Abstract

AbstractThe lateral (L) cilia on an isolated filament from the gill of Mytilus edulis remain arrested at the end of their recovery stroke (hands up) when perfused with artificial sea water (ASW). The laterofrontal (LF) cilia continue to be active. The addition of 10% ethanol (ETOH) to the ASW perfusate arrests the LF cilia in a hands‐up posture; the L cilia remain undisturbed. By contrast, 10−6 M 5‐hydroxytryptamine (5HT) in ASW activates the L cilia and arrests the LF cilia at the end of their effective stroke (hands down). Continued perfusion with 10% ETOH (v/v) in ASW/5HT restores activity to the LF cilia but arrests the L cilia (hands up). These effects are reversible and independent of external Ca2+.Following the detergent extraction of the filament, all gill cilia are inactive. The addition of 0.2 mM ATP in the presence of low Ca2+ (< 10−7 M) reactivates all model cilia. Under these conditions, 5HT can no longer inhibit the activity of LF cilia and is not required for the activation of the L cilia. This suggests that 5HT acts at a membrane level. An increase in free Ca2+ (> 10−6 M) arrests the L cilia hands up; the LF cilia remain active. Further Ca2+ increase (> 10−3 M) induces hands‐up arrest of the LF cilia, confirming that the Ca2+ threshold of the two ciliary types is different by several orders of magnitude.The addition of 10% ETOH in low Ca2+ to demembranated reactivated cilia arrests the L cilia hands up while the LF cilia continue to beat. Ten percent ETOH appears to interact with the axoneme, mimicking the effect of high Ca2+ and with the membrane to increase Ca2+ permeability and possibly to inactivate 5HT receptors. These results are discussed in terms of axonemal switching mechanisms and the physiological control of filter feeding in the lamellibranch gill.

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