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)

Somatostatinergic projections of the amygdala to the bed nucleus of the stria terminalis (BST) and medial preoptic-hypothalamic region were examined using a technique that combines retrograde axonal transport with peroxidase-antiperoxidase immunohistochemistry. With injections of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) into either the BST or medial preoptic-hypothalamic region numerous double-labeled cells exhibiting both retrograde labeling and somatostatin-like immunoreactivity were observed in the medial amygdaloid nucleus and intra-amygdaloid portion of the BST. Additional cells were seen in the central nucleus, basomedial nucleus and anterior amygdaloid area. Although WGA-HRP labeled neurons and somatostatin-positive cells were observed in the lateral and basolateral amygdaloid nuclei, few double-labeled neurons were found.
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PMID:Somatostatinergic projections from the amygdala to the bed nucleus of the stria terminalis and medial preoptic-hypothalamic region. 288 2

The distribution of somatostatinlike immunoreactivity was studied in the hippocampal formation, retrohippocampal region, and temporal cortex in the human brain. Tissues from surgical biopsy and postmortem cases were used, and the immunogold/silver method on vibratome sections was introduced for routine applications in conjunction with primary antisera that recognise somatostatin-14 or somatostatin-28. Somatostatin-28 antisera readily stained numerous neurons, dendrites, and extensive axonal networks throughout the hippocampus and neighbouring cortex. Liquid phase absorption provided controls for specificity. The most prominent accumulations of somatostatin immunoreactive neurons and axons occurred in the hilus of the area dentata, in CA1, and in the entorhinal and perirhinal cortices. Axonal plexuses occurred throughout the hippocampal subfields but were particularly dense in those regions rich in somatostatin neurons. The distribution of somatostatin immunoreactive neurons and fibers parallels the distribution of neuropeptide Y (NPY) neurons and fibers in the hippocampus and cerebral cortex to a remarkable extent. Double labelling experiments with antisera against neuropeptide Y and somatostatin indicate a considerable frequency of coexistence of the two peptides in single neurons, particularly in large multipolar cortical neurons and also in the small bipolar white matter neurons. Regional variations exist in the amounts of coexistence found in the hippocampal subfields; somatostatin-NPY coexistence is particularly high in the hilus of the area dentata, the subicular complex, and the deep layers of the entorhinal and perirhinal cortices. In the hippocampi and temporal cortices in cases of Alzheimer-type dementia compared to those of age-matched control brains, there is a significant to severe loss of somatostatin immunoreactive neurons and axons. This loss is most severe in those regions with the highest indices of neurofibrillary tangles and neuritic plaques-the hilus of the area dentata, CA1, and the entorhinal and perirhinal cortices. Surviving somatostatin neurons are distorted with short dendrites and truncated axons. Neuritic plaques identified on double label experiments with thioflavin include somatostatin axons but not neurons.
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PMID:Somatostatin immunoreactive neurons in the human hippocampus and cortex shown by immunogold/silver intensification on vibratome sections: coexistence with neuropeptide Y neurons, and effects in Alzheimer-type dementia. 288 16

