UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serotonin(2A) (5HT(2A)) receptors have been shown to play an important role in several psychiatric disorders, including depression, schizophrenia, and alcoholism. This immunohistochemical study examined the cellular localization of 5HT(2A) receptors in various rat brain structures (olfactory, striatum, cortex, hippocampus, and amygdala). The colocalization of 5HT(2A) receptors in astrocytes was performed by double-immunofluorescence staining of 5HT(2A) receptors and of glial fibrillary acidic protein (GFAP) using confocal laser microscopy. 5HT(2A) receptor immunolabeling was observed in olfactory bulbs, neostriatum, hippocampus, amygdala, and neocortex. Somata and dendrites of pyramidal cells in the frontal cortex (layer V) were densely labeled with 5HT(2A) receptors. In several other brain structures (hippocampus, amygdala, striatum, olfactory structures), 5HT(2A) receptor immunolabeling was found in cell bodies and processes of neurons. 5HT(2A) receptor immunolabeling was also observed in GFAP-positive cells of the various brain structures we investigated (layers I/VI of the neocortex, corpus callosum, hippocampal fissure and hilus, and amygdala). These results indicate that 5HT(2A) receptors are expressed in neurons and astrocytes and suggest the possibility that not only neuronal but also glial 5HT(2A) receptors have functional implications in psychiatric disorders.
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PMID:Cellular localization of serotonin(2A) (5HT(2A)) receptors in the rat brain. 1075 40

A prolonged period (48 h) of cortical spreading depression (CSD) induced resistance against severe focal cerebral ischemia (infarct tolerance), however, the mechanism behind this is unknown. The infarct tolerance was a transient phenomenon; the resistance increased linearly for the initial 12 days, peaking from 12 to 15 days after a preconditioning of CSD, and was decreased thereafter. This study examined the time course of brain-derived neurotrophic factor (BDNF), heat shock protein (hsp)27 and 70, and glial fibrillary acidic protein (GFAP) expressions after CSD in the brain. Immunohistochemical expression of BDNF, hsp27, hsp70, or GFAP following a prolonged period of CSD induced by KCl-infusion, or following NaCl-infusion was analyzed by regional densitometry for 24 days in the rat neocortex. In addition, BDNF protein was measured quantitatively by two-site ELISA assay in the neocortex (n=6 at each time point). The GFAP expression was elevated in astrocytes (compared to the normal level of immunodensity) during the period peaking on day 3-6 following the CSD. The hsp27 immunoreactivity was also elevated in astrocytes from day 1 to 12 peaking on day 1 and 6, but there was no expression of hsp70 during the period following CSD. The immunoreactivity for BDNF was elevated in neurons from day 0 to 18 peaking on day 1 and 6. The protein levels of BDNF in the neocortex were significantly elevated from day 0 to 12 peaking on days 0 and 6 (compared to the normal level) (P<0.05). Using a laser-scanning confocal imaging system, the BDNF-like immunoreactivity in neuronal nuclei was found to increase linearly peaking on day 12, which correlated well with the development of infarct tolerance. The intranuclear increase in BDNF-like protein might contribute to the induction of infarct tolerance in the brain.
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PMID:Infarct tolerance accompanied enhanced BDNF-like immunoreactivity in neuronal nuclei. 1098 48

The levels of autoantibodies and their anti-idiotypes to proteins of nervous tissue (S100b, GFAP, MP65 and nerve growth factor) were studied in 85 women of 18-48 years of age with psychogenic neurotic depressions. It was found that the changes of the levels of autoantibodies to the proteins of nervous tissue correspond to various somatoautonomic manifestations and correlate with severity of depression, its typological variations and duration of the disease. The data obtained show a close relationship between nervous and immune systems that was expressed by some parallelism of the dynamics of the changes of both neurotic depressive symptoms and serum immunoreactivity to neuroantigens.
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PMID:[The humoral immunity characteristics of women with neurotic depressions]. 1102 35

