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)

The gamma-Aminobutyric acid-A (GABAA) antagonist picrotoxin and bicuculline were administered to male rats to determine their effects on somatostatin (SRIF) release, measured in unanesthetized animals stereotaxically implanted with push-pull cannula in the median eminence (ME). I.p. injection (3 mg/kg) of picrotoxin (n = 5) or bicuculline (n = 6) significantly increased (35.4 +/- 10.8 vs 13.7 +/- 4.3 pg/15 min; P less than 0.03 and 38 +/- 3.5 vs 14 +/- 1.8 pg/15 min; P less than 0.001, respectively) SRIF release from the ME compared to baseline levels measured in the same animals. In contrast, with local perfusion of picrotoxin, (10(-4) to 10(-6) M) SRIF release from the ME was not affected. These data suggest a physiological endogenous inhibitory tone of GABA on SRIF release.
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PMID:Peripheral administration of picrotoxin and bicuculline stimulates in vivo somatostatin release from rat median eminence. 197 Aug 59

Somatostatin (SOM) synthesis and release were studied with radioimmunoassay and immunocytochemical techniques in rat fetal hippocampal neurons maintained in monolayer tissue culture. SOM immunoreactivity increased from undetectable to over 4,000 pg/ml in media and over 2,500 pg/culture in neurons by 3 to 5 weeks. After 3 weeks, approximately 11% of the neurons stained for SOM. Gamma-aminobutyric (GABA) immunoreactivity was present in hippocampal neurons from 1 day to 5 weeks with 40-50% of the neurons staining for GABA by 5 weeks in vitro. Costaining neurons for SOM and GABA revealed that 63% which were positive for SOM also stained for GABA.
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PMID:Expression of somatostatin and GABA immunoreactivity in cultures of rat hippocampus. 197 38

This study utilized the technique of in situ hybridization histochemistry to identify cells expressing neurotransmitter mRNAs in embryonic striatal tissue grafts implanted into the ibotenic acid-lesioned rat neostriatum. Synthetic 32P- or 35S-labelled oligodeoxyribonucleotide probes specific for prosomatostatin, proneuropeptide Y. proenkephalin, prodynorphin and preprotachykinin mRNAs and a 32P-labelled cRNA probe specific for glutamate decarboxylase mRNA were used to study the regional and cellular changes in these mRNA levels in the normal, lesioned and grafted neostriatum. The levels of neuropeptide Y mRNA and somatostatin mRNA were substantially increased in the striatal grafts compared with the intact control striata. The levels of glutamate decarboxylase mRNA in the grafts also appeared to be slightly elevated over those in the control striata. However, the levels of proenkephalin mRNA, prodynorphin mRNA and preprotachykinin mRNA were significantly lower in the grafts. The increased levels of neuropeptide Y mRNA and somatostatin mRNA in the grafts were due both to an increase in the number of labelled cells and to an increase in the cellular levels of each neuropeptide mRNA. In contrast, the cellular levels of proenkephalin mRNA, prodynorphin mRNA and preprotachykinin mRNA in the grafts were comparable, or elevated relative, to those in the intact striata but the density of cells expressing each of these mRNAs was reduced. Since neuropeptide Y and somatostatin are known to be present in medium to large aspiny striatal neurons (interneurons) and enkephalin, dynorphin and tachykinin peptides and GABA are localized in medium spiny striatal projection neurons, the above findings would indicate that there is a divergence in the levels of activity between these two neuronal populations in the striatal grafts. Our data suggest that the levels of gene expression and hence the functional neurotransmitter-synthesizing and releasing activity in the grafted neuron are different from those in the normal mature striatum.
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PMID:Gene expression in striatal grafts--I. Cellular localization of neurotransmitter mRNAs. 197 68

A perfusion system was used to monitor the release of [3H]-GABA from isolated retinas of Xenopus laevis. Measurable release was stimulated by glycine at concentrations as low as 200 microM. Glycine-stimulated release was blocked by strychnine, and was not reduced in "calcium-free" Ringer's solution (0 Ca2+/20 mM Mg2+). Glutamate also stimulated calcium-independent release, using concentrations as low as 100 microM. In contrast, release stimulated by 25 mM potassium was reduced by 80% in calcium-free medium. In most experiments, agonists were applied in six consecutive 4-min pulses separated by 10-min washes with Ringer's solution. Under these conditions, the release stimulated by 0.5 mM glutamate or 25 mM potassium decreased by at least 50% from the first to the second pulse, and then gradually decreased with successive applications. In contrast, the response to 0.5 mM glycine at first increased and then only gradually decreased with successive pulses. These patterns of response to different agonists were similar in calcium-free medium. Somatostatin (-14 or -28) also stimulated release, and this effect was inhibited by AOAA, an inhibitor of GABA degradation. In the presence of AOAA, somatostatin had little effect, except at high concentrations of somatostatin (5 microM), which increased both basal and glycine-stimulated release. In contrast to somatostatin, glycine-stimulated release was much larger in the presence of AOAA. Autoradiography was used to investigate which cell types released [3H]-GABA under our conditions. Autoradiograms showed that horizontal cells and a population of apparent "off" bipolar cells were well-labeled by [3H]-GABA high-affinity uptake. In addition, light labeling was seen over numerous amacrine cells. After application of glycine, glutamate, or potassium, there was a decrease in label density over horizontal cells.
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PMID:Glycine stimulates calcium-independent release of 3H-GABA from isolated retinas of Xenopus laevis. 198 Feb 4

