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)

This study was undertaken in order to establish the presence of pluripotential neuroblasts in the developing chick CNS. This has been suggested by our previous observations that expression of emerging neuronal phenotypes in the chick embryo CNS is affected by exposure to neurotrophic substances (i.e., GHRH, SRIF, NGF, EGF, muscle-derived factors) or neurotoxins such as ethanol. We have proposed that one mechanism whereby these substances elicit their effects is by shifting phenotypic expression in populations of pluripotential neuroblasts. In order to establish the presence of significant populations of pluripotential neuroblasts, cultures obtained from 3-day-old whole chick embryos (E3WE) were double-stained with antibodies to markers specific for four neuronal phenotypes in various permutations. Cultures at 6 DIV were tested for the presence of tyrosine hydroxylase (TH), choline acetyltransferase (ChAT), gamma-aminobutyric acid (GABA), and somatostatin (SRIF) alone, and in various combinations. We observed a colocalization of all phenotypic markers within neuronal perikarya and processes in more than fifty percent of neuronal cells in these cultures. These data suggest that developing neuroblasts at this stage of embryogenesis possess the machinery necessary to adopt multiple neuronal phenotypes. The colocalization of neurotransmitter proteins in early neuroblasts (60 hr of embryogenesis) supports the recent concept that these substances themselves may influence phenotypic expression and also supports our idea that microenvironmental factors (i.e., ethanol, growth factors) provide signals which affect emerging phenotypes.
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PMID:Early neuroblasts are pluripotential: colocalization of neurotransmitters and neuropeptides. 756 50

The shape, projection, ultrastructure and chemistry of interneurons that were initially identified by their immunoreactivity for somatostatin in the small intestine of the guinea pig were examined. Somatostatin immunoreactive nerve cell bodies and nerve fibres were located in the myenteric plexus. Simultaneous labelling for 2 antigens revealed that the somatostatin immunoreactive interneurons were also immunoreactive for choline acetyltransferase, but not for calbindin or neuropeptide Y. Cell shapes were determined by immunohistochemistry, ultrastructural analysis and intracellular dye filling. The neurons had large cell bodies (38 x 14 microns) which gave rise to long branched filamentous dendrites and a single axon. The projections of the somatostatin immunoreactive interneurons were determined by analysis of patterns of fibre loss and survival following degenerative section of myenteric nerve pathways and by analysis of individual neurons that were injected intracellularly with dye. The axons projected anally, sometimes after a short oral excursion, and were confined to the myenteric plexus. They gave rise to multiple varicose branches within myenteric ganglia: in the majority of cases the first branch was within 100 microns of the cell body. Synaptic inputs to the cells were examined by light and electron microscopy. All somatostatin immunoreactive neurons received numerous somatostatin immunoreactive inputs on the cell body and all filamentous processes. Ultrastructural investigation indicated that these constituted the majority of all inputs. It is concluded that cholinergic, somatostatin immunoreactive, interneurons have a unique soma morphology and form synaptically connected chains that run anally in the myenteric plexus.
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PMID:Cholinergic, somatostatin-immunoreactive interneurons in the guinea pig intestine: morphology, ultrastructure, connections and projections. 759 94

