Disease relevance of Neuroglia

• Cerebral ischemia enhances polyamine oxidation: identification of enzymatically formed 3-aminopropanal as an endogenous mediator of neuronal and glial cell death [1].
• Glioblastoma expression of vitronectin and the alpha v beta 3 integrin. Adhesion mechanism for transformed glial cells [2].
• Retinal degeneration upregulated both p75NTR and the high-affinity neurotrophin receptor TrkC in different parts of Müller glial cells [3].
• Further, we observe that TAR-deleted mutants of HIV-1 demonstrate normal late gene expression in glial cells as evidenced by syncytia formation and production of viral p24 antigen.(ABSTRACT TRUNCATED AT 250 WORDS)[4]
• Retinoic acid induces embryonal carcinoma cells to differentiate into neurons and glial cells [5].

Psychiatry related information on Neuroglia

• In this investigation, we have simultaneously assessed glial cell density and neuronal density and size in the anterior cingulate cortex in schizophrenia, major depressive disorder, and bipolar disorder [6].
• In Alzheimer's disease, there is a significant increase in the proportion of statin-negative neuroglia (range, 51 to 58%) [7].
• The inflammation-induced changes in glial cell morphology and expression of inducible nitric oxide synthase in the injected area, the release of acetylcholine, GABA and glutamate from the ipsilateral cortex, the production of nitrite levels in the injected area and ipsilateral cortex, and changes in motor activity were investigated [8].
• Moreover, neurones and glial cells do not over-express phosphorylated TIF 2 alpha in CJD [9].
• Propentofylline, a neuroprotective glial cell modulator, has been shown in preclinical studies to address some of the common pathological processes of Alzheimer's disease (AD) and vascular dementia (VaD), including glial cell activation and increased production of cytokines, free radicals, and glutamate [10].

High impact information on Neuroglia

• In addition, glial cells express various metabotropic receptors coupled to intracellular Ca2+ stores through the intracellular messenger inositol 1,4,5-triphosphate [11].
• N-CAM has now been identified as a receptor for glial cell line-derived neurotrophic factor (GDNF) [12].
• We show here that Gcm1, encoding the transcription factor glial cells missing-1 (Gcm1), is expressed in small clusters of chorionic trophoblast cells at the flat chorionic plate stage and at sites of chorioallantoic folding and extension when morphogenesis begins [13].
• We have characterized a novel member of the neurexin family, Neurexin IV (NRX), which is localized to septate junctions (SJs) of epithelial and glial cells [14].
• We have identified a gene, glial cells missing (gcm), that encodes a novel nuclear protein expressed transiently in early glial cells [15].

Chemical compound and disease context of Neuroglia

• Because increasing evidence indicates that glial cells are a target of endothelin, we have characterized endothelin-induced phosphoinositide (PI) turnover and Ca2+ homeostasis in C6 glioma cells [16].
• Mechanisms underlying human immunodeficiency virus-1 encephalopathy are not completely known; however, recent studies suggest that the viral protein gp41 may be neurotoxic via activation of inducible nitric oxide synthase (iNOS) in glial cells [17].
• The powerful trophic effects that glial cell line-derived neurotrophic factor (GDNF) exerts on midbrain dopamine neurones suggest its use in treating Parkinson's disease [18].
• Nitric oxide (NO) that is produced by inducible NO synthase (iNOS) in glial cells is thought to contribute significantly to the pathogenesis of multiple sclerosis [19].
• This study was undertaken to elucidate the roles of neurons and glial cells in the handling of glutamate and glutamine, a glutamate precursor, during cerebral ischemia [20].

