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 striatum and the mesencephalic dopamine neurons which innervate it, are each organized into developmentally and biochemically distinct compartments. Striatal patches, characterized in the neonate by high concentrations of opiate receptors and substance P, are innervated prenatally by fibers originating in one group of midbrain dopamine neurons, the ventral tier. By the third postnatal day, a dense dopamine projection from neurons in the dorsal tier of the mesostriatal group innervates non-patch areas of the striatum, i.e. the matrix, and is followed by the appearance there of neurotensin, somatostatin and calcium binding protein. We have recently observed that the period of establishment of connections between dorsal tier dopamine neurons and their target cells in the striatal matrix is accompanied by a surge in expression of the gene coding for tyrosine hydroxylase (TH). In order to determine the overall metabolic state of mesencephalic and striatal neurons during the period of up-regulation of TH gene expression, we have applied immunocytochemistry for neuron specific enolase (NSE), and cytochrome oxidase histochemistry, known markers for neuronal activity, as well as TH immunohistochemistry to the mesencephalon and striatum of postnatally developing rats. At birth, both NSE and cytochrome oxidase were expressed almost exclusively in the patches, appearing in the matrix only after the 2nd postnatal day. Patches of NSE remained visible thru the 14th day. In the mesencephalon, cytochrome oxidase and immunoreactive NSE cells in adjacent sections, were present only in the pars reticulata (i.e. ventral tier). By day 8, both techniques identified nigral cells in the dorsal as well as ventral tiers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Temporal and compartmental restriction of neuron-specific enolase expression in the rat mesostriatal system. 133 Mar 70

Immunocytochemical methods have been used to examine the localisation of 3 neurofilament proteins and the calcium binding protein, calbindin D28k, in whole mount preparations of the submucous plexus in the Wistar rat. Neurofilament-M (160 kDA protein) was present in 40% of the submucosal neurons, staining fine filaments in the soma and the axonal processes. Calbindin D28k was present in 40% of the submucosal neurons staining both the soma and nerves within the plexus. The neurofilament proteins and calbindin D28k were never observed within the same neurons. Neurofilament-M was co-localised with substance P and calcitonin gene-related peptide but not somatostatin or the other neuropeptides investigated. Calbindin D28k was co-localised with vasoactive intestinal polypeptide and neuropeptide Y. Galanin- and somatostatin-immunoreactive neurons did not contain either the neurofilament proteins or calbindin D28k. The results demonstrate the presence of subsets of submucosal neurons that can be distinguished by the presence of neurofilament-M or calbindin D28k.
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PMID:Neurofilament M and calbindin D28k are present in mutually exclusive subpopulations of enteric neurons in the rat submucous plexus. 170 5

Immunoreactivity (IR) for the calcium binding protein, calbindin, was localized in sensory ganglia (nodose, trigeminal and dorsal root), in parasympathetic ganglia (otic and sphenopalatine) in sympathetic chain ganglia and in sympathetic pre-vertebral ganglia of guinea pig. In sensory ganglia, fine nerve fibres with calbindin-IR surrounded the majority of cell bodies, a low proportion of which were themselves reactive. In cranial parasympathetic and in sympathetic chain ganglia, a small proportion of nerve cells was surrounded with baskets of calbindin-IR nerve fibres, but very few cell bodies were reactive. In prevertebral sympathetic ganglia, dense networks of terminals surrounded many cell bodies, but few somata were themselves reactive. In the coeliac and inferior mesenteric ganglia, the calbindin-IR nerve fibres surrounded somatostatin-IR cell bodies, but not those with neuropeptide Y-IR. It is concluded that specific subgroups of peripheral autonomic and sensory neurones have calbindin-IR.
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PMID:Calbindin immunoreactivity in sensory and autonomic ganglia in the guinea pig. 197 8