Brain infarction was induced in rats by injection of microspheres through the right internal carotid artery, and structural changes in the astrocytes were observed during the early period following the infarction. Necrotic foci, varying in size and shape, were found in the right hemisphere. After immunohistochemical staining for GFAP, GFAP-positive astrocytes in the perinecrotic area known as the ischemic penumbra had distinctly increased in number and size with elongation of cytoplasmic processes 3 days after infarction. Electron microscopic observation revealed that glycogen granules had markedly accumulated in the cytoplasm of astrocytes located in the ischemic penumbra 3 and 5 days after infarction. Seven days after infarction, however, the glycogen granules disappeared from the astrocytes. Intermediate filaments increasingly appeared in the protoplasmic astrocytes after 3 days and were abundant in the activated and hypertrophied astrocytes after 7 days. As a result of our present study, we conclude that: (1) the function of glucose uptake from blood vessels was not impaired in the astrocytes under hypoxic conditions; (2) the astrocytes actively ingested blood glucose through the endothelial cells and accumulated it as glycogen for activation of their functions, and the cell volume increased under hypoxic conditions; (3) the depression of energy metabolism and the decrease in the uptake of energy sources in the nerve cells promoted glycogen accumulation in the astrocytes under hypoxic conditions; (4) intermediate filaments (GFAP filaments) increased in number, coincident with the activation and enlargement of the astrocytes; and (5) protoplasmic astrocytes were transformed into fibrous astrocytes in the ischemic penumbra of the brain infarction.
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PMID:Activated astrocytes with glycogen accumulation in ischemic penumbra during the early stage of brain infarction: immunohistochemical and electron microscopic studies. 1147 25

Human and macaque retinae have similar retinal vascular anatomy. The general features of the retinal vascular anatomy of these two primates have much in common with more widely studied animal models such as rat and cat. However, primates are unique amongst mammals in having a region in temporal retina specialized for high visual acuity, which includes the fovea centralis (or 'fovea'). Several features distinguish the fovea from other parts of the retina, including a very high local density of cone photoreceptors, a high density of inner retinal cells during development, and an absence of retinal blood vessels. The retinal vascular complex comprises a number of cell types, in addition to vascular endothelial cells, including pericytes, microglia, astrocytes-none of which is intrinsic to the retina. In addition, amacrine-like cells make bouton-like associations with retinal vessels and may be involved in the autoregulation of blood flow. During development endothelial cells 'invade' the retina, accompanied by a population of microglial cells; glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes are also seen associated with the developing vasculature, and are in advance of the vascular front by a few hundred microns. Recent findings indicate that astrocytes at the vascular front proliferate in response to factors released by endothelial cells, including leukemia inhibitory factor. Better understood is the role of GFAP-immunoreactive astrocytes just in advance of the developing vessels. These astrocytes are sensitive to hypoxia and in response release vascular endothelial growth factor (VEGF) which in turn promotes the migration, differentiation and proliferation of vascular endothelial cells. This hypoxia/VEGF-mediated process of migration, proliferation and differentiation appears common to the retinae of a variety of species, including human. However, in human and macaque retina, different mechanisms appear to govern the development of the retinal vessels growing along the horizontal meridian of the retina towards the central area, which contains the fovea. Despite the relatively advanced state of differentiation and maturation of cells in the central area compared with the periphery, the growth of retinal vessels into the central area has been described as 'retarded', and the incidence of cell proliferation associated with these vessels is lower than in peripheral vessels. Furthermore, neither retinal vessels nor their accompanying astrocytes grow into a circumscribed region which, at a later stage, develops into the foveal depression. These observations suggest that molecular markers define the foveal region and inhibit cell proliferation and vascular growth at the fovea and, perhaps, along the horizontal meridian. The findings also suggest that at the fovea, the retina is adapted morphologically to its blood supply, since in the vicinity of the fovea, the development of retinal vessels is retarded or inhibited. The limitations on vascularization of central retina has implications for its vulnerability to degenerative changes, as seen in age-related macular degeneration.
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PMID:Development of the primate retinal vasculature. 1158 18

