Increasing evidences support that accessory cells in mechanosensors regulate neuronal output; however, the glial molecular mechanisms that control this regulation are not fully understood. We show here in Caenorhabditis elegans that specific glial Na+-K+-ATPase genes are needed for nose touch-avoidance behavior. Our data support the requirement of these Na+-K+-ATPases for homeostasis of Na+ and K+ in nose touch receptors. Our data add to our understanding of glial regulation of mechanosensors.
Cytochrome P450 (CYP) isozymes vary their expression depending on the brain area, the cell type, and the presence of drugs. Some isoforms are involved in detoxification and/or toxic activation of xenobiotics in central nervous system. However, their role in brain metabolism and neurodegeneration is still a subject of debate. We have studied the inducibility of CYP isozymes in human neuroblastoma SH-SY5Y cells, treated with β-naphtoflavone (β-NF) or ethanol (EtOH) as inducers, by qRT-PCR, Western blot (WB), and metabolic activity assays. Immunohistochemistry was used to localize the isoforms in mitochondria and/or endoplasmic reticulum (ER). Tetrazolium (MTT) assay was performed to study the role of CYPs during methylphenyl pyridine (MPP+) exposure. EtOH increased mRNA and protein levels of CYP2D6 by 73% and 60% respectively. Both β-NF and EtOH increased CYP2E1 mRNA (4- and 1.4-fold, respectively) and protein levels (64% both). The 7-ethoxycoumarin O-deethylation and dextromethorphan O-demethylation was greater in treatment samples than in controls. Furthermore, both treatments increased by 22% and 18%, respectively, the cell viability in MPP+-treated cells. Finally, CYP2D6 localized at mitochondria and ER. These data indicate that CYP is inducible in SH-SY5Y cells and underline this in vitro system for studying the role of CYPs in neurodegeneration.
Cellular function is regulated by the concentration of intracellular and extracellular ions, including pH. Ion channels and transporters that mediate the flux/transport of protons and bicarbonate (HCO
3
–
) are the chief regulators of pH. In the nervous system, due to their high electrical activity, neurons tend to produce and excrete large amounts of acids. On the contrary, glial cells have been proposed to be key contributors of pH buffering. We published that the Cl
–
/HCO
3
–
permeable channel CLH-1 mediates intracellular pH buffering of
C. elegans
Amphid sheath (AMsh) glia at baseline. We show here that, under physiological conditions,
clh-1
knock out worms show reduced HCO
3
–
extrusion from AMsh glia, suggesting that CLH-1 may help prevent cellular alkalinization. This function becomes even more apparent when animals are grown on plates enriched with HCO
3
–
. We speculate that CLH-1 might function as a regulator of extracellular pH.
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