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)

Brains of 49 patients who had died with Alzheimer's disease and 54 controls were examined. The Alzheimer group exhibited noticeably reduced activity of the cholinergic marker enzyme choline acetyltransferase in the cerebral cortex, but cortical concentrations of noradrenaline, gamma-aminobutyric acid, and somatostatin were also significantly reduced. Analysis of the results according to age at death showed that the older patients, dying in their 9th and 10th decades, had a relatively pure cholinergic deficit confined to temporal lobe and hippocampus, together with a reduced concentration of somatostatin confined to temporal cortex. By contrast, the younger patients, dying in their 7th and 8th decades, had a widespread and severe cholinergic deficit together with the abnormalities of noradrenaline, gamma-aminobutyric acid, and somatostatin, and the younger patients accounted for most of the abnormalities in these systems observed in the overall group. Comparison of the young subjects with Alzheimer's disease with the older controls did not support the concept of Alzheimer's disease representing an acceleration of the aging process. These results suggest that Alzheimer's disease in people aged under 80 may represent a distinct form of presenile dementia which differs in important respects from the dementia of old age.
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PMID:Neurochemical characteristics of early and late onset types of Alzheimer's disease. 614 50

The coexistence of gamma-aminobutyric acid (GABA), glutamate decarboxylase (GAD), and cholecystokinin (CCK)- or somatostatin-immunoreactive material in the same neurons was studied in the hippocampus and visual cortex of the cat. One-micrometer-thick serial sections of the same neuron were reacted to reveal different antigens by the unlabeled antibody enzyme method. All CCK- and somatostatin-immunoreactive neurons in the cortex and all CCK-immunoreactive and the majority of somatostatin-immunoreactive neurons in the hippocampus that could be examined in serial sections were also immunoreactive for GABA. In neurons that were immunoreactive for GAD it was often possible to demonstrate immunoreactivity for one of the peptides as well as for GABA. GABA-immunoreactive neurons, as revealed by an antiserum to GABA, were present in all layers of the cortex and hippocampus, and their shape, size, and distribution were similar to GAD-immunoreactive neurons. All GAD-immunoreactive neurons were also positive for GABA, but the latter staining revealed additional neurons. CCK/GABA- and somatostatin/GABA-immunoreactive neurons were present mainly in layers II and upper III and in layers V and VI in the visual cortex. CCK/GABA-immunoreactive neurons were most frequently present in the strata oriens, pyramidale, and moleculare of the hippocampus and in the polymorph cell layer of the dentate gyrus. Somatostatin/GABA-immunoreactive neurons were localized mainly in the stratum oriens and in the hilus of the fascia dentata. The two peptides could not be found in the same neuron. The majority of neurons that were GABA immunoreactive did not stain for either peptide. The presence of CCK- and somatostatin-immunoreactive material in GABAergic cortical neurons raises the possibility that neuroactive peptides affect GABAergic neurotransmission.
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PMID:Different populations of GABAergic neurons in the visual cortex and hippocampus of cat contain somatostatin- or cholecystokinin-immunoreactive material. 614 75

Neurons in the cat and monkey cerebral cortex were stained immunocytochemically for glutamic acid decarboxylase (GluDCase; L-glutamate 1-carboxy-lyase, EC 4.1.1.15), somatostatin (SRIF), neuropeptide Y (NPY), and cholecystokinin octapeptide (CCK). In all areas of cortex examined (somatic sensory, motor, parietal and visual areas), neurons displaying immunoreactivity for each of these molecules were nonpyramidal cells. Co-localization of GluDCase immunoreactivity with peptide immunoreactivity in the same cells was demonstrated by (i) the antibody elution method, staining the same cells by immunofluorescence, first for a peptide and then for GluDCase; (ii) double staining of the same sections with sheep anti-GluDCase and rabbit anti-peptide antisera, the bound antibodies being localized by rhodamine-conjugated donkey anti-sheep and fluorescein-conjugated swine anti-rabbit secondary antisera. With both procedures, cell bodies immunoreactive for GluDCase and for each of the peptides were found in all areas of cortex examined. With double labeling on single sections, it was found that all CCK-, SRIF-, and NPY-immunoreactive cells in cat cortex and 90%-95% in monkey cortex are also GluDCase positive. Many more cells, however, are immunoreactive for GluDCase alone. GluDCase was co-localized with CCK, SRIF, or NPY not only in cell somata, but also in small punctate structures, which are likely to be axon terminals. From the data gained in previous electron microscopic studies, we postulate that neurons displaying GluDCase- and CCK-like immunoreactivity are a class separate from those displaying GluDCase- and SRIF-like immunoreactivity. NPY, however, is co-localized with SRIF immunoreactivity. These results imply that classes of cortical interneuron contain a conventional neurotransmitter (gamma-aminobutyric acid) and a neuromodulator (one of the peptides).
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PMID:Neuropeptide-containing neurons of the cerebral cortex are also GABAergic. 614 47