Biological context of Neuroglia

• In ana mutants, quiescent postembryonic central brain and optic lobe neuroblasts enter S phase precociously. ana encodes a novel secreted protein of 474 amino acids that is expressed not in the affected neuroblasts, but rather in a subclass of neighboring glial cells [21].
• Primary cultures containing CNS glial cells have been shown to respond to beta-adrenergic agonists with an increase in cyclic AMP and, as a result, with an increase in glycogenolysis and have also been shown to respond to a variety of peptides with changes in cyclic AMP [22].
• Thus, complement activation provides a specific mechanism for recruiting reactive glial cells to the site of the fibrillar amyloid beta-protein plaque, which could lead to inflammatory events, neuronal dysfunction and degeneration [23].
• Here we searched for neurogenesis in adult macaques by using immunofluorescent triple labeling for the DNA-replication indicator, bromodeoxyuridine (BrdU), and neuronal and glial cell markers [24].
• DFGF-R1 (breathless), a Drosophila FGF receptor homolog, is required for the migration of tracheal cells and the posterior midline glial cells during embryonic development [25].

Anatomical context of Neuroglia

• Glutamate is taken up avidly by glial cells in the central nervous system [26].
• On mesencephalic glial cells the majority of DA neurones develop a great number of highly branched and varicose neurites, whereas on striatal glia they only exhibit one long, thin and rather linear neurite [27].
• Epidermal growth factor (EGF), which can be purified from the mouse submaxillary gland or from pregnant human urine, is a potent multiplication-stimulating factor for several types of cultured cells, including human fibroblasts and glial cells [28].
• The gfa gene encodes glial fibrillary acidic protein, an intermediate filament protein expressed in glial cells [29].
• Previously, we reported the structure and sleep-inducing properties of cis-9-octadecenamide, a lipid isolated from the cerebrospinal fluid of sleep-deprived cats. cis-9-Octadecenamide, or oleamide, has since been shown to affect serotonergic systems and block gap-junction communication in glial cells (our unpublished results) [30].

Associations of Neuroglia with chemical compounds

• These results demonstrate a non-vesicular mechanism for the release of glutamate from glial cells and neurons [31].
• Our experiments show that glial cells possess quisqualate- and kainate-receptor channels but lack receptors for NMDA [32].
• Possible relationship between glial cells, dopamine and the effects of antipsychotic drugs [33].
• Uptake into glial cells helps to terminate glutamate's neurotransmitter action and to keep its extracellular concentration, [Glu]o, below neurotoxic levels [34].
• These results suggest that neuropeptides influence glial cells as well as neurones in the CNS and, in the case of somatostatin and substance P, provide further examples of neuropeptides modulating the response to another chemical signal without having a detectable action on their own [22].

Gene context of Neuroglia

• Brain lipid-binding protein is a direct target of Notch signaling in radial glial cells [35].
• breathless, a Drosophila FGF receptor homolog, is essential for migration of tracheal and specific midline glial cells [36].
• We showed that radial glial cells isolated from the cortex of Pax6 mutant mice have a reduced neurogenic potential, whereas the neurogenic potential of non-radial glial precursors is not affected [37].
• Removal of gcm and gcm2 function shows that the two genes act redundantly and are required for the formation of a subset of glial cells [38].
• CasR deficiency was transferred onto the glial cells missing 2-deficient (Gcm2-deficient) background by intercrossing CasR- and Gcm2-deficient mice [39].

Analytical, diagnostic and therapeutic context of Neuroglia

• Using a similar approach in which the morphology of individual DA cells can be studied after 3H-DA uptake and autoradiography, we now report on in vitro neurone-glia interactions and show that glial cells exert a morphogenetic effect on DA neurones [27].
• Bergmann glial cells in mouse cerebellar slices revealed a kainate-type glutamate receptor with a sigmoid current-to-voltage relation, as demonstrated with the patch-clamp technique [40].
• We demonstrate by immunocytochemistry that NGF exerts its antiinflammatory effect by downregulating the production of interferon gamma by T cells infiltrating the CNS, and upregulating the production of interleukin 10 by glial cells in both inflammatory lesions of EAE and normal-appearing CNS white matter [41].
• Immunofluorescence microscopy analysis showed HMIT expression in glial cells and some neurons [42].
• In a neuron-glia coculture system, wild-type glial cells protected neurons against mutant htt-mediated neurotoxicity, whereas glial cells expressing mutant htt increased neuronal vulnerability [43].

References