques showed that NADPH-d, somatostatin, and neuropeptide Y coexisted within the same neurons in controls and patients with HD. The density of these neurons was greater in the ventral putamen and the nucleus accumbens than in the remainder of the striatum. The distinctive AChE pattern of high and low enzyme activity was altered in HD. The AChE-rich matrix zone was markedly reduced in size, while the total area of zones of low enzyme activity was not different from that found in control striatum. The relation between these AChE chemical compartments and the distribution of preserved diaphorase neurons remained intact; NADPH-d neurons were predominantly observed in the matrix zone.
 ...
PMID:Morphologic and histochemical characteristics of a spared subset of striatal neurons in Huntington's disease. 294 77

A combination of immunocytochemical and enzyme histochemical methods have been used to study those neurons which survive lesions of the rat striatum, produced by low doses of the excitotoxin quinolinic acid. Nissl-stained sections revealed that following injection of this toxin many large neurons remained within areas of extensive cell loss. These large cells were found to express both the enzyme acetylcholinesterase and choline acetyltransferase-like immunoreactivity. The surviving cells did not contain the enzyme reduced nicotinamide adenine dinucleotide phosphate or the peptides, somatostatin and neuropeptide Y. This pattern of selective cell sparing was also found following lesions induced by low doses of the toxins ibotenic acid and kainic acid. The survival of large neurons indicates that the excitotoxin-lesioned rat striatum shares common features with the pattern of cell loss found in the caudate-putamen in Huntington's disease. The major difference between these two examples of striatal nerve cell degeneration is, however, the selective preservation of somatostatin/neuropeptide Y/nicotinamide adenine dinucleotide phosphate-diaphorase-containing neurons found in Huntington's disease but not observed following quinolinic acid lesions.
 ...
PMID:Sparing of cholinergic neurons following quinolinic acid lesions of the rat striatum. 297 92

Contracting muscle cells release K ions into their surrounding interstitial fluid, and some of these ions, in turn, enter venous plasma. Thereby, intense or exhaustive exercise may result in hyperkalemia and potentially dangerous cardiotoxicity. Training not only reduces hyperkalemia produced by exercise but in addition, highly conditioned, long-distance runners may show resting hypokalemia that is not caused by K deficiency. To examine the factors underlying these changes, dogs were studied before and after 6 wk of training induced by running on the treadmill. Resting serum [K] fell from 4.2 +/- 0.2 to 3.9 +/- 0.3 meq/liter (P less than 0.001), muscle intracellular [K] rose from 139 +/- 7 to 148 +/- 14 meq/liter (P less than 0.001), and directly measured muscle cell membrane potential (Em) in vivo rose from -92 +/- 5 to -103 +/- 5 mV (P less than 0.001). Before training, resting Em of isolated intercostal muscle in vitro was -87 +/- 5 mV, and after incubation in 10(-4) M ouabain, Em fell to -78 +/- 5 mV. After training, resting Em of intercostal muscle rose to -95 +/- 4, but fell to -62 +/- 4 mV during incubation in 10(-4) M ouabain. The measured value for the Em was not completely explained by the increased ratio of intracellular to extracellular [K] or by the potassium diffusion potential. Skeletal muscle sarcolemmal Na,K-ATPase activity (microM inorganic phosphate mg-1 protein h-1) increased from 0.189 +/- 0.028 to 0.500 +/- 0.076 (P less than 0.05) after training, whereas activities of Mg2+ -dependent ATPase and 5'nucleotidase did not change. In untrained dogs, exercise to the point of exhaustion elevated serum [K] from 4.4 +/- 0.5 to 6.0 +/- 1.0 meq/liter (P less than 0.05). In trained dogs, exhaustive exercise was associated with elevation of serum [K] from 3.8 +/- 0.3 to 4.2 +/- 0.4 (NS). The different response of serum [K] to exercise after training was not explainable by blood pH. Basal insulin levels rose from 7.0 +/- 0.7 microU/ml in the untrained dogs to 9.9 +/- 1.0 microU/ml (P less than 0.05) after training. Although insulin might have played a role in the acquired electrical hyperpolarization, the reduced exercise-produced hyperkalemia after training was not reversed by blockade of insulin release with somatostatin. Although the fundamental mechanisms underlying the cellular hyperpolarization were not resolved, our observations suggest that increased Na-K exchange across the sarcolemmal membrane, the increase of Na,K-ATPase activity and possibly increased electrogenicity of the sodium pump may all play a role in the changes induced by training.
 ...
PMID:Muscle cell electrical hyperpolarization and reduced exercise hyperkalemia in physically conditioned dogs. 298 19

The effects of pertussis toxin on the responses of rat pituitary-tumour (GH) cells to thyrotropin-releasing hormone (thyroliberin, TRH) were examined. Treatment of cells with pertussis toxin did not alter the affinity or concentration of TRH receptors, or the sensitivity of the TRH receptor to inhibition by guanine nucleotides. TRH caused an increase in low-Km GTPase activity in membrane-containing fractions from both control and pertussis-toxin-treated cells. TRH stimulation of inositol phosphate formation was insensitive to pertussis toxin. TRH caused a biphasic increase in the concentrations of cytosolic free Ca2+ as monitored by intracellularly trapped Quin 2, and this increase was the same in control and toxin-treated cultures. The toxin did not alter the increase in prolactin and growth-hormone (somatotropin) release stimulated by TRH or shift the TRH dose-response curve, and it did not affect the TRH-induced rise in prolactin synthesis measured over 24 h. However, pertussis toxin did block the ability of somatostatin and muscarinic agonists to inhibit prolactin and growth-hormone secretion stimulated by vasoactive intestinal peptide when analysed under the same conditions as those in which the TRH system was unaffected. These data indicate that the guanine nucleotide effects on TRH binding and activity are not mediated by Ni, but possibly by another member of the family of guanine-nucleotide-dependent regulatory proteins.
 ...
PMID:Thyroliberin action in pituitary cells is not inhibited by pertussis toxin. 302 9

