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)

Effects of intraventricular injection of sheep anti-somatostatin gamma-globulin (anti-SSG) on strychnine-induced seizures, strychnine LD50, and pentobarbital LD50 were examined in male rats under light ether anesthesia. Ten microliters of anti-SSG given 2 h earlier significantly decreased the duration of strychnine-induced seizures as compared with that in the control rats pretreated with normal sheep gamma-globulin (NSG). This effect of anti-SSG seemed to be specific, as there was no difference in seizure duration between sheep anti-LHRH gamma-globulin (anti-LHRHG)- and NSG-pretreated rats. Survival rates in anti-SSG-pretreated rats after injection of strychnine and pentobarbital were significantly larger (P less than 0.01 and P less than 0.05, respectively) than those in the control rats receiving NSG. The administration of anti-SSG resulted in 26.7% and 22.9% increases in the LD50 of strychnine and pentobarbital, respectively. These results indicate that endogenous somatostatin in the cerebrospinal fluids and/or the periventricular tissue nodulates the response of the central nervous system to strychnine and pentobarbital in rats.
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PMID:Effect of intraventricular administration of anti-somatostatin gamma-globulin on the lethal dose-50 of strychnine and pentobarbital in rats. 8 54

Major phases of the physiology of food intake regulation remain hypothetical. There is a central regulatory mechanism for hunger and satiety, but the signals and messages that activate the brain centers remain conjectural. The alimentary tract regulation, the regulation by osmoreceptors, the thermostatic, the glucostatic, the lipostatic, the amino acid, and the hormonal food intake regulation theories leave many questions unanswered. Low molecular weight peptides appear to have an important effect on brain functions. Hypothalamic peptides such as thyrotropin-releasing hormone, gonadotropin-releasing hormone, and somatostatin have been assigned new roles in various brain functions. The hypothalamus and probably other parts of the brain produce also anorexigenic peptides. Anorexia is a common manifestation of cancer. It is proposed that peptides, oligonucleotides, and other small metabolites produced by the cancer and by the tumor-bearing host are responsible for the genesis of the anorexia. They produce the anorexia through a peripheral effect on neuroendocrine cells and neuroreceptors and through a direct effect on hypothalamic and other central nervous system sensor and responder cells.
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PMID:Anorexia-producing intermediary metabolites. 17 68

Neuronal compartments can be separated by differential spinning or by centrifugation on continuous or discontinuous density gradients. Application of these fractionation techniques to brain structures containing neurosecretory neurons shows that LHRH, somatostatin and a non dopamine prolactin inhibiting factor (PIF) are exclusively recovered from synaptosomal fractions. This indicates that biologically and/or immunologically reactive forms of these hormones are almost entirely concentrated in nerve-endings of neurosecretory neurons. In contrast, other neuropeptides - posterior pituitary hormone, but also TRH, a vasoactive intestinal peptide (VIP), substance P or endorphins - are also found in supernatant fractions. The existence of multiple molecular forms of neuropeptides is likely to explain these differences. Current theories postulate that they are synthetized on ribosomes as precursor forms. Their active structure is only achieved by enzymatic splitting of the pre- or the prohormone within nerve endings. This mode of synthesis is probably common to all neuropeptides, although it has only been well substantiated in a few cases, in particular for the hormones of the posterior pituitary. Thus, the lack of immunologically detectable LHRH or SRIF outside the synaptosomal fraction may reflect masking of the active immunological sites by inert peptide chains associated with prohormonal forms. Fractionation methods can also be applied to physiological or pharmacological experiments. In particular, they permit to characterize, on presynaptic membranes of neurosecretory neurons, specific receptors to neurotransmitters involved in the control of neurohormone secretion. Interaction of dopamine and acetylcholine with LHRH and CRF release are presented as examples of such applications.
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PMID:[Subcellular distribution of hypothalamic neurohormones and in vitro stimulation of their release]. 20 91

