A Neuromuscular Junction-like Calcium Release Mechanism In A Unicellular Organism

Abstract

When a myocyte is depolarized by an action potential, calcium ions enter the cell through L-type calcium channels located on the sarcolemma. This calcium, or the physical interaction between the activated L-type calcium channel, triggers a subsequent release of calcium that is stored in the sarcoplasmic reticulum (SR) through calcium-release channels ryanodine receptors. Crypthecodium cohnii is an unicellular dinoflagellate (phyloge-netically related to malarial parasite) with cortical multi-membranous structures apparently similar to the SR. In the present study, both fluorescence-conjugated ryanodine and dihydropyridine gave positive labellings on the cortical area of dinoflagellate cells in where the chlortetracycline-stained calcium stores were located. Either mechanical stimulations or potassium ions could induce membrane potential changes and calcium mobilizations. In addition, cytosolic calcium mobilizations induced by L-type calcium channel agonist (Bay K) was inhibited by ryanodine receptor antagonist (dantrolene). When the membrane potentials were disrupted by sodium ionophore, both mechanically-induced cytosolic calcium mobilizations and membrane potential changes were reduced. This indicated that the dihydropyridine receptor-like protein was upstream of the ryanodine receptor-like channel. Accumulated data, therefore, are consistent with a neuromuscular type excitation-contraction coupling-like mechanism in the dinoflagellates. Acknowledgement: Part of this research was supported by HKUST’s EHIA05/06.SC04 in Molecular Medicine awarded to J.T.Y.W. and S.Y.W.S).