Somatostatin 28- and neuropeptide Y-containing innervations were mapped in the human medial forebrain (eight control brains) with immunohistochemistry, using the sensitive avidin-biotin-peroxidase method. Peptidergic perikarya and fibers had an extensive distribution: they were densest in the ventral striatum (nucleus accumbens, olfactory tubercle and bed nucleus of the stria terminalis) and infralimbic cortex, of intermediate density in the medial septal area and of lowest density in the dorsal and caudal lateral septal nucleus. Somatostatin-like immunoreactive perikarya and fibers were generally more numerous than the neuropeptide Y-like immunoreactive ones, but more faintly labeled. Their pattern of distribution was strikingly similar in some of the limbic structures studied but clearly distinct in others. Excellent overlap of neuropeptide Y and somatostatin-like immunoreactivity was detected in: (1) the medial septal area, where innervation occasionally formed perivascular clusters; (2) the nucleus accumbens and olfactory tubercle, characterized by dense patchy innervation; and (3) the laterodorsal septal nucleus, scarcely innervated. In the latter structures, most peptidergic neurons were double-labeled. On the other hand, both peptidergic innervations clearly differed in the lateroventral septal nucleus and the bed nucleus of the stria terminalis which contained distinct clusters of somatostatin-like immunoreactive neurons devoid of neuropeptide Y-like immunoreactivity. Also, the perineuronal and peridendritic axonal plexuses ('woolly fibers') present in these structures were only labeled with somatostatin. In the infralimbic cortex, the relation between the peptides varied according to the cortical laminae. Coexistence of somatostatin and neuropeptide Y frequently occurred in layer VI and in the subcortical white matter, whereas layer V and particularly layers II and III contained a contingent of neurons labeled only with somatostatin. Dense horizontal terminal networks in layers I and VI however were similar for both peptides. These findings support the existence of two different types of somatostatin-like immunoreactive perikarya as regards colocalization with neuropeptide Y. Their particular topographical segregation within the cortical and subcortical structures analysed suggest that they could have different connections and functional properties.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Somatostatin 28 and neuropeptide Y innervation in the septal area and related cortical and subcortical structures of the human brain. Distribution, relationships and evidence for differential coexistence. 288 48

Three adults with progressive cognitive decline and extrapyramidal dysfunction were studied. They were all mentally retarded women without known chromosomal abnormalities, ranging in age at the time of onset from 31 to 42 yrs with an average duration of illness of 6 yrs. Neurological signs were stereotyped and consisted of a unilateral equinovarus foot posture followed by progressive dementia, rigidity and quadriparesis. Identical pathological findings were noted in all cases. There was marked deposition of iron-containing pigments in the globus pallidus and reticulate zone of the substantia nigra. Numerous axonal spheroids were noted in these areas and in the gracile and cuneate nuclei. In addition to these typical changes of Hallervorden-Spatz disease (HSD), abundant neurofibrillary tangles (NFTs) were found within the hippocampus, neocortex, nuclei of basal forebrain, subthalamic nucleus and brainstem reticular formation. Rare Hirano bodies and granulovacuolar degeneration were noted within the hippocampus; neuritic plaques and amyloid deposits were absent. Ultrastructurally the NFTs were mostly paired helical filaments (PHFs) with a diameter of 20 to 25 nm and a half-periodicity of 80 nm. Straight filaments and incompletely twisted forms were also seen. Immunocytochemistry with polyclonal antibodies to PHFs was positive in a distribution identical to that of Bodian-positive NFTs. Biochemical analysis of frozen frontal cortex from 1 case revealed a 94% depletion of the cholinergic marker enzyme choline acetyltransferase. Somatostatin-like immunoreactivity was within normal range. Study of 1 case with laser microprobe mass analysis revealed evidence of aluminium accumulation in tangle-bearing hippocampal neurons. Adjacent tangle-free neurons failed to show comparable accumulations. These findings indicate that adult onset HSD occurring in mentally retarded individuals may represent a distinct clinicopathological entity associated with neurofibrillary pathology without amyloid deposition.
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PMID:Adult onset Hallervorden-Spatz disease with neurofibrillary pathology. A discrete clinicopathological entity. 288 13

