Up-regulation of the transient A-type K+ current (IA) in the differentiation of neural stem cells of the early postnatal rat hippocampus / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Neural stem cells (NSCs) not only are essential to cell replacement therapy and transplantation in clinical settings, but also provide a unique model for the research into neurogenesis and epigenesis. However, little attention has been paid to the electrophysiological characterization of NSC development. This work aimed to identify whether the morphological neuronal differentiation process in NSCs included changes in the electrophysiological properties of transient A-type K(+) currents (I(A)).</p><p><b>METHODS</b>NSCs were isolated from early postnatal rat hippocampus and were multiplied in basic serum-free medium containing basic fibroblast growth factor. Potassium currents were investigated and compared using whole-cell patch-clamp techniques and one-way analysis of variance (ANOVA), respectively.</p><p><b>RESULTS</b>Compared with NSC-derived neurons, cloned NSCs (cNSCs) had a more positive resting membrane potential, a higher input resistance, and a lower membrane capacitance. Part of cNSCs and NSC-derived neurons possessed both delayed-rectifier K(+) currents (I(DR)) and I(A), steady-state activation of I(A) in cNSCs (half-maximal activation at (21.34 +/- 4.37) mV) occurred at a more positive voltage than in NSC-derived neurons at 1-6 days in vitro (half-maximal activation at (12.85 +/- 4.19) mV).</p><p><b>CONCLUSIONS</b>Our research revealed a developmental up-regulation of the I(A) component during differentiation of postnatal NSCs. Together with the marked developmental up-regulation of I(DR) in vitro neuronal differentiation we have previously found, the voltage-gated potassium channels may participate in neuronal maturation process.</p>

Protection mechanisms of ATP-sensitive K channels on hippocampal CA1 neurons during chronic severe hypoxia / 中国应用生理学杂志

<p><b>AIM</b>To study the protection mechanisms of K(ATP) channels on hippocampal CA1 neurons during chronic severe hypoxia.</p><p><b>METHODS</b>p53 expression, DNA fraction, and cell apoptosis were examined in cultured hippocampal neurons in control group, hypoxia group, hypoxia group treated with K(ATP) channels antagonist and hypoxia group treated with K(ATP) channels agonist.</p><p><b>RESULTS</b>In the group of a 12 h long exposure to oxygen concentration of 0%, diazoxide (100 micromol/L), the K(ATP) channels agonist, reduced p53 expression and the hypoxia-induced apoptosis. In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA.</p><p><b>CONCLUSION</b>K(ATP) channels protect hippocampal neurons against chronic severe hypoxia by suppressing p53 expression.</p>