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)

A depletion of large cholinergic neurons in the nucleus basalis of Meynert is a consistent finding in Alzheimer's disease (AD). The nucleus basalis of Meynert also contains interneurons and afferents that may modulate its functioning. In the present study we examined neurochemical markers for neuropeptides, amino acid neurotransmitters, and monoaminergic neurotransmitters in postmortem samples of the nucleus basalis in 16 control subjects and 30 patients with AD. There were no significant changes in glutamate, aspartate, taurine, gamma-aminobutyric acid (GABA), and catecholamines; however, concentrations of serotonin, 5-hydroxyindoleacetic acid, and 5-hydroxytryptophol were significantly reduced. Choline acetyltransferase activity was significantly reduced, consistent with previous reports. Galanin immunoreactivity was significantly increased twofold in the patients with AD, but there were no significant changes in substance P, somatostatin, or neuropeptide Y immunoreactivity. Since galanin inhibits acetylcholine release, and produces cognitive deficits in animals, increased galanin immunoreactivity in the nucleus basalis of Meynert in AD may contribute to the cognitive deficits that characterize the illness.
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PMID:Galanin immunoreactivity is increased in the nucleus basalis of Meynert in Alzheimer's disease. 169 71

In the mammalian cerebral cortex, neurons destined for layers 2-6 are generated only after the period of genesis for a group of transient neurons that populate the subplate and marginal zones. Although a number of molecular markers for the subplate zone exist, most are also expressed by other cell populations in the cortical plate. To begin to study molecular properties of the subplate, we generated monoclonal antibodies against homogenates of cat cortical subplate zone. One monoclonal antibody, termed subplate 1 (SP1), recognized a polypeptide of 56 kDa. This antigen was strongly expressed within the subplate neurons only during a 3-week period beginning at birth and extending until 3 weeks after birth. From postnatal day 1, the number of SP1-immunoreactive neurons below the visual cortex increased until the end of second postnatal week and then declined thereafter. This period coincides with the period when a majority of the subplate neurons undergo naturally occurring cell death. The antigen was not expressed by subplate neurons surviving in the adult white matter. At the peak of antigen expression, 14% or less of the immunoreactive neurons also coexpressed gamma-aminobutyric acid, somatostatin, or neuropeptide Y. Biochemical and immunocytochemical properties of the SP1 antigen were also compared with the Alz-50 antigen (A68), a marker for dying neurons. On Western blots, SP1- and Alz-50-reactive polypeptides were selectively enriched in cytosolic fractions of kitten cerebral cortex, but each marker recognized different molecular weight polypeptides. In tissue sections many subplate, cortical plate, and layer 1 neurons were Alz-50 immunoreactive. In contrast, a rarer subpopulation of neurons restricted to the subplate was labeled by SP1. We propose that the SP1 antigen is a protein expressed within dying cortical subplate neurons, at the commencement of cell death.
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PMID:Expression of a unique 56-kDa polypeptide by neurons in the subplate zone of the developing cerebral cortex. 170 94

Areas 20, 21 and 22 of the temporal neocortex of the macaque monkey (Macaca fascicularis) were studied with immunocytochemical and electron-microscopic techniques to localise neurons immunoreactive to the neuropeptides vasoactive intestinal polypeptide, substance P and somatostatin, and to gamma-aminobutyric acid (GABA). GABAergic neurons were found in all cortical layers, but especially in layers II, IV and VI. They were all of non-pyramidal morphology, comprising small round cells, and bipolar or multipolar forms. Presumed GABAergic axon terminals were also common. Peptidergic neurons were also found in all layers, but they consisted of cells of many morphological types, including pyramidal cells. Compared with previous descriptions in other cortical areas and in other animals, we find a greater proportion of peptidergic temporal cortical neurons compared to the GABAergic population. The immunopositive neurons were easily recognisable ultrastructurally from non-reactive neurons by the dense labelling of the cytoplasm and nucleus. Immunopositive and negative neuronal somata were often contiguous, providing evidence for the specificity of the immune reaction. Stem dendrites were often labelled for a short distance from the soma, and other strongly reacting dendritic segments were found in the neuropil, as were labelled axons. Neurons labelled for GABA had features typical of non-pyramidal cells, but neuropeptides were also found in cells with pyramidal characteristics.
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PMID:Pyramidal neurons are immunopositive for peptides, but not GABA, in the temporal cortex of the macaque monkey (Macaca fascicularis). 170 16

