Ca²⁺ modulates morphine and/or HIV-1 Tat-induced trafficking of the p65 (RelA) subunit of NF-κB into the nucleus of astrocytes.

<p>Chelating [Ca²⁺]_i with 10 µM BAPTA significantly delays Tat and/or morphine-(Morph or MOR) induced nuclear import of p65(RelA), while artificially elevating [Ca²⁺]_i by excessive (5 mM) Ca²⁺ outside the cell ([Ca²⁺]_o), accelerates p65 subunit trafficking into the nucleus. Note that p65 nuclear shuttling occurs both in vehicle and in BAPTA-treated astrocytes, suggesting that nucleocytoplasmic shuttling occurs continuously. It also infers that other events such as the phosphorylation of specific NF-κB subunits are operative (^§<i>P</i><0.05, vehicle vs. BAPTA -treated cells; ^†<i>P</i><0.05, control vs. 5 mM [Ca²⁺]_o-treated cells).