Changes of emotional behavior and neuronal cell loss in the hippocampus were investigated after pentylenetetrazol (PTZ) induced kindling in rats. Behavioral and morphological changes were studied in partially and fully kindled rats and after different postkindling periods comparing to the controls. The resident-intruder test indicated a diminished offensive behavior in partially and fully kindled animals. The open-field and the cat-odor exposition tests reveal changes in defensive behavioral pattern only in fully kindled rats. A decrease of exploratory locomotion and an increase in freezing were assessed in the open-field and the cat-odor exposition test, respectively, up to 10 weeks after the end of kindling. The first damaged neurons (CA4 region) were observed in the partially kindled group (PK), correlating with an increase in the glial fibrillary acidic protein (GFAP)-immunoreactivity (GFAP-IR) and hypertrophy of astrocytes. The most significant increase in the number of damaged neurons was detected 24 h after completion of kindling (selective vulnerability: CA4/CA1>DG>CA2+CA3). The neuronal loss went on for 10 weeks postkindling. A low correlation between the number of Stage 4 kindling seizures and the number of damaged hippocampal neurons was found 24 h after the end of kindling in individual rats. The present results demonstrate that PTZ kindling goes along with long-lasting changes in emotional behavior. The alterations of the defensive behavior after the termination of kindling can be interpreted as depression-like and are obviously associated with a characteristic pattern of neuronal loss in various hippocampal regions.
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PMID:Morphological alterations of neurons and astrocytes and changes in emotional behavior in pentylenetetrazol-kindled rats. 1170 Dec

GFAP (glial fibrillary acidic protein) is an intermediate filament protein found exclusively in the astrocytes of the central nervous system. We studied the role of GFAP in the neuronal degeneration in the hippocampus after transient ischemia using knockout mice. Wild-type C57 Black/6 (GFAP(+/+)) mice and mutant (GFAP(-/-)) mice were subjected to occlusion of both carotid arteries for 5-15 min. Hippocampal slices were prepared 3 days after reperfusion and the field excitatory postsynaptic potentials (fEPSP) in the CA1 were recorded. High frequency stimulation induced robust long-term potentiation (LTP) in GFAP(-/-), as in GFAP(+/+) mice. After ischemia, however, the LTP in GFAP(-/-) was significantly depressed. Similarly, paired pulse facilitation (PPF) displayed little difference between GFAP(+/+) and GFAP(-/-), but after ischemia, the PPF in GFAP(-/-) showed a depression. Histological study revealed that loss of CA1 and CA3 pyramidal neurons after ischemia was marked in GFAP(-/-). MAP2 (dendritic) immunostaining in the post-ischemic hippocampus showed little difference but NF200 (axonal) immunoreactivity was reduced in GFAP(-/-). S100beta (glial) immunoreactivity was similar in the post-ischemic hippocampus of the GFAP(+/+) and GFAP(-/-), indicating that reactive astrocytosis did not require GFAP. Our results suggest that GFAP has an important role in astrocyte-neural interactions and that ischemic insult impairs LTP and accelerates neuronal death.
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PMID:Disturbance of hippocampal long-term potentiation after transient ischemia in GFAP deficient mice. 1175 76

