Variation potential in higher plants: Mechanisms of generation and propagation

Abstract

Long-distance intercellular electrical signals, including variation potential (VP) in higher plants, are a potential mechanism of coordinate functional responses in different plant cells under action of stressors. VP, which is caused by damaging factors (e.g., heating, crushing), is transient depolarization with an irregular shape. It can include a long-term depolarization and fast impulse depolarization ('AP-like' spikes). Mechanisms of VP generation and propagation are still under investigation. It is probable that VP is a local electrical response induced by propagation of hydraulic wave and (or) chemical agent. Both hypotheses are based on numerous experimental results but they predict VP velocities which are not in a good accordance with speed of variation potential propagation. Thus combination of hydraulic and chemical signals is the probable mechanism of VP propagation. VP generation is traditionally connected with transient H(+)-ATPase inactivation, but AP-like spikes are also connected with passive ions fluxes. Ca(2+) influx is a probable mechanism which triggers H(+)-ATPase inactivation and ions channels activation at VP.

Keywords: generation; higher plants; propagation; simulation; variation potential.

Figure 1.

Electrical signals in hypocotyl of pumpkin seedling induced by different stimuli. (a) action potential induced by ice water; (b) variation potential without spikes induced by leaf burning; (c) variation potential with AP-like spikes induced by leaf burning. Electrical signals were registered in 7 cm from zone of stimulation. Redrawn from works.

Figure 2.

Hypothetical mechanism of VP generation and propagation. Propagation of chemical signal, hydraulic signal or combination of these signals (hydraulic dispersion and turbulent diffusion) activated ligand-dependent or mechano-sensitive Ca²⁺ channels. Ca²⁺ influx inactivates H⁺-ATPase and induces long-term depolarization. Depolarization to AP threshold activates potential-dependent Ca²⁺ channels. Additional Ca²⁺ influx and plasma membrane depolarization activate potential-dependent Cl⁻ channels, and, later, K⁺-channels. As a result AP-like spike is formed.