Suppression of ciliary movements by a hypertonic stress in the newt olfactory receptor neuron

Author:

Wakazono Yoshihiko12,Sakurai Takashi1,Terakawa Susumu13

Affiliation:

1. Medical Photonics Research Center, Hamamatsu University School of Medicine, Hamamatsu, Japan;

2. Department of Physiology, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan; and

3. Faculty of Health Science, Tokoha University, Shizuoka, Japan

Abstract

Olfactory receptor neurons isolated from the newt maintain a high activity of the ciliary beat. A cilium of neuron is so unique that only little is known about regulatory factors for its beat frequency. We examined the olfactory receptor neuron immersed in various extracellular media under the video-enhanced differential interference contrast microscope. The activation of voltage-gated Ca2+ channels by K+ depolarization or by application of Ca2+ to membrane-permeabilized olfactory cells did not affect the ciliary movement, suggesting that Ca2+ influx through the cell membrane has no direct effect on the movement. However, when an extracellular medium contained NaCl or sucrose at concentrations only 30% higher than normal levels, ciliary movement was greatly and reversibly suppressed. In contrast, a hypotonic solution of such a solute did not change the ciliary movement. The hypertonic solutions had no effect when applied to permeabilized cells. Suction of the cell membrane with a patch pipette easily suppressed the ciliary movement in an isotonic medium. Application of positive pressure inside the cell through the same patch pipette eliminated the suppressive effect. From these findings, we concluded that the hypertonic stress suppressed the ciliary movement not by disabling the motor proteins, microtubules, or their associates in the cilia, but rather by modifying the chemical environment for the motor proteins. The ciliary motility of the olfactory receptor cell is directly sensitive to the external environment, namely, the air or water on the nasal epithelium, depending on lifestyle of the animal.

Funder

Hamamatsu University School of Medicine

Ministry of Education, Culture, Sports, Science, and Technology (MEXT)

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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