The effect of altering gamma-aminobutyric acid (GABA) activity on growth hormone (GH) secretion of freely moving chronically cannulated male rats was studied. Systemic injection of the GABA agonist muscimol (2 mg/kg i.v.) inhibited the anticipated secretory episode. Increasing brain GABA levels by gamma-acetylenic-GABA (50 mg/kg i.v.) also inhibited the expected GH rise. When injected before the expected secretory episode, the GABA receptor antagonist bicuculline methiodide (2 mg/kg i.v.) triggered an early secretory peak. GABA and muscimol failed to change GH secretion by cultured anterior pituitary cells. When the somatostatin input to the stalk-median eminence region was interrupted by an anterolateral cut around the medial basal hypothalamus, the GH level was steadily increased and muscimol injections caused a prompt decrease of plasma GH levels. These results are consistent with the hypothesis that GABAergic tonic inhibition participates in the control of GH secretion and that GABA inhibits spontaneous GH release by inhibiting the secretion of a GH-releasing factor.
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PMID:Site of gamma-aminobutyric acid (GABA)-mediated inhibition of growth hormone secretion in the rat. 615 Nov 30

The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulus-evoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic gamma-aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.
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PMID:Regulation of neuropeptide release. 615 55

Homogenates of rat dorsal or ventral spinal cord were subjected to centrifugation on a continuous density gradient. The gradient was generated according to a new method with the aid of a microprocessor-controlled HPLC pump. The distribution of substance P-like immunoreactivity (SPI) and somatostatin-like immunoreactivity (SRIFI) across the gradient showed two peaks. The SPI peak seen at lower density was found only in dorsal spinal cord tissue. No peak of SPI was seen at this position in homogenates prepared from the spinal cords of capsaicin-pretreated rats. The second peak of SPI, found at a higher density, was accompanied by peaks in the levels of endogenous 5-hydroxytryptamine (5-HT), [14C]glycine, and [3H]norepinephrine uptake. This peak was seen at the same density in the dorsal and the ventral spinal cord. Tissue derived from capsaicin-pretreated rats exhibited one peak of SPI, accompanied by a maximum of [14C]glycine uptake. The uptake of [3H]gamma-aminobutyric acid ( [3H]GABA) was found to have a maximum at a somewhat lower density than that of [14C]glycine. It is concluded that the peak of SPI found at lower density in the dorsal spinal cord is associated with nerve endings belonging to capsaicin-sensitive primary afferents, while other endings, including those also containing 5-HT, are probably associated with the peak of SPI found at higher density.
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PMID:Distribution of spinal cord nerve endings containing various neurotransmitters on a continuous density gradient. 619 68

Classical and 'new' neurotransmitters appear in a certain sequence which seem to be similar in rat and man. Serotonin is one of the earliest transmitter which can be detected at a gestational age of 8 days in the rat. A couple of days later noradrenergic and dopaminergic fluorescence can be detected. The development of neurons with gamma-aminobutyric acid and acetylcholine lags behind the monoaminergic neurons. Endorphin is found in high concentrations at an early stage, while substance P, enkephalin and hypothalamic peptides like thyrotropin releasing hormone appear later in development. Inhibitory transmitters like GABA, somatostatin and endorphins reach their maximal concentrations in CNS during infancy, which might have some functional implications. The classical neurotransmitter noradrenaline might have certain unique functions during fetal and perinatal life. It seems to be important for the development of the cerebral cortex. It is released in high quantities at birth and might be of importance for the neonatal adaptation such as inducing arousal. The function of all the newly detected neuropeptides is far from elucidated even in adult life. Some of them seem to have important functions during perinatal life, while perhaps they occur in the adult organism only as evolutionary residues. For example endorphins seem to affect respiratory control in the fetus and the newborn in ways not seen in the adult. So called neuromodulators, for example adenosine, might also have particular functions during perinatal life.
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PMID:Classical and 'new' neurotransmitters during development--some examples from control of respiration. 620 44