The anlages of the medial-basal hypothalamus (MBH), septopreoptic area (POA), Rathke's pouch, and the parietal cortex (CC) of rats (at 12.5, 14.5 and 16.5 days of gestation) were transplanted singly or in combination into the third ventricle of adult female rats, and the development of neurons in the grafts was investigated immunohistochemically with the use of antisera to tyrosine hydroxylase (TH), somatostatin (SRIH), ACTH, methionine enkephalin-Arg6-Gly7-Leu8 (Enk-8), rat corticotropin-releasing factor (rCRF), rat hypothalamic growth hormone-releasing factor (rhGRF), and luteinizing hormone-releasing hormone (LHRH). TH and all the peptides examined except LHRH were detected in distinct neurons in MBH grafts and in cografts of MBH plus Rathke's pouch from 12.5-day-old embryos. SRIH, rCRF, Enk-8, and TH were found in POA grafts from embryos of the same age. Although immunoreactive LHRH was first detected in neurons in POA grafts from 16.5-day-old embryos, it appeared in cografts of POA and MBH from 12.5-day-old embryos. The immunoreactive fibers developed in the grafts expressed the same characteristic behaviors as in intact brain; the fibers containing hormonal substances formed complexes with the vasculature like in the organum vasculosum laminae terminalis (OVLT) or in the median eminence, while the fibers containing neurotropic signals formed fiber networks surrounding other nerve cell bodies as if they synaptically associate. In CC grafts, the neurons contained TH, SRIH, rCRF, or Enk-8, and their axonal processes formed fiber networks. These findings suggest that all the hypothalamic neurons examined are committed by 12.5 days of gestation to develop maintaining transmitter phenotype and target recognition capacity.
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PMID:Development of hypothalamic neurons in intraventricular grafts: expression of specific transmitter phenotypes. 289 28

Double immunolabelling on semithin sections revealed glutamate decarboxylase immunopositive dots surrounding somatostatin-containing cell sections in the rat periventricular hypothalamic area. Up to 12 appositions were observed per cell section with an average number of 2-3 and a unimodal distribution. At the electron microscopical level pre-embedding staining of glutamate decarboxylase showed that most immunoreactive elements consisted of immunolabelled axonal endings. Most of these glutamate decarboxylase immunopositive boutons were found within the neuropil where they frequently made synapses on unidentified dendrites. Some of them were apposed to somatostatin-containing cell bodies that were identified according to the presence of immunolabelled granules using combined immunogold post-embedding staining. In many instances glutamate decarboxylase immunoreactive endings were also found to be involved in synaptic contact with somatostatin-labelled perikarya, or neuronal processes. These contacts provide the morphological basis for a direct GABAergic control of the somatostatin-containing cells regulating the secretion of growth hormone.
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PMID:GABAergic innervation of somatostatin-containing neurosecretory cells of the anterior periventricular hypothalamic area: a light and electron microscopy double immunolabelling study. 289 59

Immunohistochemical and axonal transport methods were used to chart the distribution of somatostatin-immunoreactive (SS-IR) fibres in the paraventricular (PVH) and supraoptic (SO) nuclei of the rat hypothalamus and to identify the cell group(s) from which they originate. Fibres and varicosities immunoreactive for SS-28 and/or SS-281-12 are found primarily in the parvocellular division of the PVH, though aspects of the magnocellular division, and of the SO, in which oxytocinergic neurons are clustered also receive moderate inputs. Combined retrograde transport-immunohistochemical studies indicated that these arise principally from non-catecholaminergic neurons in the lateral aspect of the commissural part of the nucleus of the solitary tract (NTS). SS-28 has been shown to act within the central nervous system to elicit both oxytocin and vasopressin secretory responses, and may be involved in mediating vasopressin secretory responses to haemorrhage. Direct SS-28-IR inputs to the magnocellular cell groups from the NTS, which receives primary visceral sensory inputs, are in a position to play a role in mediating oxytocin secretory responses to interoceptive stimuli; the pathway(s) and mechanism(s) which allow SS-28 to interact with vasopressinergic neurons are not clear.
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PMID:Somatostatin 28-immunoreactive inputs to the paraventricular and supraoptic nuclei: principal origin from non-aminergic neurons in the nucleus of the solitary tract. 290 91