To clarify the functional role of the brain somatostatinergic system in cognitive processes, changes in the performance in passive avoidance and water maze tasks and in brain somatostatin contents were comparatively investigated in young Fischer rats subjected to brain cholinergic and somatostatinergic depletion, and in aged Fischer rats. Lesioning of the nucleus basalis magnocellularis and administration of cysteamine (200 mg/kg, s.c.), a depletor of somatostatin, resulted in significant deficits in passive avoidance, but complete transection of the fimbria-fornix hardly affected the performance in the task. When cognitive performance was assessed in the Morris water maze, lesions of the nucleus basalis magnocellularis and the fimbria-fornix, and administration of cysteamine, significantly impaired the acquisition of navigatory spatial memories of rats. On the other hand, aged rats (24-27 months) showed severe impairments of memory acquisition in both tasks. Neurochemistry measurements showed that lesions of the nucleus basalis magnocellularis produced a selective reduction both in the cortical cholinergic marker choline acetyltransferase and in striatal somatostatin level, whereas lesioning of the fimbria-fornix caused a marked loss of choline acetyltransferase in the hippocampus and posterior cortex, and a significant reduction in hippocampal somatostatin. On the other hand, treatment with cysteamine significantly reduced the contents of somatostatin in all the brain regions examined, but minimally affected choline acetyltransferase activity. However, significant reduction in the striatal choline acetyltransferase activity and elevation in somatostatin content in the frontal cortex were found in aged rats compared with young rats. Taken together, these results strongly suggest that changes in the brain somatostatinergic transmission are involved in the cognitive deficits in the experimental animal models of dementia presently employed. Furthermore, the present comparative study further implies that there are differences in the relative involvement of the cholinergic and somatostatinergic systems in the performance of rats on two different tests of mnemonic function.
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PMID:Changes in brain somatostatin in memory-deficient rats: comparison with cholinergic markers. 764 25

Immunocytochemical techniques were employed to examine the temporal ordering whereby amyloid beta-protein (A beta P) and neuronal elements collectively come together to form senile plaques in Alzheimer's disease (AD). Specifically, we addressed three questions: (1) whether A beta P deposition precedes or follows neuritic changes; (2) whether paired helical filament (PHF) formation is an early or late event in the genesis of the dystrophic neurites which participate in plaque formation; and (3) whether the density of senile plaques displays any relationship with the prevalence of PHF or Alz-50 containing neurons. To address these questions we studied the amygdala from a group of patients with AD, a group of nondemented age-matched individuals exhibiting a sufficient number of senile plaques to be classified by neuropathological criteria as AD, and a group of age-matched controls without AD pathology. Amyloid-bearing plaques were demonstrated by A beta P immunolabeling and thioflavine-S staining. Neuritic changes in the form of dystrophic neurites were observed with the aid of antibodies against PHF, Alz-50, as well as antibodies against several neuropeptides (i.e., substance P, somatostatin, and neurotensin) and the acetylcholine biosynthetic enzyme, choline acetyltransferase. By using a graded range of pathologic changes both within and across the patient population to provide us with a means of evaluating plaque deposition from its earliest to most advanced stages of development, we observed in patients and/or regions of the amygdala displaying a mild degree of pathologic change A beta P deposition in the absence of any neuritic changes. With increasing density of A beta P, however, we began to observe dystrophic neurites within plaques. In regions of relatively few plaques, the dystrophic neurites were immunolabeled only with antibodies against the various neurotransmitters and they lacked evidence of cytoskeletal pathology (i.e., Alz-50 or PHF). Only as the density of A beta P increased further within a region, were dystrophic neurites observed that exhibited Alz-50 or PHF. In no instance did we observe a relationship between the density of A beta P deposition and the density of Alz-50 or PHF-immunoreactive neurons. Collectively, our data suggest that the deposition of A beta P is an early pathologic event in senile plaque formation. Thereafter, swollen neurites can be seen in the vicinity of A beta P. This early neuritic response, which can first be visualized by immunolabeling for one or another transmitter substance, is followed by alterations in the cytoskeleton as recognized initially by antibodies to Alz-50 and subsequently by the presence of PHF.
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PMID:Evidence that transmitter-containing dystrophic neurites precede paired helical filament and Alz-50 formation within senile plaques in the amygdala of nondemented elderly and patients with Alzheimer's disease. 769 48