The host response to peripheral inflammation induces fever and behavioural depression that are supposed to be centrally mediated by cytokines. Several proinflammatory cytokines activate 'signal transducer and activator of transcription' 3 (STAT3) via gp130-like receptor signaling. In order to determine which cells in the rat brain and pituitary are activated during bacterial inflammation, we investigated in a spatiotemporal manner the activation of STAT3 in these organs following peripheral lipopolysaccharide (LPS) challenge. Under basal conditions, STAT3 immunoreactivity was observed in neurones and some glial cells throughout the brain. Two hours after the administration of LPS, nuclear localisation of STAT3 (hallmark of activation) was observed in zones at the interface between brain and blood or cerebrospinal fluid such as pituitary, ependymal layer, meninges, glia limitans, circumventricular organs and surrounding nervous parenchyma. Four hours after LPS, the nuclear activation of STAT3 propagated to cells located inside the parenchyma (cortex, hypothalamus, corpus callosum and hippocampus among others) and declined 8 h after treatment. Double labelling of STAT3 and glial fibrillary acidic protein identified activated cells in the parenchyma as astrocytes. These data show that STAT3 is activated in the pituitary and in brain astrocytes after a peripheral LPS challenge as demonstrated by immunohistochemistry. Astrocytes may therefore play a key role in the brain response to peripheral inflammation.
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PMID:Spatiotemporal analysis of signal transducer and activator of transcription 3 activation in rat brain astrocytes and pituitary following peripheral immune challenge. 1207 13

Using a human glial fibrillary acidic protein (hGFAP) promoter-driven cre transgene, we have achieved efficient inactivation of a floxed connexin43 (Cx43) gene in astrocytes of adult mice. The loss of Cx43 expression was monitored in a cell-autonomous manner via conditional replacement of the Cx43-coding region by a lacZ reporter gene. In this way, we bypassed the early postnatal lethality previously reported for Cx43 null mice and characterized the phenotypic consequences of Cx43 deficiency in the CNS. Mice lacking Cx43 in astrocytes were viable and showed no evidence of either neurodegeneration or astrogliosis. Spreading depression (SD) is a pathophysiological phenomenon observed in the CNS that is characterized by a propagating wave of depolarization followed by neuronal inactivation. Inhibitors of gap junctional communication have previously been shown to block initiation and propagation of SD. In contrast, we observed an increase in the velocity of hippocampal SD in the stratum radiatum of mice lacking Cx43 in astrocytes. In the same brain subregion, dye-coupling experiments revealed a reduction in overall astrocytic intercellular communication by approximately 50%. This strongly suggests separate and different neuronal and glial contributions of gap junctional intercellular communication to SD. Concomitant with increased velocity of spreading depression, we observed enhanced locomotory activity in mice lacking Cx43 in astrocytes.
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PMID:Accelerated hippocampal spreading depression and enhanced locomotory activity in mice with astrocyte-directed inactivation of connexin43. 1257 5

Previously, we cloned a gene from rat hippocampus that now shows homology to Ndrg2, a member of the N-myc downregulated gene (NDRG) family with putative roles in neural differentiation, synapse formation, and axon survival. Following adrenalectomy, hippocampal Ndrg2 mRNA increased in response to glucocorticoids. Ndrg2 mRNA was also upregulated by corticosterone in cerebral cortex and heart. Since Ndrg2 mRNA increased in response to glucocorticoid treatment of cultured astrocytes, we examined its cellular localization in adult brain by in situ hybridization. Ndrg2 mRNA is a prevalent message that is widely expressed throughout the brain, but is more abundant in gray matter than in white matter. Predominant mRNA expression was found in neurogenic regions of the adult brain. Furthermore, Ndrg2 mRNA in these regions was localized to GFAP-positive astrocytes or radial glia. In one of these regions, the subgranular zone of the dentate gyrus, Ndrg2 expression was decreased after adrenalectomy, and was restored to sham-operated levels by corticosterone, indicating that it is under positive regulation by glucocorticoids in vivo. Recently, another group reported that Ndr2/Ndrg2 transcripts in rat frontal cortex were decreased by chronic antidepressant treatment. Because antidepressants may alleviate symptoms of depression by reversing the effects of glucocorticoids, these data suggest that further study of Ndrg2 regulation and function in glia could contribute to understanding the pathogenesis and treatment of depression.
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PMID:Ndrg2, a novel gene regulated by adrenal steroids and antidepressants, is highly expressed in astrocytes. 1499 68

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