Considering the initial expression of neurotransmitters and neuropeptides immediately after neural induction in amphibian embryos, we previously pointed out that a neuronal cell population emerges from neural plate (NP) and neural fold (NF) expressing very early specific cholinergic, catecholaminergic, GABAergic and peptidergic traits. The purpose of the present work was to investigate the extent to which the neuroblasts that are present in the neurectoderm immediately after gastrulation are committed to give rise to multiple subsets of neurons containing various combinations of neuroactive transmitters rather than to different subpopulations of neurochemically homogeneous neurons. By means of double immunocytochemical localization with a monoclonal TOH-antibody and polyclonal antibodies against GABA or somatostatin, no coexistence of neurotransmitters and neuropeptide was ever found in neuronal subpopulations arising in vitro from NP or NF. The early emergence, under the same conditions, of distinct neuronal subpopulations as a consequence of neural induction strongly suggests that, at the gastrula stage, the neural precursor population most probably does not constitute a homogeneous set of cells.
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PMID:Are neuronal precursor cells committed to coexpress different neuroactive substances in early amphibian neurulae? 198 84

In the mammalian intestine serotonin (5-hydroxytryptamine, 5-HT) is present in high concentrations in the enterochromaffin cells. The release of 5-HT from the intestinal mucosa is regulated by a complex pattern of neuronal and humoral inputs to the enterochromaffin cells. The enterochromaffin cells appear to be endowed with different inhibitory (alpha 2-adrenoceptors, GABAA- and GABAB-receptors, histamine H3-receptors, receptors for vasoactive intestinal polypeptide and somatostatin) as well as stimulatory receptors (beta-adrenoceptors, muscarine and nicotine receptors). The physiological significance of this complex system of receptors is suggested by experiments which demonstrate that the respective intrinsic neurotransmitters (catecholamines, acetylcholine, GABA and vasoactive intestinal polypeptide) released within the gut are involved in the regulation of the release of 5-HT from the enterochromaffin cells.
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PMID:Regulation of serotonin release from the intestinal mucosa. 204 57

NPY-neurons in the striatum and cortex have many morphological and chemical features in common. They are intrinsic, medium sized, aspiny and exhibit ultrastructural characteristics typical of neurons undergoing active synthesis and release of peptides. Most of the NPY-neurons in the two regions coexist with somatostatin, exhibit high levels of NADPH-diaphorase and are resistant to degeneration associated with Huntington's disease. Ultrastructural analysis suggests that the ensheathment by glia and sparsity of asymmetric (putatively excitatory) inputs may render NPY neurons resistant to excitotoxicity. Although NPY-neurons receive few inputs, they make numerous contacts with dendrites within a small region of the neuropil. Among their targets are GABAergic neurons. These NPY-receptive GABA neurons differ from other GABAergic neurons in the vicinity in that they receive few other inputs along their somata and proximal dendrites. This suggests that NPY may exert more influence on a specific class of GABAergic neurons. Many more of the NPY-terminals are found at sites that would be strategic for the simultaneous modulation of the release of transmitters and postsynaptic responses. The differences among NPY-neurons in the striatum versus cerebral cortex are mainly chemical. Most notably, the NPY-neurons are GABAergic in the cortex and not GABAergic in the striatum. In addition, some of the NPY-axons in the ventral portions of striatum and cerebral cortex may be catecholaminergic, and thus originate in brainstem areas recognized to contain NPY and epinephrine or norepinephrine. NPY- and catecholaminergic fibers converge onto same dendrites. Thus, the two transmitters may interact through intercellular biochemical pathways postsynaptically. Finally, the sites where the two fibers directly contact each other may be where NPY stimulates the turnover of dopamine.
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PMID:Neuropeptide Y in cortex and striatum. Ultrastructural distribution and coexistence with classical neurotransmitters and neuropeptides. 217 19