beta-Endorphin, Met-enkephalin, substance P, and somatostatin concentrations were evaluated in the hypothalami of rats treated either acutely or chronically (15 days) with sodium valproate, diphenylhydantoin, phenobarbital, or ethosuximide. All of these drugs, with the exception of ethosuximide, induced significant decreases in beta-endorphin concentrations after acute treatment, while only sodium valproate induced a decrease after chronic treatment. The acute and chronic effects of sodium valproate were also produced by aminooxyacetic acid, an inhibitor of gamma-aminobutyric acid (GABA) transaminase, while another GABA transaminase inhibitor, ethanolamine-O-sulphate, and THIP, a GABA receptor agonist, were effective after acute administration. Metenkephalin, substance P, and somatostatin concentrations were never affected by the drugs used. The present results, indicating that antiepileptic agents specifically decrease beta-endorphin concentrations, seem to correlate well with the capacity of these agents to blunt the epileptic activity of the peptides tested. Moreover, our data suggest that GABA may be involved in the anticonvulsant-induced reduction of beta-endorphin concentrations.
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PMID:Antiepileptic agents affect hypothalamic beta-endorphin concentrations. 620 24

Effects of neuroactive peptides on the release of labeled 5-hydroxytryptamine (5-HT) from preloaded rat spinal cord slices were investigated. The 5-HT release was significantly stimulated by somatostatin (10-50 microM) and substance P (10-50 microM), but not by neurotensin (50 microM), beta-endorphin (30 microM) and methionine-enkephalin (met-enk) (100 microM). Somatostatin-stimulated 5-HT release was markedly inhibited by gamma-aminobutyric acid (GABA) (30 microM), but not by baclofen (30 microM) and met-enk (100 microM). Substance P-stimulated 5-HT release was strongly inhibited by GABA (30 microM) and baclofen (30 microM), but not by met-enk (100 microM). High concentrations (20 mM) of potassium also stimulated 5-HT release. The high potassium-stimulated 5-HT release was not affected by GABA (30 microM) and met-enk (100 microM). These results suggested further evidence on the important role of somatostatin and substance P as modulators of serotonergic neurones.
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PMID:Effect of neuroactive peptides on labeled 5-hydroxytryptamine release from rat spinal slices in vitro. 620 42

Phorbol diester tumor promoters are potent cocarcinogens which also possess activity in a variety of biological assays. We have examined the effect of phorbol diesters on secretion of somatostatin-like immunoactivity (SRIF-LI) by dispersed cells of fetal rat brain maintained in long term culture. Phorbol-12-myristate-13-acetate (PMA) and phorbol 12, 13-dibutyrate stimulate SRIF-LI secretion in a dose-dependent fashion. 4-O-Methyl-PMA is approximately 100 times less potent than phorbol 12, 13-dibutyrate. 4-beta-Phorbol was inactive. Treatment with a nonphorbol irritant, teleocidin, also was associated with significantly augmented release of SRIF-LI. Significant stimulation is seen within 7.5 min of treatment and response is linear over 1 h. Administration of phorbol diesters in low calcium buffer (0.1 mM) with or without cobalt or pretreatment with verapamil are associated with significantly diminished secretion. Substitution for sodium ion by choline or pretreatment with tetrodotoxin (10(-7) M) also inhibits response to PMA. gamma-Aminobutyric acid (50 microM) or the gamma-aminobutyric acid agonist muscimol (5 microM) decrease response to PMA as does sodium pentobarbital (IC50 approximately 30 microM). Phenobarbital is less potent as an inhibitor; significant suppression is not seen until approximately 300 microM. The data are consistent with an action for phorbol diesters mediated at least in part by voltage dependent sodium channels and calcium influx into excitable cells. Inhibition by hyperpolarizing agents is compatible with this mechanism. Phorbol diesters may thus mimic endogenous modulator substances active at the nerve cell membrane.
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PMID:Phorbol diesters stimulate somatostatin secretion from cultured brain cells. 640 21


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