Zinc-dependent gene expression in neurons upon glutamate stimulation

Zinc (Zn2+) has been increasingly recognized to function as an important neurotransmitter, although how it functions in the context of signaling cascades is as yet unknown. In dissociated rat hippocampal neuron cultures, we stimulated neurons with glutamate, with or without additional exogenous ZnCl2 or a cell-permeable zinc chelator TPA. We found considerable heterogeneity among biological replicates which complicated zinc-dependent gene expression analysis. In general, we saw upregulation of genes implicating ER stress in glutamate-stimulated neurons that experience a zinc signal. 5 replicates of each of 4 conditions (unstimulated control, glutamate treatment, glutamate/Zn treatment, glutamate/TPA treatment). Glutamate treatment was used as the reference condition for most comparisons. TPA = tris(2-pyridylmethyl)amine, a Zn2+ chelator.