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Fig. 7. Model of transmitter and neuropeptide action on CPE cells. Binding of dopamine (DA) or TPep-NLS to a receptor leads to a reduction in I_Cl(Ca), carried by Ca²⁺ dependent Cl^- channels (CaCC) and I_(Cl-)leak, also carried by CaCC channels. We hypothesize that the blockage of Cl^- currents leads to a depolarization of the cell and the activation of voltage-gated Ca²⁺ channels (Ca_vC) leading to an influx of Ca²⁺. This initial influx triggers the release of further Ca²⁺ from ryanodine receptor channel (RyR)-gated endoplasmic reticulum (ER) stores. The sharp rise of [Ca²⁺]_in activates the Ca²⁺-calmodulin complex, which in turn, upregulates kinases and phosphodiesterases critical for increasing ciliary beating rate. Also present are voltage activated proton channels that play a significant role in pH maintenance and may activate after long depolarizations to aid in the repolarization of the membrane potential. Pluses indicate molecules or actions that increase current amplitude or beating rate, minuses represent inhibitory molecules or actions.

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