Reduction of mechanical sensitivity in an insect mechanoreceptor correlated with destruction of its tubular body.

The modified cilium (dendrite) of epithelial mechanoreceptors of insects contains microtubules in different arrangements: (1) microtubules distributed over the entire receptor and not fixed in a special configuration, therefore called free microtubules, (2) densely packed, interconnected microtubules called the tubular body, and (3) 9 doublet microtubules. These groups of microtubules have been discussed in relation to mechanotransduction. In a preceding paper the free microtubules were proved to be not involved in mechanotransduction. In this paper the hypothesis is examined that the tubular body may be essential to mechanotransduction. For this purpose the effect of the microtubule-disassembling drug vinblastine on both the tubular body and the sensitivity is examined in a femoral mechanoreceptor of the cricket Acheta domesticus. After 6- to 26-h exposure to vinblastine the tubular body is partially or totally destroyed. Simultaneously, mechanical sensitivity decays to zero. In contrast, the pacemaker property for nerve impulses of the apical dendritic segment is only slightly altered. We conclude from these results that the tubular body is essential to mechanotransduction. Three experiments in which a (small) response persisted, despite a totally destroyed tubular body, suggest that receptor potentials can in principle be evoked without an intact tubular body. In addition to the irreversible reduction of receptor sensitivity, vinblastine causes a reversible reduction during repetitive stimulation. This adaptation is supposed to be the consequence of altered properties of the tubular body.