Journal
JOURNAL OF INORGANIC BIOCHEMISTRY
Volume 179, Issue -, Pages 54-59Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jinorgbio.2017.11.014
Keywords
Zinc deficiency; Neuronal apoptosis; Amino acid neurotransmitters; GluR2; NR2B
Funding
- Natural Science Foundation of Tianjin City [15JCYBJC24500]
- National Natural Science Foundation of China [31272317]
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In the present study, a model of zinc deficiency was developed by exposing primary neurons to an N,N,N',N'-Tetrakis (2-pyridylmethyl) ethylenediamine (TPEN)-containing medium. The cell survival rate, apoptosis rate, intracellular and extracellular concentrations of 4 amino acids, and the expression of 2 glutamate receptor subtypes alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor (GluR2)and N-methyl-D-aspartate receptor subtype 2B (NR2B) were evaluated in zinc-deficient cells. The results revealed that zinc deficiency led to a decrease in cell viability and an increase in the apoptosis rate. Additionally, in cultured neurons, zinc deficiency led to an increase in the concentration of aspartic acid (Asp) and a decrease in the concentrations of glutamate (Glu), glycine (Gly), and gamma-aminobutyric acid (GABA). These changes were reversed by concurrent zinc supplementation. Furthermore, zinc deficiency led to an increase in the secreted amounts of Glu, Gly, and Asp but a decrease in secreted amounts of GABA, as measured using the concentrations of these amino acids in the cell-culture medium. These changes were partially reversed by zinc supplementation. Finally, zinc deficiency led to a significant decrease in GluR2 expression and an increase in NR2B expression in cultured neurons, whereas simultaneous treatment with zinc sulfate (ZnSO4) prevented these changes. These results suggest that zinc deficiency-induced neuronal death/apoptosis involves changes in the concentrations of 4 amino acid neurotransmitters and the expression of 2 glutamate receptor subtypes.
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