Abstract
The effect of three different anion channel inhibitors, namely (5-nitro-2-3-phenylpropyl-amino)benzoic acid (NPPB), Zn 2+ and anthracene-9-carboxylic acid (A-9-C) on the action potential in the liverwort Conocephalum conicum were tested. All three caused an increase of the excitability threshold and a decrease of action potential amplitudes. This confirms the involvement of anion channels in the action potentials in Conocephalum. In plants treated with 1 or 2 mM A-9-C but not with NPPB (50 or 100 //M) and Zn 2+ (100 or 500 //M), a light-induced transient depolarization occurred. In contrast to action potentials, the amplitude of this voltage transient depended on the light intensity and on the duration of preceding dark period. Also in contrast to action potentials, which are blocked by TEA, when applied together with A-9-C, TEA even increased the amplitudes of the light-induced voltage transients to up to 170 mV. The depolarization was obviously limited by the voltage-dependent opening of K + channels in the absence of TEA. The amplitude of the light-induced voltage transients (in the presence of TEA) increased in elevated CaCI2 concentrations pointing to a Ca 2+ permeability giving rise to the depolarization. However, none of the Ca 2+ channel blockers tested, La 3+ , Gd 3+ , nifedipine, verapamil or diltiazem, had an effect. The light-induced voltage transients in A-9-C treated plants are quite different from light- and electrically triggered action potentials but share some similarities with light-induced generator potentials.
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