Thiel and colleagues demonstrated that the all-or-none nature of Chara action potential(AP) is determined by formation of a second messenger, probably inositol triphosphate (IP3), whichin turn releases Ca2+ from internal stores. The Ca2+-activated Cl– channels are the main agent of thedepolarization phase of the AP. Once the Ca2+ is re-sequestered by the calcium pumps, the chlorideconductance drops and depolarization-activated outward rectifier current, the background current andthe proton pump current return the membrane potential difference (PD) to resting level. Departingfrom the Thiel model of transient increase of Ca2+ concentration, we set up membrane PD rate ofchange equation to calculate the AP form by numerical integration. Compared to data, this model APdepolarized more gradually. We introduced a prompt Ca2+ transient from the outside, achieving agood correspondence with the experimental AP. In Chara cells subjected to 50 mM NaCl/0.1 mMCa2+ medium, the AP duration increased from 2 s to up to 50 s and the APs were often spontaneous.The lack of stimulating pulse revealed a sharp positive spike at the beginning of each AP, confirmingthat Chara plasma membrane may contain transient receptor potential (TRP)-like channels, possiblyactivated by another second messenger diacylglycerol (DAG) formed at the same time as IP3. Thelong duration of the saline AP can be modeled by decreasing the coefficients in the Hill equationdescribing the Ca2+ pumps on the internal stores. The model provides new insights into the characeanAP and suggests a range of experiments.
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Beilby et al. (2016) studied this question.
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