In addition to proposing the nematocyst release response, we hypothesize that the response is controlled by prey-derived chemicals, as are nematocyst-mediated prey capture (Thorington and Hessinger, 1988b) and the subsequent feeding response (Lindsted, 1971; Lenhoff and Heagy, 1977).
Using methoxyverapamil (D-600) to selectively inhibit discharge from Type Bs, we show that (i) NANA inhibits the intrinsic adherence of nematocysts discharged from Type C CSCCs and, therefore, controls the release response of Type Cs; and (ii) glycine inhibits the intrinsic adherence of nematocysts discharged from Type B CSCCs and, therefore, controls the release response of Type Bs.
To test our hypotheses that a nematocyst release response exists and is under the control of prey-derived chemicals, we ask the research question: Do known chemosensitizers of nematocyst discharge lower, in a dose-dependent manner, the values of [i.
We proposed a so-called nematocyst release response controlled by soluble, prey-derived chemicals also known to both chemosensitize nematocyst discharge and initiate the feeding response.
b] over a wide range of values, in a dose-dependent manner, but without affecting the release response of nematocysts discharged from Type Bs.
Glycine inhibits discharge from Type Cs, but it does not affect the Type C nematocyst release response.
Our present work shows that NANA controls the release response of nematocysts discharged from Type Cs [ILLUSTRATION FOR FIGURE 2D OMITTED], whereas glycine controls the release response of nematocysts from the more numerous Type Bs [ILLUSTRATION FOR FIGURE 3D OMITTED].
On the other hand, the subsequent release response and prey ingestion take place on a much longer timescale than prey capture.