UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin (SS)-containing perikarya located within the hypothalamic periventricular nucleus (PeVN) comprise a heterogenous population of neurons with both local intrahypothalamic and distant extrahypothalamic axonal projection sites. The close proximity of SS perikarya and their dendrites to dopaminergic (DA) neuronal processes in the PeVN suggests that these peptidergic neurons may be regulated by DA receptor-mediated mechanisms. To test this, the effects of the D1 agonist SKF 38393 and D2/3 agonist quinelorane were examined on expression of the immediate early gene products Fos and its related antigens (FRA) in SS-immunoreactive (IR) neurons in the PeVN. SS-IR neurons were located in the most medial portion of the PeVN bordered medially by the third ventricle and laterally by tyrosine hydroxylase (TH)-IR neurons. In control rats, 10-15% of all SS-IR neurons contained FRA-IR. Activation of D1 receptors with SKF 38393 had no effect on either the total number of SS-IR neurons or the number of SS-IR neurons containing FRA-IR. In contrast, activation of D2/3 receptors with quinelorane decreased the number of SS-IR neurons containing FRA-IR, without affecting the total number of SS-IR neurons. The D2/3 antagonist raclopride had no effect per se, but prevented the quinelorane-induced decrease in the number of SS neurons expressing FRA-IR. These results reveal that activation of D2/3 (but not D1) receptors inhibits expression of the immediate early gene products FRA in SS-containing neurons in the PeVN, but expression of FRA in SS neurons is not tonically inhibited by dopamine acting on D2/3 receptors.
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PMID:Dopamine receptor-mediated regulation of expression of Fos and its related antigens (FRA) in somatostatin neurons in the hypothalamic periventricular nucleus. 937 17

In previous studies m2 muscarinic acetylcholine receptor-immunoreactive interneurons and various types of m2-positive axon terminals have been described in the hippocampal formation. The aim of the present study was to identify the types of interneurons expressing m2 receptor and to examine whether the somadendritic and axonal m2 immunostaining labels the same or distinct cell populations. In the CA1 subfield, neurons immunoreactive for m2 have horizontal dendrites, they are located at the stratum oriens/alveus border and have an axon that project to the dendritic region of pyramidal cells. In the CA3 subfield and the hilus, m2-positive neurons are multipolar and are scattered in all layers except stratum lacunosum-moleculare. In stratum pyramidale of the CA1 and CA3 regions, striking axon terminal staining for m2 was observed, surrounding the somata and axon initial segments of pyramidal cells in a basket-like manner. The co-localization of m2 with neurochemical markers and GABA was studied using the "mirror" technique and fluorescent double-immunostaining at the light microscopic level and with double-labelling using colloidal gold-conjugated antisera and immunoperoxidase reaction (diaminobenzidine) at the electron microscopic level. GABA was shown to be present in the somata of most m2-immunoreactive interneurons, as well as in the majority of m2-positive terminals in all layers. The calcium-binding protein parvalbumin was absent from practically all m2-immunoreactive cell bodies and dendrites. In contrast, many of the terminals synapsing on pyramidal cell somata and axon initial segments co-localized parvalbumin and m2, suggesting a differential distribution of m2 receptor immunoreactivity on the axonal and somadendritic membrane of parvalbumin-containing basket and axo-axonic cells. The co-existence of m2 receptors with the calcium-binding protein calbindin and the neuropeptides cholecystokinin and vasoactive intestinal polypeptide was rare throughout the hippocampal formation. Only calretinin and somatostatin showed an appreciable degree of co-localization with m2 (20% and 15%, respectively). Using retrograde tracing, some of the m2-positive cells in stratum oriens were shown to project to the medial septum, accouting for 38% of all projection neurons. The present results demonstrate that there is a differential distribution of m2 receptor immunoreactivity on the axonal vs the somadendritic membranes of distinct interneuron types and suggest that acetylcholine via m2 receptors may reduce GABA release presynaptically from the terminals of perisomatic inhibitory cells, while it may act to increase the activity of another class of interneuron, which innervates the dendritic region of pyramidal cells.
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PMID:Distinct interneuron types express m2 muscarinic receptor immunoreactivity on their dendrites or axon terminals in the hippocampus. 946 48

