Pressure-induced changes in Ca2+-channel excitability in Paramecium.
The behaviour of swimming Paramecium is markedly affected by hydrostatic pressure (50-200 atm, 1 atm = 101 325 Pa). To investigate whether pressure might alter behaviour by acting directly on specific ion channels that mediate the behavioural responses, we examined the effects of K+, Na+ and Ba2+ ions on swimming speed and the reversal response during pressurization and decompression. If pressure acted on the channels that transport these ions, then the pressure-induced responses of swimming Paramecium should be exaggerated or diminished, according to which ions were present in the experimental buffer. Pressurization to 100 atm in standard buffer inhibited the brief reversal of swimming direction that occurred at atmospheric pressure when a paramecium encountered the wall of the pressure chamber. To determine whether pressure impaired mechanoreceptor function or directly blocked the Ca2+-channels that control ciliary reversal, we added Ba2+ or Na+ to standard buffer to induce multiple spontaneous reversals. Pressurization blocked these reversals, suggesting that channel opening is directly inhibited by pressure. Decompression in standard buffer elicited momentary ciliary reversal and backward swimming. Buffers with a high ratio of K+ to Ca2+ suppressed this response, and the decompression-induced reversal was exaggerated in the presence of Ba2+ or Na+, consistent with the effects that these ions are known to have on Paramecium's reversal response. These data imply that, upon decompression, the Ca2+-channels that mediate ciliary reversal open transiently. In addition to blocking the reversal response, pressurization slowed forward swimming. By examining the response to pressurization of Paramecium immobilized by Ni2+, we found that hydrostatic pressure apparently slows swimming by reorientating the direction of ciliary beat.
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D000818:Animals; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002923:Cilia / Q000187:drug effects; D007473:Ion Channels / Q000502:physiology*; D009068:Movement; D010247:Paramecium / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D011312:Pressure; D012964:Sodium / Q000494:pharmacology
D007473:Ion Channels; D001464:Barium; D012964:Sodium; D011188:Potassium; D002118:Calcium