Human platelet membrane proteins were phosphorylated by exogenous, partially purified Ca2+-activated phospholipid-dependent protein kinase (protein kinase C). The phosphorylation of one of the major substrates for protein kinase C (Mr = 41 000) was specifically suppressed by the beta subunit of the inhibitory guanine-nucleotide-binding regulatory component (Gi, Ni) of adenylate cyclase. The free alpha subunit of Gi (Mr = 41 000) also served as an excellent substrate for the kinase (greater than 0.5 mol phosphate incorporated per mol of subunit), but the Gi oligomer (alpha X beta X gamma) did not. Treatment of cyc- S49 lymphoma cells, which are deficient in Gs/Ns (the stimulatory component) but contain functional Gi/Ni, with the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate, a potent activator of protein kinase C, did not alter stimulation of adenylate cyclase catalytic activity by forskolin, whereas the Gi/Ni-mediated inhibition of the cyclase by the hormone, somatostatin, was impaired in these membranes. The results suggest that the alpha subunit of the inhibitory guanine-nucleotide-binding regulatory component of adenylate cyclase may be a physiological substrate for protein kinase C and that the function of the component in transducing inhibitory hormonal signals to adenylate cyclase is altered by its phosphorylation.
 ...
PMID:Protein kinase C phosphorylates the inhibitory guanine-nucleotide-binding regulatory component and apparently suppresses its function in hormonal inhibition of adenylate cyclase. 316 29

This study was undertaken to elucidate the mechanism(s) involved in glucocorticoid-induced insulin antagonism. Male Sprague-Dawley rats (200 to 210 g) were injected with 1 mg/kg dexamethasone-phosphate (Dex) or the vehicle every other day for 10 days. Two days after the last injection, fasted anesthetized animals were infused (per kg body weight per min) with 8 mg glucose, 5 mU porcine insulin and 1.4 micrograms somatostatin with blood sampling before, and at 10 min intervals between 90 and 130 min after the pancreatic suppression test was begun. At the end of the test, abdominal muscle was quickly freeze-clamped and the substrate and products of the rate-determining reactions of glycolysis and glycogenesis were measured. Dex-treated rats had higher basal (0 min) and steady-state levels (90-130 min) of both glucose and insulin signifying insulin antagonism. The pattern of muscle tissue metabolites revealed no free intracellular glucose in either group and concentrations of all other metabolites in the Dex-treated rats were less than those in the control animals (except for a small increase in glycogen). These results suggest a site of insulin antagonism between (and including) insulin binding and glucose transport. Further studies in the Dex-treated rats revealed normal: a) insulin binding to freshly isolated hepatocytes; b) basal and insulin-stimulated xylose transport in soleus muscle; c) basal and insulin-stimulated glucose uptake in hemidiaphragms. These normal in-vitro results suggested that a circulating factor may be responsible. Repeat pancreatic suppression tests in the Dex-treated rats revealed blunted suppression of serum FFA concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Possible role for the glucose-fatty acid cycle in dexamethasone-induced insulin antagonism in rats. 330 80

The ultrastructure of reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase-positive neurons in cat cerebral cortex, amygdala and caudate nucleus was investigated by electron microscopy using a modified method applicable to aldehyde-fixed tissues. These NADPH diaphorase-positive neurons were morphologically similar to neurons immunohistochemically positive for somatostatin. They had large amounts of electron-dense formazan reaction products scattered through the whole cytoplasm but not in the mitochondria or nucleus. Similar electron-dense reaction products were visible in the dendrites of these neurons. The results indicate that NADPH diaphorase histochemistry is a useful method for the ultrastructural examination of particular groups of neurons.
 ...
PMID:Ultrastructure of reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase-positive neurons in the cat cerebral cortex, amygdala and caudate nucleus. 340 36

Four weeks after 70% resection of the pancreas in the rat, serum levels of calcium, inorganic phosphate, magnesium, parathyroid hormone and calcitonin, as well as femur dry weight, volume, mean specific density, and mineral content were investigated. The urinary excretion of cAMP and hydroxyproline was measured. Additionally, residual pancreatic amylase content, fasting blood levels of insulin, glucagon, somatostatin and glucose were determined, and the mineral balance (calcium, phosphate) studied. Residual pancreatic amylase content was decreased to 22% of control values, fasting serum glucose and plasma glucagon were increased. Fecal excretion of calcium and phosphate was unchanged, but their balance was increased. Serum calcitonin and the mean specific density of femurs were decreased. All the other variables were unchanged. We conclude that in the rat, 70% pancreatic resection 1) probably does not have any harmful effects on calcium metabolism and bone mineralization in the short term postoperatively, 2) provokes mild hyperglucagonemia, the molecular nature and the origin of which need further elucidation.
 ...
PMID:Influence of 70 percent pancreatic resection on serum and bone calcium in the rat--a preliminary report. 342 61


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>