Analysis of the connectivity between different neuronal cell types is dependent on an appreciation of their dendritic and axonal arborizations. A detailed study of the dendrites and axons of GABAergic neurons has been thwarted by the lack of a suitable technique for enhancing GABA immunoreactivity. This article describes a procedure using tetanus toxin which, when applied to organotypic hippocampal cultures, considerably enhances the immunoreactivity in the dendrites and axons of the GABA- and somatostatin-containing neurons and clearly demonstrates the co-localization of GABA and somatostatin immunoreactivities in the same neuron. Tetanus toxin was applied to the culture medium on Day 14 for a 24-hr period and the cultures were fixed at the end of Day 18. Tetanus toxin-treated cultures (n = 30) or untreated cultures (n = 40) were incubated for either GABA or somatostatin immunoreactivity. Tetanus toxin-treated cultures used for co-localization studies (n = 20) were incubated for both GABA and somatostatin immunoreactivity.
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PMID:Tetanus toxin-enhanced GABA immunoreactivity in living neurons. 948 13

Physiological and morphological properties of large non-pyramidal cells immunoreactive for cholecystokinin, parvalbumin or somatostatin were investigated in vitro in the frontal cortex of 18-22-day-old rats. These three peptides were expressed in separate populations including large cells. Cholecystokinin cells and parvalbumin cells made boutons apposed to other cell bodies, but differed in their firing patterns in response to depolarizing current pulses. Parvalbumin cells belonged to fast-spiking cells. Parvalbumin fast-spiking cells also included chandelier cells. In contrast, cholecystokinin cells were found to be regular-spiking non-pyramidal cells or burst-spiking non-pyramidal cells with bursting activity from hyperpolarized potentials (two or more spikes on slow depolarizing humps). Large somatostatin cells belonged to the regular-spiking non-pyramidal category and featured wide or ascending axonal arbors (wide arbor cells and Martinotti cells) which did not seem to be apposed to the somata so frequently as large cholecystokinin and parvalbumin cells. For electron microscopic observations, another population of eight immunohistochemically-uncharacterized non-pyramidal cells were selected: (i) five fast spiking cells including one chandelier cell which are supposed to contain parvalbumin, and (ii) three large regular-spiking non-pyramidal cells with terminals apposed to somata, which are not considered to include somatostatin cells, but some of which may belong to cholecystokinin cells. The fast-spiking cells other than a chandelier cell and the large regular-spiking non-pyramidal cells made GABA-positive synapses on somata (4% and 12% of the synapses in two small to medium fast-spiking cells, 22% and 35% of the synapses in two large fast-spiking cells, and 10%, 18% and 37% of the synapses in three large regular-spiking non-pyramidal cells). A few terminals of the fast-spiking and regular-spiking non-pyramidal cells innervated GABAergic cells. About 30% of the fast-spiking cell terminals innervated spines, but few of the regular-spiking non-pyramidal cell terminals did. A fast-spiking chandelier cell made GABA-positive synapses on GABA-negative axon initial segments. These results suggest that large GABAergic cells are heterogeneous in neuroactive substances, firing patterns and synaptic connections, and that cortical cells receive heterogeneous GABAergic somatic inputs.
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PMID:Neurochemical features and synaptic connections of large physiologically-identified GABAergic cells in the rat frontal cortex. 963 65

The release of serotonin may occur throughout the sleep-wake cycle according to 2 different modalities: - by the axonal nerve endings during waking; - by the dendrites and/or the soma of the nucleus raphe dorsalis (nRD) during sleep. Neuronal nitric oxide (NO), synthesised by constitutive NO synthase (NOS), is colocalized with neurotransmitters such as GABA, acetylcholine, somatostatin, serotonin, etc. In order to evaluate its modalities of release throughout the rat sleep-wake cycle, a sensor allowing its specific detection in freely moving animals was prepared. In the cortex, the highest NO signal occurs during the waking state (W=100%) versus slow wave sleep (SWS=-6%) and paradoxical sleep (PS=-9%). The mild variations observed might reflect a mean of the individual sleep-wake cycle variations attached to each NO source (GABAergic interneurons, cholinergic and serotoninergic axonal nerve endings, etc.).
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PMID:5-Hydroxyindoles compounds and nitric oxide voltammetric detection in the rat brain: changes occurring throughout the sleep-wake cycle. 966 98