In a patient with hypogonadotropic hypogonadism treated with luteinizing hormone releasing hormone (LHRH), secondary failure of both subjective and hormone responses occurred at the time of appearance of binding of 125I-LHRH by the patient's serum. On electrophoresis of the patient's serum with 125I-LHRH, label was found only in the gamma globulin region. 125I-LHRH added to the patient's serum was precipitated by sheep anti-human immunoglobulin G (anti-IgG) but not by sheep anti-human immunoglobulin M (anti-IgM). Competitive displacement of 125I-LHRH by unlabeled LHRH was demonstrated while TSH releasing hormone (TRH), somatostatin and rat pituitary hormones showed no displacement when tested at concentrations 5 X 10(6) greater than that of LHRH. Studies using 14 different analogs of LHRH revealed that those with changes at the carboxy terminus showed binding similar to LHRH. It is concluded that IgG antibody to LHRH was produced in this patient by repeated administration of synthetic LHRH. It is further concluded that antibody specificity is directed toward the N terminus region.
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PMID:Characteristics of antibody produced during chronic treatment with LHRH. 32 67

Somatostatin and LHRH were detected by radioimmunoassay in the synaptosome fraction obtained by homogenization and differential centrifugation of the rat median eminence. Both somatostatin and LHRH were demonstrated by electron microscopic immunocytochemistry in secretory granules within synaptosomes.
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PMID:Immunoreactive somatostatin and luteinizing hormone releasing hormone in median eminence synaptosomes of the rat: detection by immunohistochemistry and quantification by radioimmunoassay. 33 89

Since both TRH and somatostatin (SRIF) are localized to the ventromedial hypothalamic nucleus, a region known to be involved in control of food intake, the possibility that these peptides might alter food intake was evaluated. The peptides were dissolved in 0.9% NaCl and injected into the 3d ventricle in a volume of 2 micron1 in animals bearing 3d ventricular cannulae. Food and water had been removed from the cages the night before and the intake was measured at 1 and 6 h after injection. Control injections of 0.15M NaCl or glutathione (3 nmoles) had no effect on food or water intake. At a dose of 3 nmoles, LHRH, SRIF, and TRH suppressed water intake alh. Lowering the dose of LHRH and SRIF to 0.6 nmoles led to loss of this inhibition but the suppressive effect of TRH, which was more pronounced at the higher dose than that of the other two peptides, persisted. Lowering the dose of TRH to 0.3 nmoles led to loss of the inhibitory effect. The dose of 3 nmoles of LHRH did not suppress food intake but this dose of both SRIF and TRH had a significant suppressive effect on food intake at 1 h. There was no suppressive action of a lower dose of 0.6 nmoles of SRIF, but TRH was still effective to suppress food intake at this dose. A dose of 0.3 nmoles of TRH had no effect on food intake. It is suggested that TRH, and possibly SRIF may play a physiological role in control of food intake, perhaps by altering the neural activity within the ventromedial nucleus.
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PMID:Suppression of feeding and drinking activity in rats following intraventricular injection of thyrotropin releasing hormone (TRH). 40 33

In the hypothalamus of the adult domestic mallard, small to medium-sized perikarya are stained specifically with rabbit antiserum against cyclic somatostatin (PAP technique of Sternberger). The somatostatin-immunoreactive material is located in neurons different from those containing immunoreactive LHRH, vasotocin or mesotocin. Somatostatin-containing perikarya are observed 1) in a chain-like arrangement extending from the area of the median division of the supraoptic nucleus to the caudal end of the paraventricular nucleus; 2) as single cells in the preoptic region; and 3) as a conspicuous formation in the optic tract division of the supraoptic nucleus. In the rostral portion of the median eminence, somatostatin-immunoreactive axons penetrate into the external zone. Fine accessory fiber bundles project to the neural lobe.
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PMID:Immunocytochemical demonstration of somatostatin-containing neurons in the hypothalamus of the domestic mallard. 73 8

