| pubmed-article:16809466 | pubmed:abstractText | The physiological mechanisms controlling ciliary beating remain largely unknown. Evidence exists supporting both hormonal control of ciliary beating and control via direct innervation. In the present study we investigated nervous control of cilia based locomotion in the nudibranch mollusc, Tritonia diomedea. Ciliated pedal epithelial (CPE) cells acting as locomotory effectors may be electrically excitable. To explore this possibility we characterized the cells' electrical properties, and found that CPE cells have large voltage dependent whole cell currents with two components. First, there is a fast activating outward Cl(-) current that is both voltage and Ca(2+) influx dependent (I(Cl(Ca))). I(Cl(Ca)) is sensitive to DIDS and 9-AC, and resembles currents of Ca(2+)-activated Cl(-) channels (CaCC). Ca(2+) dependence also suggests the presence of voltage-gated Ca(2+) channels; however, we were unable to detect these currents. The second current, a voltage dependent proton current (I(H)), activates very slowly and is sensitive to both Zn(2+) and changes in pH. In addition we identify a new cilio-excitatory substance in Tritonia, viz., dopamine. Dopamine, in the 10 mumol l(-1)-1 mmol l(-1) range, significantly increases ciliary beat frequency (CBF). We also found dopamine and Tritonia Pedal Peptide (TPep-NLS) selectively suppress I(Cl(Ca)) in CPE cells, demonstrating a link between CBF excitation and I(Cl(Ca)). It appears that dopamine and TPep-NLS inhibit I(Cl(Ca)) not through changing [Ca(2+)](in), but directly by an unknown mechanism. Coupling of I(Cl(Ca)) and CBF is further supported by our finding that DIDS and zero [Cl(-)](out) both increase CBF, mimicking dopamine and TPep-NLS excitation. These results suggest that dopamine and TPep-NLS act to inhibit I(Cl(Ca)), initiating and prolonging Ca(2+) influx, and activating CBF excitation. | lld:pubmed |