A double-labeling immunofluorescence colocalization technique was used to examine the extent of coexistence of somatostatin (SOM)-like immunoreactivity with neuropeptide Y (NPY)-, tyrosine hydroxylase (TH)- and vitamin D-dependent calcium binding protein (D-CaBP)-like immunoreactivities in neurons of the rat main olfactory bulb. SOM-like immunoreactivity (SOM-I) was distributed within restricted populations of periglomerular neurons and deep short-axon cells, and rarely within superficial short-axon cells at the glomerular layer/external plexiform layer (GL/EPL) border region. Double-labeling analysis revealed that all of the SOM-I deep and superficial short-axon cells also contained NPY-I. Colocalization of SOM-I and TH-I or of SOM-I and D-CaBP-I was infrequently observed within periglomerular neurons. The rare SOM-I short-axon cells at the GL/EPL border always exhibited D-CaBP-I. These results demonstrate virtual complete coexistence of SOM and NPY in short-axon neurons of the main olfactory bulb. With a few exceptions, however, bulbar SOM neurons appear to constitute subclasses of periglomerular cells immunohistochemically distinct from those containing TH or D-CaBP.
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PMID:Somatostatin-like immunoreactivity in rat main olfactory bulb: extent of coexistence with neuropeptide Y-, tyrosine hydroxylase- and vitamin D-dependent calcium binding protein-like immunoreactivities. 257 95

Adrenalectomy of adult male rats resulted in a nearly complete loss of hippocampal granule cells 3 to 4 months after surgery. Nissl and immunocytochemical staining of hippocampal neurons revealed that the granule cell loss was selective; there was no apparent loss of hippocampal pyramidal cells or of gamma-amino butyric acid (GABA)-, somatostatin-, neuropeptide Y-, calcium binding protein-, or parvalbumin-containing hippocampal interneurons. The hippocampal CA1 pyramidal cells of adrenalectomized animals exhibited normal electrophysiological responses to afferent stimulation, whereas responses evoked in the dentate gyrus were severely attenuated. Corticosterone replacement prevented both the adrenalectomy-induced granule cell loss and the attenuated physiological response. Thus, the adrenal glands play a role in maintaining the structural integrity of the normal adult brain.
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PMID:Selective loss of hippocampal granule cells in the mature rat brain after adrenalectomy. 291 56

The morphology and distribution of perikarya positive for choline acetyltransferase, somatostatin, calcium binding protein (calbindin D28K) and nicotinamide adenine dinucleotide phosphate diaphorase were surveyed in the human striatum. Choline acetyltransferase and somatostatin antibodies labeled separate populations of large striatal interneurons. Somatostatin immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (nitric oxide synthase) activity were completely co-localized. Calbindin antibody identified two distinct groups of striatal neurons: (1) numerous medium-sized, lightly stained neurons, probably analogous to striatopallidal projection neurons in the rat, and (2) much less numerous, large, darkly stained neurons. Half of the latter group, but none of the former, were also nicotinamide adenine dinucleotide phosphate diaphorase-positive. Somatostatin-positive and medium-sized, calbindin-positive neurons were more numerous in the caudate nucleus than in the putamen or ventral striatum. By contrast, large calbindin-immunoreactive neurons were more frequently encountered in the putamen. Choline acetyltransferase-positive neurons were evenly distributed across striatal components. In aged control subjects, the size of large, darkly stained calbindin-positive neurons was reduced relative to young subjects. Aging had no effect on somatostatin-, medium-sized calbindin-, or choline acetyltransferase-positive neurons. However, in histologically confirmed cases of Alzheimer's disease, there was a selective, 75% loss of choline acetyltransferase-immunoreactive perikarya from the ventral striatum, but not from the dorsal striatum, compared to aged controls. Furthermore, the remaining cholinergic neurons in the ventral striatum of Alzheimer's disease cases were significantly smaller than similar neurons in controls. These results indicate that various striatal components which have been shown to differ in their anatomical connectivity and functional specialization, also differ in their neurochemical signatures. The specific and marked loss of choline acetyltransferase-positive neurons from the ventral striatum in Alzheimer's disease is consistent with the characteristic cholinergic and 'limbic' pathology in this disease.
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PMID:Human striatum: chemoarchitecture of the caudate nucleus, putamen and ventral striatum in health and Alzheimer's disease. 752 83

