Experiments were carried out to determine the role of the plasma membrane in the control of tentacle contraction in Heliophrya erhardi. Intracellular recordings gave membrane potentials between −20 and −30 mV. In a Ca2+-containing medium mechanical stimulation induced tentacle contraction but no associated electrical events were recorded. Intracellular stimulation with 50 nA, 100 ms hyperpolarizing current induced contraction, but no significant changes in membrane potential, whereas up to 100 nA, 100 ms depolarizing current had no effect. In a Ca2+-free medium neither mechanical stimulation nor electrical stimulation induced contraction. Extracellular stimulation of 15 V, 100 ms induced a Ca2+-dependent, unilateral (anodal) contraction response with a threshold of 5x10−9M-Ca2+. At concentrations above this neither latency to contraction nor contraction time showed significant variation. In a standard concentration of 10−4M-Ca2+ the sensitivity to extracellular stimulation was increased and latency to contraction was reduced in the presence of a phorbol ester (TPA), which mimics the second messenger diacylglycerol in stimulating the activity of protein kinase C. It is suggested that control of tentacle contraction is unlikely to be mediated by stimulus-activated ion channels in the plasma membrane, and the possibility that the polyphosphoinositide signalling pathway is involved is discussed.

This content is only available via PDF.