Subplate neurons, the first neurons of the cerebral cortex to differentiate and mature, are thought to be essential for the formation of connections between thalamus and cortex, such as the system of ocular dominance columns within layer 4 of visual cortex. To learn more about the requirement for subplate neurons in the formation of thalamocortical connections, we have sought to identify the neurotransmitters and peptides expressed by the specific class of subplate neurons that sends axonal projections into the overlying visual cortex. To label retrogradely subplate neurons, fluorescent latex microspheres were injected into primary visual cortex of postnatal day 28 ferrets, just prior to the onset of ocular dominance column formation. Subsequently, neurons were immunostained with antibodies against glutamate, glutamic acid decarboxylase (GAD-67), parvalbumin, neuropeptide Y (NPY), somatostatin (SRIF), or nitric oxide synthase (NOS). Retrograde labeling results indicate that the majority of subplate neurons projecting into the cortical plate reside in the upper half of the subplate. Combined immunostaining and microsphere labeling reveal that about half of cortically projecting subplate neurons are glutamatergic; most microsphere-labeled subplate neurons do not stain for GAD-67, parvalbumin, NPY, SRIF, or NOS. These observations suggest that subplate neurons can provide a significant glutamatergic synaptic input to the cortical plate, including the neurons of layer 4. If so, excitation from the axons of subplate neurons may be required in addition to that from lateral geniculate nucleus neurons for the activity-dependent synaptic interactions that lead to the formation of ocular dominance columns during development.
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PMID:Major glutamatergic projection from subplate into visual cortex during development. 970 30

Noradrenaline (NA) from the locus coeruleus and GABA from intracortical nonpyramidal cells exert strong influences on cortical activity. To assess possible interaction between the two, the effects of noradrenergic agonists on spontaneous GABAergic IPSCs as well as on the activity of identified GABAergic cell types were investigated by in vitro whole-cell recordings from the frontal cortex of 18- to 22-d-old rats. NA (3-50 microM) and an alpha-adrenergic agonist, 6-fluoronorepinephrine (FNE; 30-50 microM), induced an increase of IPSC frequency in pyramidal cells, but a beta-adrenergic agonist did not. This increase was reduced by tetrodotoxin, bicuculline, and alpha-adrenergic antagonists, suggesting that GABAergic cells are excited via alpha-adrenoceptors. Fast-spiking or late-spiking cells were depolarized by application of NA or FNE, but none demonstrated spike firings. The former morphologically included common multipolar cells with extended axonal arborizations as well as chandelier cells, and the latter neurogliaform cells. Most somatostatin-immunoreactive regular or burst-spiking cells, including Martinotti cells and wide arbor cells, were depolarized and accompanied by spike firing. In a few cases this was preceded by hyperpolarization. Cholecystokinin-immunoreactive regular or burst-spiking nonpyramidal cells, including large basket cells, were affected heterogeneously: depolarization, hyperpolarization followed by depolarization, or hyperpolarization resulted. The findings suggest that, similar to the effects of acetylcholine, the excitability of cortical GABAergic cell types is differentially regulated by NA and that NA actions are similar to cholinergic ones in some GABAergic cell types but not in others.
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PMID:Noradrenergic excitation and inhibition of GABAergic cell types in rat frontal cortex. 971 65

Most of the smaller diameter neurons of dorsal root and trigeminal ganglia in adult rats expressed latexin, which has the inhibitor activity of carboxypeptidase A. Most of the dorsal root ganglion (DRG) neurons containing either calcitonin gene-related peptide (CGRP), substance P (SP) or somatostatin (SST) coexpressed latexin. Latexin was widely distributed in the cytoplasm of the cell body and in axonal fibers of cultured DRG neurons which were sensitive to capsaicin. In addition, latexin-immunoreactivity was observed throughout lamina II of the spinal cord in normal animals, but was lost following sciatic nerve-axotomy, suggesting the presence of latexin-immunoreactive axonal fibers and/or terminals from DRG neurons. Immunoelectron microscopy indeed revealed latexin-immunoreactive axonal terminals and thinly myelinated and unmyelinated axonal fibers within the dorsal horn. These observations suggest that latexin may be involved in nociceptive information transmission or its modulation.
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PMID:Latexin expression in smaller diameter primary sensory neurons in the rat. 972 42