The morphological substrate for the central mechanisms that control growth hormone (GH) release in the rat hypothalamus was investigated immunohistochemically by light and electron microscopy. In electron-microscopic studies, a dual immunolabeling technique was employed to demonstrate pairs of peptides, i.e. rat hypothalamic growth hormone-releasing factor (rhGRF) and somatostatin (SRIH), rhGRF and substance P (SP), and rhGRF and methionine-enkephalin-Arg6-Gly7-Leu8 (Enk-8), in different neuronal structures. Immunoreactivity of rhGRF was detected as silver-gold particles and those of the other substances as diaminobenzidine products by preembedding immunostaining procedures. In the external layer of the median eminence, axonal terminals immunolabeled for rhGRF and for SRIH showed the same pattern of distribution and close proximity. The neuronal inputs to GRF cell bodies in the arcuate nucleus were examined, and SRIH, SP and Enk-8 fibers with varicosities were found to form dense networks around the perikarya of GRF neurons, suggesting the presence of synaptic associations. Axonal terminals immunolabeled for SRIH, SP or Enk-8, and unlabeled terminals appeared to form coincidental synaptic junctions on GRF perikarya. These findings suggest that the central regulation of GH release occurs at the levels of the median eminence and the cell bodies.
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PMID:Ultrastructural evidence for neuronal regulation of growth hormone secretion. 313 6

Microscopic studies have shown the saccopleural membrane in the respiratory system of the domestic fowl to consist of a sheet of three dense layers of collagen fibres covered dorsally and ventrally by mainly simple squamous epithelium. On the ventral surface, which faces into the caudal thoracic air sac, there are occasional ridges of pseudostratified ciliated epithelium. Many nerve bundles are present throughout the membrane, the larger bundles of myelinated and unmyelinated axons being confined to the lamina propria under the dorsal epithelium (parietal pleura). In addition to axonal profiles with the ultrastructural appearance of cholinergic or adrenergic axons, peptidergic-type axons were identified. Immunofluorescence studies demonstrated VIP-, substance P-, somatostatin- and enkephalin-immunoreactive fibres in the membrane. Although it has been suggested that receptors may be present in this region of the respiratory system, none of the axons have features suggestive of sensory terminals, although many axonal profiles are closely associated with the epithelia where no obvious effector cells are present.
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PMID:The structure and innervation of the saccopleural membrane of the domestic fowl, Gallus gallus: an ultrastructural and immunohistochemical study. 365 25

The lateral bed nucleus of the stria terminalis (BSTL) and central nucleus of the amygdala (Ce) are amygdaloid nuclei that have similar afferent and efferent connections within the brain. Previous studies have demonstrated that both regions send axonal projections to the dorsal vagal complex (dorsal motor nucleus and nucleus tractus solitarii). The present study used the combined retrograde fluorescence-immunofluorescence method to examine whether cells contributing to this pathway contained any of the following neuropeptides: corticotropin-releasing factor, neurotensin, somatostatin, substance P, enkephalin, or galanin. The inputs to the dorsal vagal complex originated mainly from ventral BSTL and medial Ce, although a significant number of neurons within the dorsal BSTL and lateral Ce also contributed. Corticotropin-releasing factor, neurotensin, and somatostatin neurons mainly located within the dorsal BSTL and the lateral Ce contained retrograde tracer after injections into the vagal complex. Substance P neurons in the ventral BSTL and medial Ce provide a sparse input to the dorsal vagal complex. Enkephalin and galanin neurons within the BSTL and Ce did not appear to project to the dorsal vagal complex. Corticotropin-releasing factor and neurotensin neurons within the lateral hypothalamus also project to the dorsal vagal complex. Approximately 22% of the Ce and 15% of the BSTL retrogradely labeled neurons were peptide immunoreactive. Thus, it is concluded the Ce and BSTL are sources of a significant peptidergic pathway to the dorsal vagal complex. However, it is also apparent that the majority of putative transmitter types within the amygdaloid vagal projection still are unknown. The results suggest that the dorsal and ventral BSTL and the lateral and medial Ce, respectively, are homologous zones with regard to chemoarchitecture and connections. The data is discussed considering the possible function of peptides within descending amygdaloid pathways to the brainstem.
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PMID:Neuropeptide neuronal efferents from the bed nucleus of the stria terminalis and central amygdaloid nucleus to the dorsal vagal complex in the rat. 365 18


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