The objective was to determine the distribution of growth hormone-release-inhibiting hormone (somatostatin) in the rat brain using the peroxidase-antiperoxidase immunocytochemical method with antisera prepared against unconjugated, synthetic somatostatin. Somatostatin occurred in low quantity in the organum vasculosum of the lamina terminalis. It was present throughout the full length of the median eminence and occupied the entire width between the tuberoinfundibular sulci. Most somatostatin was located in the dorsal portion of the external lamina, and the amount varied according to the mediolateral position. The bodies labeled for somatostatin were most often granules; occasionally they appeared as clusters of granules that seemed to be membrane-enclosed. Some of these bodies appeared to be portions of axons. Many of the larger bodies were arranged alongside tanycytes, but no label was distributed generally in tanycyte cytoplasm. Somatostatin was highly concentrated in the proximal one-quarter of the infundibular stem and appeared in lower concentration throughout the distal portion of the stem. It was absent from the pars nervosa and pars intermedia of the pituitary gland. The distribution of somatostatin in the median eminence differed considerably from that of gonadotropin-releasing hormone. Somatostatin was identified in the ventromedial and/or dorsomedial hypothalamic nuclei of only two animals. Here it was probably located in axons that terminated on neuronal cell bodies but also may have been present in a restricted portion of the perikaryonal cytoplasm.
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PMID:Distribution of growth hormone-release-inhibiting hormone (somatostatin) in the rat brain as observed with immunocytochemistry. 79 45

The reaction products of plasma enzyme degradation of TRH were identified by thin layer chromatography. The enzyme in normal rat plasma yields proline and pGlu-His as major reaction products. High concentrations of proline decrease peptide cleavage, resulting in greater amounts of acid TRH. The apparent Km of the enzyme is 4.1 X 10(-6) M. LHRH and neurotensin are competitive inhibitors with Ki of 5 X 10(-6) M and 1.5 X 10(-5) M, respectively. Somatostatin, MIF, oxytocin, arg-vasopressin, arg-vasotocin, neurophysin II and glucagon do not compete; and pGlu-His-Pro-OH, Glu-His-Pro-OH, pGlu-His, His-Pro-NH2, and Pro-NH2 do not affect enzyme activity. These data suggest that the substrated requires pGlu and a terminal or internal amide to complex with the enzyme. The enzyme is markedly inhibited by Cu++, Bal, benzamadine, p-(chloromercuri)-benzoic acid, moderately affected by EDTA and puromycin, and unaffected by mercaptoethanol. TSH does not affect enzyme activity while LH inhibits it moderately at high concentrations (300-600 pg/ml).
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PMID:Characteristics of the plasma TRH-degrading enzyme. 81 19

Pregnant guinea pigs were given a daily oral dose of 0, 5.5, or 11 mg lead (as lead acetate) per kg body weight during days 22-52 or 22-62 of gestation. Maternal serum progesterone levels were measured at the end of treatment, as well as hypothalamic levels of gonadotropin-releasing hormone (GnRH) and somatostatin (SRIF) in both the mothers and fetuses. Lead-treated dams had lower serum concentrations of progesterone at the end of treatment than did vehicle-treated animals. This effect was statistically significant for the higher Pb dose only. Hypothalamic levels of GnRH and SRIF were reduced in a dose-dependent manner by lead treatment in both dams and fetuses. The reduction of SRIF levels in 52-day-old fetuses was particularly severe (92%) in the 11 mg group. However, neither litter size nor body and organ weights, including placental weight, of the dams and fetuses was significantly affected. The relevance of these hormonal decreases is unknown, but could include decreased reproductive capacity in both the dams and fetuses that does not become apparent until later in the life-cycle.
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PMID:Effects of low-level lead exposure on hypothalamic hormones and serum progesterone levels in pregnant guinea pigs. 134 82


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