Previous studies have shown that experimentally induced lysosomal dysfunction elicits various features of aging in the cortical telencephalon. The present study used cultured slices to test if: (1) it causes similar changes in the hypothalamus, and/or (2) modifies the processing of two releasing factors important to aging. A 2-day exposure to N-CBZ-L-phenylalanyl-L-alanine-diazomethylketone (ZPAD), a selective inhibitor of cathepsins B and L, triggered a pronounced increase in the numbers of lysosomes in the ventromedial and dorsomedial nuclei, and in lateral hypothalamus. Continued incubation with the inhibitor for 3-12 days resulted in the spread of endosomes-lysosomes into dendrites and, in the lateral hypothalamus, the formation of massive, lysosome-filled expansions of neuronal processes (meganeurites). These effects did not occur in the arcuate nucleus, making it the first region so far examined in which lysosomal proliferation is not initiated by hydrolase inhibitors. Despite this, a dense plexus of axons and terminals in the median eminence was partially depleted of growth hormone releasing hormone (GHRH) within 48 hours after addition of ZPAD. Moreover, the inhibitor caused axonal GHRH to become collected into large puncta, an effect highly suggestive of a partial failure in axonal transport. GHRH mRNA levels were not greatly affected by 6 days of ZPAD exposure, indicating that reduced expression did not play a major role in the peptide changes seen at 48 hours. Similar but less pronounced immunocytochemical changes were recorded for the somatostatin system in the arcuate and periventricular nucleus. It is concluded that lysosome dysfunction: (1) has different consequences for the arcuate nucleus than other brain regions, and (2) disrupts transport of hypothalamic releasing factors. The potential significance of the results to endocrine senescence is discussed.
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PMID:Experimentally induced lysosomal dysfunction disrupts processing of hypothalamic releasing factors. 981 Nov 15

Nerve circuits within the proximal duodenum were investigated using a combination of immunohistochemistry for individual neuron markers and lesion of intrinsic nerve pathways to determine axon projections. Cell shapes and axonal projections were also studied in cells that had been injected with a marker substance. Several major neuron populations were identified. Calbindin immunoreactivity occurred in a population of myenteric nerve cells with Dogiel type II morphology. These had axons that projected to other myenteric ganglia, to the circular muscle and to the mucosa. All were immunoreactive for the synthesizing enzyme for acetylcholine, choline acetyltransferase, and some were also immunoreactive for calretinin. Myenteric neurons with nitric oxide synthase immunoreactivity projected anally to the circular muscle. These were also immunoreactive for vasoactive intestinal peptide, and proportions of them had enkephalin and/or neuropeptide Y immunoreactivity. It is suggested that they are inhibitory motor neurons to the circular muscle. A very few (about 2%) of nitric oxide synthase-immunoreactive neurons had choline acetyltransferase immunoreactivity. Tachykinin (substance P)-immunoreactive nerve cells were numerous in the myenteric plexus. Some of these projected orally to the circular muscle and are concluded to be excitatory motor neurons. Others projected to the tertiary plexus which innervates the longitudinal muscle and others provided terminals in the myenteric plexus. Two groups of descending interneurons were identified, one with somatostatin immunoreactivity and one with vasoactive intestinal peptide immunoreactivity. The two most common nerve cells in submucous ganglia were neuropeptide Y- and vasoactive intestinal peptide-immunoreactive nerve cells. Both provided innervation of the mucosa. There was also a population of calretinin-immunoreactive submucous neurons that innervated the mucosal glands, but not the villi. Comparison with the ileum reveals similarities in the chemistries and projections of neurons. Differences include the almost complete absence of nitric oxide synthase immunoreactivity from vasoactive intestinal peptide-immunoreactive interneurons in the duodenum, the projection of calbindin-immunoreactive Dogiel type II neurons to the circular muscle and the absence of tachykinin-immunoreactivity from these neurons.
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PMID:Morphological and immunohistochemical identification of neurons and their targets in the guinea-pig duodenum. 988 79

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