Characean internodal cells generate receptor potential (ΔE m) in response to mechanical stimuli. Upon a long-lasting stimulus, the cells generated ΔE m at the moment of both compression and decompression, and the amplitude of ΔE m at the moment of decompression, (ΔE m)E, was larger than that at compression. The long-lasting stimulus caused a membrane deformation (ΔD m) having two components, a rapid one, (ΔD m)rapid, at the moment of compression and a slower one, (ΔD m)slow, during the long-lasting compression. We assumed that (ΔD m)slow might have some causal relation with the larger ΔE m at (ΔE m)E. We treated internodal cells with either HgCl2 or ZnCl2, water channel inhibitors, to decrease (ΔD m)slow. Both inhibitors attenuated (ΔD m)slow during compression. Cells treated with HgCl2 generated smaller (ΔE m)E compared to nontreated cells. On the other hand, cells treated with ZnCl2 never attenuated (ΔE m)E but, rather, amplified it. Thus, the amplitude of (ΔD m)slow did not always show tight correlation with the amplitude of (ΔE m)E. Furthermore, when a constant deformation was applied to an internodal cell in a medium with higher or lower osmotic value, a cell having higher turgor always showed a larger (ΔE m)E. Thus, we concluded that changes in tension at the membrane may be the most important factor to induce activation of mechanosensitive Ca2+ channel.
The Journal of Membrane Biology – Springer Journals
Published: Nov 17, 2007
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