Within the amygdala of elderly subjects and patients with Alzheimer's disease (AD), we recently found evidence suggesting amyloid beta-protein (A beta P) deposition occurs before the appearance of dystrophic neurites. Moreover, these data suggested dystrophic neurites initially lack evidence of cytoskeletal pathology although with time and further maturation, the dystrophic neurites display an altered cytoskeleton as evidenced by their immunoreactivity to Alz-50 and paired-helical filaments (PHF). These findings are of particular relevance to our understanding of the sequence of pathologic events in AD and thus it has become important to determine whether these events are unique to the amygdala or are representative of a more general pattern which can be found throughout the brain. Using a battery of antibodies to markers that are characteristic of AD pathology (i.e., A beta P, PHF, and Alz-50), three peptidergic neurotransmitters (neurotensin, somatostatin, and substance P), and one neurotransmitter biosynthetic enzyme (choline acetyltransferase), we examined the entorhinal cortex (EC) of three groups of subjects (AD, normal elderly, and a group of nondemented elderly with numerous senile plaques). The EC was studied, in part, because it is well recognized as a brain region displaying severe and, most importantly, early pathologic changes. Like the amygdala, we found evidence that amyloid beta-protein immunoreactive (A beta P-IR) and thioflavine-S-positive senile plaques occur within the EC prior to the appearance of transmitter-, Alz-50-, or PHF-immunoreactive dystrophic neurites. We also observed transmitter-immunoreactive dystrophic neurites in the absence of Alz-50 or PHF-immunolabeled dystrophic neurites and transmitter- and Alz-50-IR dystrophic neurites in the absence of those containing PHF. Collectively, these findings were similar to those seen within the amygdala and thus reinforced the concept that A beta P deposition is the primary event in plaque pathology, and this deposition is subsequently followed by the appearance of dystrophic neurites which retain their transmitter phenotype yet lack an altered cytoskeleton. With time, these dystrophic neurites develop cytoskeletal alterations and become immunoreactive to Alz-50 and PHF.
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PMID:Evidence that transmitter-containing dystrophic neurites precede those containing paired helical filaments within senile plaques in the entorhinal cortex of nondemented elderly and Alzheimer's disease patients. 769 Jun 77

This study examines the properties of neurons differentiating in cultures of mammalian neural crest cells. The neurons fall into two categories: (1) a population of early differentiating (ED) neurons generated from precursors that are postmitotic at the time of plating; and (2) a late differentiating (LD) population of neurons arising from dividing precursor cells. The ED population of neurons survive for only 2-3 days while the LD neurons survive for many weeks. Both groups of neurons express the neuronal marker, neurofilament, as well as adrenergic and cholinergic characteristics. The latter two traits are evident as immunoreactivity for tyrosine hydroxylase (TH)/dopamine-beta-hydroxylase (D beta H) and choline acetyltransferase (ChAT), respectively. The LD neurons also contain immunoreactivity for a number of neuropeptides including, substance P (SP), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), calcitonin gene related polypeptide (CGRP), and somatostatin (SOM). Immunoreactivity for SP, CGRP, and VIP are found in virtually all of the LD neurons while SOM and NPY are found in a smaller percentage of the neurons.
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PMID:Neuronal differentiation in cultures of murine neural crest. I. Neurotransmitter expression. 769 63

An in situ hybridization procedure that identifies cells expressing D2 dopamine receptor mRNA was combined in double-labelling studies with immunohistochemical procedures that identify cells expressing either choline acetyltransferase (ChAT) or somatostatin. D2 receptor mRNA was detected in almost all of the ChAT positive caudate-putamen cells, approximately half of the ChAT positive nucleus accumbens cells and none of the somatostatin-positive cells in either brain region.
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PMID:D2 dopamine receptor mRNA distribution in cholinergic and somatostatinergic cells of the rat caudate-putamen and nucleus accumbens. 770 May 82

