Carbon monoxide augments electrical signaling in cultured neural networks of hippocampal neurons partly through activation of BKCa channels

Carbon monoxide (CO) is often viewed as a lethal gas in light of its capacity to prevent oxygen uptake in hemoglobin; however, it also functions to regulate a variety of proteins and physiological processes. Here we show that CO is an important chemical cue, to which neurons respond strongly, and this response is then integrated into neural network activity. In cultured mouse hippocampal neurons, CO enhanced synchronized spontaneous cytosolic Ca(2+) oscillations which arose from periodic action potentials through synaptic transmission. We used single-cell patch-clamp recording to investigate the neural network. Our results showed that the frequency of spontaneous and miniature post synaptic current was increased in neurons cultured for 14-18 days after addition of CO, with no change in current amplitude. BK channels have recently been demonstrated to be important in the action of CO. Our results showed that the effect of CO on neural network electrical activity was partly abolished after blocking the BK channels. Altogether, our results suggest that CO can influence neural network electrical activity and that BK channels participate in this regulation process.