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INTRODUCTION: The EBI2 receptor is one of the key mediators of innate immune responses. In cooperation with its ligand, oxysterol 7α,25HC, EBI2 coordinates immune cell positioning in the secondary lymphoid tissue, enabling appropriate humoral and cellular immune responses. EBI2 is also expressed in the central nervous system (CNS), where it regulates inflammatory signalling and myelination. Importantly,...
BACKGROUND AND AIMS: The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. METHODS: Exposition of cAMP/RA-differentiated (DC) and nondifferentiated (NC) cells cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent accumulation. The level of Zn was measured by fluorimetric method with TSQ....
Acetyl-CoA synthesized from glucose-derived pyruvate by pyruvate dehydrogenase complex (PDHC) is a main substrate, for mitochondrial energy production and cytoplasmic synthetic pathways in all types of brain cells. Activities of mitochondrial PDHC, and several enzymes of acetyl-CoA metabolism, and ZnT1 transporter level in cholinergic septal SN56 cells were from 2 to 8 times higher than those in microglial...
Inhibition of pyruvate (PDHC) and ketoglutarate (KDHC) dehydrogenase complexes induced by thiamine pyrophosphate deficits is known to cause disturbances of cholinergic transmission in the brain, yielding clinical symptoms of cognitive and motor deficits. However, particular alterations in distribution of acetyl-CoA, in the glial cells of thiamine pyrophosphate-deficient brain remain unknown. Therefore,...
Zinc excess in the synaptic cleft may be one of pathologic signals triggering chronic neurodegenerative events. The aim of this work was to find relationships between Zn accumulation and integrity of cholinergic and astroglial cells. Exposition of cAMP/RA-differentiated (DC) and nondifferentiated cells (NC) cholinergic SN56 neuroblastoma and astroglial C6 cells to Zn yielded its concentration dependent...
Preferential loss of septal cholinergic neurons is a main cause of cognitive deficits in various encephalopathies. Zinc excess is one of multiple pathologic signals contributing to mechanisms of Alzheimer’s and other neurodegenerative diseases. We suggest that zinc may be involved in early excitotoxic phase of neuronal injury. In homogenates of SN56 cholinergic neuroblastoma cells, Zn caused instant...
Neurodegenerative lesions in cholinergic encephalopathies include an excessive activation of microglia, which may aggravate this process. Infl amatory cytokines were reported to affect viability of cultured cholinergic cells, through the infl uence on their acetyl-CoA metabolism. The aim of this work was to investigate whether phenotypic modifi cations of N9 microglia by common neuron-differentiating...
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