If we consider the chemical messengers in the central nervous system, there are about ten classic transmitters--the catecholamines, biogenic amines and amino acids--as opposed to over 50 different neuropeptides. These include previously well-established circulating hormones such as angiotensin, atrial natriuretic peptide, vasopressin and oxytocin, calcitonin and calcitonin gene related peptide (CGRP), the opioid family of peptides, gastrointestinal peptides, pituitary peptides and their releasing factors, and miscellaneous peptides such as the kinins, bombesin, gallanin, and others; all occur as neuropeptides in the brain. There is evidence supporting a role in central cardiovascular control for angiotensin, opioid peptides, substance P, neuropeptide Y, vasopressin, atrial natriuretic peptide, kinins, corticotropin releasing factor, bombesin, somatostatin, and some other peptides. They have been localized in brain areas known to be important for blood pressure regulation, and specific high-affinity peptide receptors have also been discovered. Upon central administration, these peptides produce cardiovascular effects, partly by interacting with other blood pressure-controlling neuroregulators, e.g. catecholamines and GABA. Central inhibition of brain peptide synthesis or interaction with competitive antagonists at the receptor site results in marked cardiovascular effects. Altered peptide levels and activity of synthesizing enzymes, as well as supersensitivity to the pressor action of some brain peptides, have been described in experimental models of hypertension. We are using angiotensin as a model peptide to study the peptidergic control of cardiovascular function.
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PMID:Peptidergic control of cardiovascular function: the angiotensin paradigm. 219 11

The arcuate nucleus surrounds the ventral part of the third ventricle and contains densely packed small neurons with 1-3 dendrites. At least fifteen transmitters and neuropeptides have been found in perikarya of arcuate neurons. Each transmitter and neuropeptide have a characteristic distribution. In many cases distributions overlap (for example, dopamine and somatostatin, dopamine and neurotensin, neuropeptide Y and somatostatin) and alpha-MSH and beta-endorphin seem to have identical distributions but there are also distinctive neuronal populations containing only one of the described transmitters or neuropeptides (neuropeptide Y and alpha-MSH). Studies show extensive colocalization of dopamine and neurotensin and sparse colocalization of dopamine and GABA, neuropeptide Y and FMRF-NH2 and neuropeptide Y and somatostatin. Colocalization does not seem to be the rule in the arcuate, however, it is possible that colocalization may vary with the physiological state or sex of the animal. It also should be noted that our techniques may not be sensitive enough. To study efferent projections as a possible organizing principle within the arcuate, retrograde fluorescent tracing was combined with transmitter and neuropeptide immunohistochemistry. Mainly NPY and alpha-MSH neurons were studied and both peptides are present in projections to the preoptic area as well as to the midbrain periaqueductal gray. Some arcuate neurons were found to have collateral axons to both these areas. The arcuate communicates primarily with the pituitary gland, hypothalamus, limbic system, midbrain periaqueductal gray and autonomic nuclei of the brain stem. In this way, the arcuate may be involved in integrating emotional, sensory, vegetative homeostatic and autonomic functions with endocrine functions.
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PMID:Anatomy and physiology of the neuroendocrine arcuate nucleus. 241 5

We have developed a dissociated primary cell culture of noradrenergic neurons from the locus ceruleus of postnatal (1- to 5-d-old) mice or rats. Slices of the brain stem were made on a Vibratome. Then the region of locus ceruleus, which was identified by observing the slices under a dissecting microscope, was dissected out from the slices. The removed fragments of brain slices were dissociated and cultured up to 3 weeks on a non-neuronal feeder layer, which consisted predominantly of astroglial cells, or on a fibronectin-treated collagen substratum. After 2 weeks of culture, about 70% of total neuronlike cells revealed positive catecholamine histofluorescence, indicating that they were probably noradrenergic neurons. About 98% of large- and medium-sized cultured neurons (soma diameter greater than or equal to 20 microns) was histofluorescence positive. The fluorescence-positive cells had long processes rich in varicosities, and the shape of their soma was either multipolar or fusiform. Electron microscopy using permanganate fixation revealed that the varicosities along their processes had small granular vesicles, which may contain norepinephrine. Physiological properties of these noradrenergic neurons were investigated with intracellular microelectrodes or with the whole-cell version of the patch clamp. We observed that many cells were producing spontaneous firing. Many of these spontaneously firing cells had no obvious contact with neighboring cells. The neurons were depolarized when glutamate was applied by pressure ejection. They also responded to GABA and glycine with either hyperpolarization or depolarization, and these responses were antagonized by picrotoxin and strychnine. Application of substance P generally produced depolarization with an increase in input resistance. The neurons responded with hyperpolarization to somatostatin, beta-endorphin, and enkephalin. This culture system will become a useful tool for elucidating the cellular and molecular properties of the central noradrenergic neurons.
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PMID:Noradrenergic neurons from the locus ceruleus in dissociated cell culture: culture methods, morphology, and electrophysiology. 243 74


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