Different subpopulations of GABA neurons containing the neuropeptides somatostatin and neuropeptide Y, and the calcium binding protein parvalbumin were studied by immunocytochemistry using light and electron microscopy in the dorsomedial cortex of the lizard Psammodromus algirus to investigate the connectivity of different subsets of GABA neurons in the lizard dorsomedial cortical circuitry and to compare cortical regions of reptiles and mammals. GABA neurons were classified into different subsets by using the peroxidase anti-peroxidase immunohistochemical method on adjacent Araldite-embedded semithin sections. GABA neurons in the dorsomedial cortex fall into three major subsets: 1) neurons with somatostatin (and neuropeptide Y), which accounted for about 44% of the GABA population; 2) neurons with parvalbumin, which accounted for about 13% of the GABA neurons; and 3) neurons without parvalbumin or neuropeptides, which represented 40% of all GABA cells. This division of GABA neurons in non-overlapping subpopulations of neuropeptide- and parvalbumin-containing cells is similar to that found in the mammalian hippocampal formation. On the basis of the nerve terminal fields, somatostatin- and parvalbumin-immunoreactive neuronal populations appear to be functionally different, acting on different portions of the projection neurons. Parvalbumin-immunoreactive neurons inhibit the pyramidal neurons at the cell body level, whereas somatostatin-immunoreactive neurons inhibit them on distal dendrites. The results of the present study add more similarities between the lizard dorsomedial cortex and parts of the mammalian hippocampus.
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PMID:Subpopulations of GABA neurons containing somatostatin, neuropeptide Y, and parvalbumin in the dorsomedial cortex of the lizard Psammodromus algirus. 790 63

The mechanism of delayed death of pyramidal cells in the hippocampal CA1 region and the acute death of various types of hilar neurons after ischemia is still unknown. Excitotoxicity may play a role in ischemic cell death, a prerequisite of which is the development of increased excitability or an enhanced excitatory transmission in the selectively vulnerable subfields of the hippocampus. Such changes may take place upon the loss or malfunction of local inhibitory neurons in the early postischemic period. In the present study we examined the vulnerability of non-pyramidal neurons containing a recently discovered calcium binding protein, calretinin, in the rat hippocampus following 15 min ischemia induced by four-vessel occlusion. Immunostaining for calretinin enabled us to visualize a new type of spiny non-pyramidal cell in the hippocampus specifically associated with the mossy fiber system. This cell type is present exclusively in regions where mossy fiber terminals occur, i.e. in the hilus of the dentate gyrus and in stratum lucidum of the CA3 subfield. A selective loss of immunoreactivity in these neurons was already observed at 12-24 h after ischemia, when the pyramidal cells in the CA1 region showed no signs of damage. At a survival time of two to three days, most if not all spiny calretinin-immunoreactive cells had disappeared from the hippocampus. Other types of calretinin-containing GABAergic neurons were also reduced in number, but only at a time when CA1 pyramidal cells also started to degenerate, i.e. two to three days after ischemia. We speculate that the early loss of spiny calretinin-containing cells, together with other non-pyramidal cells associated with the mossy fiber system (somatostatin-containing neurons and mossy cells of the hilus), may result in pathological network activity in the hippocampus, which may ultimately lead to an increased excitatory transmission and delayed pyramidal cell death in the CA1 region.
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PMID:Early degeneration of calretinin-containing neurons in the rat hippocampus after ischemia. 825 22