Antibodies were used to identify neurons in human frontal and temporal cortex that were immuno-positive to gamma-aminobutyric acid (GABA) and the neuropeptides vasoactive intestinal polypeptide (VIP), substance P (SP) and somatostatin (SOM). Specimens were taken at surgical biopsy and fixed immediately after removal. The results described for both light and electron microscopy were obtained when relatively high concentrations of glutaraldehyde (2.5-3%) were present in the fixative. Specimens were examined from three adults and an infant aged 5 months. GABAergic neurons were present in all cortical layers, with fewest in layers I, deep III and V, and were mainly small, and round or oval. No labelled pyramidal neurons were detected. GABAergic puncta were common in the neuropil, probably representing axonal profiles. VIP-neurons were also found in all layers, including layer I, and were approximately twice as numerous as GABA-cells. SP-positive cells were found throughout the layers, but were sparse in layers I and VI. They were about three times commoner than GABAergic neurons. SOM-reactivity was demonstrated in about the same number of cells as that for SP. Again, this involved all layers, but layer I least. Peptidergic neurons were larger, on the average, than GABAergic cells, and were frequently pyramidal in character. In the infant, the distribution, size and frequency of immunoreactive neurons were similar to those in the adult. However, GABAergic puncta were commoner.
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PMID:Distribution of GABA and neuropeptides in the human cerebral cortex. A light and electron microscopic study. 171 55

This study deals with the synaptology, morphologically identified postsynaptic targets, and origin of somatostatin (SOM) fibers in the rat lateral septal area (LSA) with special reference to those forming pericellular baskets. Septal vibratome sections were immunostained for SOM-14 in 3 experimental groups: control animals, rats subjected to a chronic transection of the ascending afferents to the septum, and animals with acute fimbria-fornix lesion. Light microscopy revealed that the SOM-immunoreactive fibers form pericellular baskets predominantly in the intermediate and ventral parts of the caudal half of the LSA. Electron microscopic analysis showed that the somatospiny neurons are postsynaptic targets of these pericellular baskets. Eight days after a unilateral cut placed at the ventral border of the septum, virtually all SOM-immunoreactive axon terminals disappeared from the ipsilateral intermediate and ventral LSA, and they were substantially reduced in the dorsal LSA. However, in these rats SOM-positive neurons could be observed in the LSA on the lesioned, but not on the contralateral side. Furthermore, on the lesion side of the anterior periventricular hypothalamus an increase was detected both in the number and the intensity of immunostaining of SOM-positive neurons. Thirty-six h following a unilateral transection of the fimbria-fornix, the SOM-immunoreactive axon terminals in the LSA remained intact; only immunonegative degenerated hippocamposeptal boutons were detected forming synaptic contacts with somatospiny neurons. Axosomatic synapses of SOM-positive boutons regularly appeared at the neck of somatic spines which were postsynaptic to degenerated hippocamposeptal fibers. The results indicate that the septal SOM fibers are of multiple origin. Those forming pericellular baskets in the LSA originate in ventral extraseptal, probably periventricular hypothalamic areas. SOM fibers scattered in the dorsal LSA are most likely processes of local SOM neurons. The accumulation of immunoreactive SOM in some cells of the undercut septum is a sign of axonal lesion, indicating that these neurons project outside the septum. The SOM innervation of somatospiny neurons which also receive hippocampal input and have been reported to contain gamma-aminobutyric acid (GABA) may be a morphological substrate of the SOM-related disinhibition in the LSA.
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PMID:Synaptology and origin of somatostatin fibers in the rat lateral septal area: convergent somatostatinergic and hippocampal inputs of somatospiny neurons. 172 20

The basal forebrain-neocortex pathway--involved in higher cognitive processing, selective attention, and arousal--is considered one of the functionally most important ascending subcortical projections. The mechanism by which this relatively sparse subcortical pathway can control neuronal activity patterns in the entire cortical mantle is still unknown. The present study in the cat provides evidence that gamma-aminobutyric acid-containing basal forebrain neurons participate in the neocortical projection and establish multiple synaptic connections with gamma-aminobutyric acid-releasing interneurons containing somatostatin or parvalbumin. We propose that a mechanism by which the numerically small ascending pathways can exert a powerful global effect in the neocortex is by the selective innervation of gamma-aminobutyric acid-releasing interneurons, which, in turn, control the activity of large populations of pyramidal cells through their extensive axon arborizations. Finally, these results demonstrate a direct anatomical link between two cell populations implicated in Alzheimer disease pathology: basal forebrain neurons and cortical somatostatin cells.
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PMID:gamma-Aminobutyric acid-containing basal forebrain neurons innervate inhibitory interneurons in the neocortex. 173 48

Several neurologic illnesses in which excitotoxic mechanisms may play a role increase in prevalence with age. In the present study we examined the susceptibility of rats to quinolinic acid striatal lesions at 1, 4 and 20 months of age, and susceptibility to N-methyl-D-aspartate (NMDA) at 1 and 4 months of age. The extent of the lesions was quantitated with measurements of substance P-like immunoreactivity (SPLI) and gamma-aminobutyric acid (GABA). The lesions in the 4- and 20-month-old age groups showed significantly smaller depletions of SPLI and GABA than those in 1-month-old animals. Neuropeptide Y-like immunoreactivity (NPYLI) and somatostatin-like immunoreactivity (SLI) were unchanged in the lesioned striata. NMDA lesions were also attenuated in 4-month- and 12-month-old animals as compared with 1-month-old animals. Uric acid concentrations showed marked dose-dependent increases in the lesioned striatum, and to a lesser extent in the overlying cerebral cortex, in all 3 age groups. There were no changes of SLI, NPYLI or SPLI with aging in the cerebral cortex or hippocampus. Kynurenine and kynurenic acid concentrations showed significant increases with aging in frontal cortex. The present results show a reduced susceptibility of animals to striatal quinolinic acid and NMDA lesions with normal aging. The delayed onset of several neurodegenerative illnesses is therefore unlikely to be due to an increasing susceptibility to excitotoxin lesions with aging.
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PMID:Effects of aging on quinolinic acid lesions in rat striatum. 183 50

