Life in the Open Ocean. Joseph J. Torres

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Figure 3.14 Cubomedusae. (a) Cross section through the bell of Carybdea; (b) longitudinal section through Tripedalia; (c) the Chirodropid medusa Carybdea. (d) The Chirodropid medusa Chiropsalmus.

      Sources: (a–c) Conant (1898); (d) Redrawn from Mayer (1910), plate 47.

      General Considerations

      Perspective is important when evaluating the foraging behavior of medusae. Equipped with rudimentary sensory systems and limited locomotory capabilities, they forage in a profoundly three‐dimensional environment. Prey are captured on tentacles deployed in a stationary ambush or a slowly moving array as the animal swims forward. Stinging cells (nematocysts) on the tentacles paralyze the prey, which are then conveyed to the mouth and digested. Since both locomotion and the sensory field are quite limited, feeding success of a medusa will be determined by the number of its physical encounters with prey and the effectiveness of its tentacles in subduing the prey item.

In their mathematical model of predator–prey interactions in zooplankton, Gerritsen and Strickler (1977) assumed that the “encounter radius” of a predator was determined by its sensory system. In the case of medusae, it is determined by the volume enclosed within their tentacle array and the likelihood that a prey item once within the “kill zone” will contact a tentacle and be trapped (Madin 1988).

      The Cnidae

      The stinging organelles, or cnidae, that give the phylum Cnidaria its name are highly complex intracellular structures unique to the phylum. They are formed inside cells called cnidoblasts (Brusca and Brusca 2003), which are formed from interstitial cells in the epidermis and gastrodermis. The mature cnida in its cell is a cnidocyte. The majority of cnidocytes are located on the tentacles in small, blister‐like groups called “batteries” or in the epidermis of the oral region.

The cnida in its discharged state consists of a cup‐shaped basal capsule, a basal “shaft” or “butt” (Hyman 1940; Arai 1997), and ends in a long hair‐like tubule that is often invested with a spiny armor (Figure 3.15). The venom used to subdue prey is either “injected” from a pore at the end of the tubule, much like a syringe works, or is introduced as a coating on the tubule, much like a poisoned dart. The trick to understanding the process of eversion or discharge is to understand how the cnida is coiled in its resting state. If you can imagine poking your finger into that of an empty rubber glove from the wrong side so that it turns “outside in”. you will have a good idea of how the cnida is coiled. In its resting state, it is literally turned outside in. When discharged, the pressure from within the cnida’s basal capsule causes it to evert, just as the finger on the rubber glove would pop back out to normal if you blew into the bottom of the glove. Cnidae can only be discharged once.

      Their older name, nematocysts, is still very much in use, and the term cnidocyte then becomes nematocyte. In the newer terminology, only the stinging cnidae are termed nematocysts, to distinguish them from other types of cnidae that, for example, stick to prey (spirocysts) instead of envenomating them (Brusca and Brusca 2003).

      Nematocysts, or cnidae, are considered to be “independent effectors”: their discharge is not governed by the nervous system of the medusa but will discharge when stimulated directly by prey contact. The nematocyst has a “lid” or operculum (Figure 3.15) that covers the capsule and acts as a trapdoor. When the cnidocyte discharges, the operculum is flung open. The cnidocil, a bristle located next to the operculum, is believed to be the mechanoreceptor or “trigger” responsible for nematocyst discharge. Though the cnidocytes are considered independent effectors, their sensitivity threshold can be modified by the nutritional state of the medusa. A starved medusa will have a lower threshold for discharge than a well‐fed one.

What causes the cnidocyte to discharge? At least three theories purport to explain how a discharge is achieved. The first is the osmotic hypothesis, wherein a high osmotic pressure (high ion concentration) is maintained inside the nematocyst capsule by active ion transport and perhaps by sequestration of small organic osmolytes. Discharge of the cnidae is effected by a change in permeability of the capsule, causing water to rush down its concentration gradient, swell the capsule, and evert the nematocyst tubule. The second explanation is that the cnida formed within the cnidocyte is already in a state of tension owing to the coiling of its collagen‐like structure, much like a jack‐in‐the‐box with the lid closed. The third is that contractile proteins in the cnidocyte squeeze the basal capsule and pop out the tubule. All three explanations are feasible, but the process happens so quickly that it has not been possible to pin one down as the most likely.