Interruption of a chronic GABA infusion into the rat somatosensory cortex induces the appearance of focal epileptic manifestations, known as the 'GABA withdrawal syndrome' (GWS). The aim of the present study was to determine, by immunocytochemistry, if neurotransmitters other than GABA are involved in GWS, namely: noradrenaline (NA), serotonin, choline acetyltransferase (CAT), cholecystokinin, neuropeptide Y, somatostatin and glial fibrillary acid protein (GFAP). Immunocytochemical data were compared in three animal groups: GABA-, saline- and L-aspartate (L-Asp)-infused rats. Only GABA-infused rats presented epileptic manifestations after interruption of the infusion. Saline- and L-Asp-infused rats served as controls. Observations were limited to the region surrounding the cortical infusion site. GABA-infused rats showed in the zone of the epileptic focus a number of cell bodies strongly immunoreactive to NA antibodies much larger than control rats. In addition, NA-immunoreactive fibers formed a dense plexus and some of them were observed around perikarya. In saline- and L-Asp-infused rats, the NA-immunolabelled fibers were sparse and NA immunolabelling was rarely observed in cell bodies. These results contrast to those obtained for the serotonergic system, where no significant difference was observed among the three groups of rats. CAT immunolabelling was observed in cell bodies, but not in nerve terminals in rats of the three groups. The number of CAT-immunoreactive cell bodies was much greater in GABA-infused rats than in the control animals. GFAP immunolabelling showed an important number of astrocytes throughout the cortex of the GABA-infused hemisphere, whereas, astrocytic reaction was limited to the infusion site in controls. Immunocytochemical data concerning peptides revealed cortical neuronal elements labelled similarly in the three groups of rats. Noradrenergic, cholinergic and glial modifications observed mainly in GABA-infused rats can result from lesion and from a specific action of GABA in chronic infusion. These modifications may contribute to the epileptogenesis of GWS, as recently demonstrated by electrophysiological recordings that show a modulating action of NA on firing activity of neurons involved in the epileptic focus.
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PMID:High expression of noradrenaline, choline acetyltransferase and glial fibrillary acidic protein in the epileptic focus consecutive to GABA withdrawal. An immunocytochemical study. 781 66

Cholinergic markers, neuropeptides, and amines and their metabolites were sampled from identical specimens across 10 neocortical regions in a large sample of Alzheimer's disease (AD) cases and controls. Levels of choline acetyltransferase, acetylcholinesterase, somatostatin, corticotropin-releasing factor, serotonin, and 5-hydroxyindoleacetic acid were significantly reduced in AD versus controls. After data reduction, the most descriptive neurochemical indices were used to examine the relationship of neurochemical measures and dementia severity within the AD sample, controlling for age effects. Dementia severity ratings were based on antemortem assessments (46.9% of AD sample) and postmortem chart review (53.1% of the AD sample). Choline acetyltransferase activity was highly correlated with clinical dementia ratings across the neocortex of the AD cases. Somatostatin and corticotropin-releasing factor levels were correlated with dementia severity only when control cases were included in the analyses. None of the amines, their metabolites, or the neuropeptides quantified related significantly to dementia severity in the AD cohort. These data (a) confirm the strong association of cholinergic deficits with functional impairment in AD and show that this association is independent of age and (b) suggest that of all the neurochemical species quantified, the cholinergic indices may be unique in their association with dementia severity.
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PMID:Neurochemical correlates of dementia severity in Alzheimer's disease: relative importance of the cholinergic deficits. 783 69

beta-Amyloid protein (beta-AP) deposits, analoguous to those found in Alzheimer's disease (AD) are observed in the brain of aging Microcebus murinus. Because choline acetyltransferase (ChAT) activity and somatostatin (SRIH) content are consistently decreased in AD, we tested whether such changes could be observed in middle aged to aged Microcebus cerebral cortex and whether they were accompanied by beta-AP deposits. A positive correlation was observed between age and ChAT activity. By HPLC, SRIH immunoreactivity eluted as four peaks, two of which being identical with SRIH-28 and SRIH-14 while the other two likely represented precursor forms. Cortical SRIH content was not significantly affected by age. ChAT activity and SRIH content were not significantly correlated. Amyloid angiopathy was observed in every brain examined and the presence of cortical lesions analoguous to senile plaques observed in the oldest case only which did not demonstrate important alterations in ChAT and somatostatin levels.
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PMID:Choline acetyltransferase and somatostatin levels in aged Microcebus murinus brain. 789 28


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