Electrically triggered action potentials in the giant alga Chara corallina are associated with a transient rise in the concentration of free Ca2+ in the cytoplasm (Ca2+cyt). The present measurements of Ca2+cyt during membrane excitation show that stimulating pulses of low magnitude (subthreshold pulse) had no perceivable effect on Ca2+cyt. When the strength of a pulse exceeded a narrow threshold (suprathreshold pulse) it evoked the full extent of the Ca2+cyt elevation. This suggests an all-or-none mechanism for Ca2+ mobilization. A transient calcium rise could also be induced by one subthreshold pulse if it was after another subthreshold pulse of the same kind after a suitable interval, i.e., not closer than a few 100 ms and not longer than a few seconds. This dependency of Ca2+ mobilization on single and double pulses can be simulated by a model in which a second messenger is produced in a voltage-dependent manner. This second messenger liberates Ca2+ from internal stores in an all-or-none manner once a critical concentration (threshold) of the second messenger is exceeded in the cytoplasm. The positive effect of a single suprathreshold pulse and two optimally spaced subthreshold pulses on Ca2+ mobilization can be explained on the basis of relative velocity for second messenger production and decomposition as well as the availability of the precursor for the second messenger production. Assuming that inositol-1,4,5,-trisphosphate (IP3) is the second messenger in question, the present data provide the major rate constants for IP3 metabolism.

Abstract. Kinetic investigations of stimulus response coupling in the green alga Chara have revealed that an intermediate second messenger is formed in the process of membrane excitation. This second messenger links electrical stimulation to the mobilization of Ca 2+ from internal stores. In the present work, the experimentally based kinetic model, which describes the stimulus-dependent production of the second messenger and Ca 2+ mobilization, is combined with a model for inositol 1,4,5-trisphosphate (IP 3 )-and Ca 2+ -sensitive gating of a Ca 2+ -release channel in endomembranes of animal cells. The combination of models allows a good simulation of experimental data, including the all-or-none-type dependence of the Ca 2+ response on stimulus duration and complex phase locking phenomena for the dependence of the Ca 2+ response on stimulation frequency. The model offers a molecular explanation for the refractory phenomenon in Chara, assigning it to the life time of an inactive state of the Ca 2+ -release channel. The model furthermore explains the steep dependence of excitation on strength/duration of electrical stimulation as a consequence of an interplay of the dynamical variables in the model.

Recent experiments demonstrate that the concentration of Ca2+ in cytoplasm of Chara corallina internodal cells plays important role in electrical excitation of the plasma membrane. The concentration of free Ca2+ in the cytoplasm -[Ca2+]c is also sensitive to visible light. Both phenomena were simultaneously studied by noninvasive measuring action potential (AP) and magnetic field with a superconducting quantum interference device magnetometer in very close vicinity of electrically excited internodal C. corallina cells. A temporal shift in the depolarization maximum, which progressively occurred after transferring cells from the dark into the light, can be explained by the extended Othmer model. Assuming that the change in membrane voltage during the depolarization part of AP is the direct consequence of an activation of [Ca2+]c sensitive Cl- channels, the model simulations compare well with the experimental data. We can say that we have an example of electrically elicited AP that is of biochemical nature. Electric and magnetic measurements are in good agreement.

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