Previous studies have reported the presence of the calcium binding protein calretinin in neurons in the striatal part of the basal ganglia in rats and primates. In the present study, immunofluorescence double-labeling techniques and immunofluorescence combined with retrograde labeling were used in rats to determine whether calretinin is found in any of the known types of striatal neurons. The results showed that a small fraction of the calretinin-containing neurons (< 10%) contain parvalbumin, but none of the calretinin-containing striatal neurons contained markers for the other two major types of striatal interneurons (i.e., choline acetyltransferase-containing cholinergic neurons and somatostatin-containing neurons). Additionally, calretinin was not found in projection neurons, using either calbindin or DARPP32 as immunofluorescent markers of striatal projections neurons in general, or using retrograde labeling to specifically identify either striatonigral or striatopallidal neurons. Thus, calretinin appears to be largely found in a unique population of striatal interneurons in rats. This population appears to be about one third the abundance of any of the previously identified populations of striatal interneurons.
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PMID:Calretinin is largely localized to a unique population of striatal interneurons in rats. 886 67

Subependymal giant cell astrocytoma (SEGA) is the most common neoplastic process involving the brain in patients with tuberous sclerosis complex (TSC). Morphologically, these tumors exhibit a wide range of cytoarchitecture with spindle and epithelioid cells resembling astrocytes, and also large, occasionally giant cells, some of which have a distinctly ganglion-like appearance. Unresolved questions regarding SEGAs center on: (a) their cytogenesis, i.e., whether they are derived from single or multiple precursors; and (b) their differentiating capacity along glial or neuronal lines. We sought to determine whether SEGAs represent truly mixed tumors or whether they consist of a single population of cells with a capacity for divergent differentiation. Twenty SEGAs were assessed for immunophenotypic features of either neuronal or glial differentiation or both. Only tumors from patients with a clinically confirmed diagnosis of TSC were included. Immunoreactivity for glial fibrillary acidic protein (GFAP) and/or S-100 protein was considered indicative of a glial phenotype, whereas the presence of neuronal differentiation was assessed by staining for cytoskeletal proteins [neurofilament epitopes, class III Beta-tubulin, microtubule-associated protein 2 (MAP2), synaptophysin], neurosecretory substances [serotonin, cholecystokinin, Beta-endorphin, substance P, somatostatin, metenkephalin, neuropeptide Y, vasoactive intestinal polypeptide (VIP), and for the 28-kDa neuron-associated calcium binding protein calbindin. Of the tumors examined, 18 exhibited both glial and neuronal epitopes, the staining pattern being variable. In 19 tumors, the constituent spindle, polygonal and giant or ganglion-like cells showed variable immunoreactivity for GFAP and S-100 proteins both within the cell body and processes. Neuron-associated cytoskeletal proteins were present in 18 cases. Class III Beta-tubulin immunoreactivity was demonstrated in 17 tumors, both within the bodies of all three cell types and to varying degrees within their processes. Neurofilament protein and calbindin staining was present in 8 tumors, with reactivity for the former being distributed in a phosphorylation-dependent manner. MAP2 was detected in a few cells of two tumors. Immunoreactivity for neuropeptides was observed in 17 lesions. Somatostatin and metenkephalin staining was noted in 10 tumors (50%) being present particularly within polygonal cells. Neuropeptide Y, serotonin and Beta-endorphin reactivity was found in 6 (30%), 5 (25%), and 4 tumors (20%), respectively; Beta-endorphin was lacking in giant cells, whereas neuropeptide Y and serotonin were seen within their cell bodies. Substance P and VIP were evident in only occasional polygonal cells of 2 (10%) and 1 tumor (5%), respectively. Stains for cholecystokinin were negative. The observation of immunoreactivity for both glial- and neuron-associated epitopes within tumor cells of the same morphology suggests that SEGAs represent proliferations of cell lineages with the capacity to undergo divergent glioneuronal as well as neuroendocrine differentiation to a greater extent than do other mixed glial-neuronal neoplasms.
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PMID:Immunohistochemical characterization of subependymal giant cell astrocytomas. 892 13


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