Evidence supports the idea that somatostatin (SO) is a neurotransmitter or neuromodulator of primary afferent neurons involved in nociception. Since gamma-aminobutyric acid (GABA), norepinephrine, and morphine alter nociception at the level of the spinal cord, we examined whether these agents could alter the potassium-stimulated release of somatostatin from rat spinal cord slices. Male Sprague-Dawley rats were decapitated and a 2 cm segment of the lumbar spinal cord removed and chopped into 0.5 x 0.5 mm pieces and perfused at 37 degrees C in individual perfusion chambers with a modified Krebs-bicarbonate buffer at a flow rate of 0.5 ml/min. Perfusates were collected at 2 min intervals and assayed for SO using radioimmunoassay. Exposure of spinal cord tissue to 50 mM KCl resulted in a 3-fold increase in release of SO from a basal level of approximately 0.2 to 0.6 pg/mg tissue/min. This evoked release was calcium dependent. Pre-exposure of tissue to GABA at 10(-4) and 10(-5) M significantly inhibited the potassium-stimulated release of SO, but did not alter basal release. The GABA receptor antagonist, bicuculline methiodide, at 10(-5) but not 10(-6) M attenuated the GABA-induced inhibition of somatostatin release. Bicuculline methiodide alone did not significantly alter either basal or stimulated release. Neither baclofen (10(-5) M, 5 x 10(-5) M), norepinephrine (10(-5) M), nor morphine (10(-5) M) had any significant effect on basal or stimulated release of SO from spinal cord tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:gamma-Aminobutyric acid inhibits the potassium-stimulated release of somatostatin from rat spinal cord slices. 196 72

Immunoreactive somatostatin (IR-SRIF) and gamma-aminobutyric acid (GABA) contents in the rat brain were investigated to study chronic effects of the treatment with anticonvulsants, carbamazepine (CBZ), valproic acid (VPA) and phenytoin (PHT). Decreased IR-SRIF levels were found in several brain regions after chronic treatment with VPA and CBZ. GABA concentrations were found to be increased significantly in chronic CBZ and VPA treatment in the rat brain, especially in limbic structures. PHT had no effect on both IR-SRIF and GABA contents in the rat brain. Effects of several GABA-mimetic drugs also were studied on IR-SRIF contents in the rat brain. Aminooxyacetic acid an inhibitor of GABA transaminase, induced a decrease in IR-SRIF concentration in the pyriform and entorhinal cortex, whereas ethanolamine-o-sulfate, another GABA-transaminase inhibitor and muscimol, a GABA receptor agonist had no effect on brain IR-SRIF after acute administration. The present results suggest that endogenous somatostatin has an important role for anticonvulsant properties of CBZ and VPA, but not of PHT. The relationship between the changes in IR-SRIF and the GABA transmitter system in the anticonvulsant action of CBZ and VPA remains to be clarified.
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PMID:Effects of anticonvulsants and gamma-aminobutyric acid (GABA)-mimetic drugs on immunoreactive somatostatin and GABA contents in the rat brain. 197 58

In the present study we investigated the relative vulnerability of neuronal subsets in the striatum to ischemia that was induced by bilateral transient ligation of the common carotid arteries in gerbils. After 4 days of survival, brains were evaluated using histochemical methods (NADPH-diaphorase and silver degeneration procedures) and neurochemical methods with radioimmunoassays for somatostatin-, neuropeptide Y-, and substance P-like immunoreactivity and measurements of amino acids using high-pressure liquid chromatography with electrochemical detection. NADPH-diaphorase-positive neurons were strikingly preserved in the ischemic dorsolateral portion of the striatum, in which there was severe neuronal loss. There was no significant depletion of NADPH-diaphorase-positive neurons in the striatum or cerebral cortex. Concentrations of neuropeptide Y-like and somatostatin-like immunoreactivity were unchanged despite a significant 25% depletion of substance P-like immunoreactivity and gamma-aminobutyric acid. Ischemic brain damage may be mediated by a neurotoxic effect of glutamate acting at the N-methyl-D-aspartate (NMDA) receptor. Previous studies of NMDA excitotoxin lesions in rat striatum have shown a sparing of neurons containing NADPH-diaphorase, somatostatin, and neuropeptide Y. The similar sparing of these neurons following ischemic lesions in gerbil striatum provides further evidence that NMDA receptor activation may play a role in ischemic injury.
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PMID:Selective sparing of NADPH-diaphorase-somatostatin-neuropeptide Y neurons in ischemic gerbil striatum. 197 76


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