Release of sialic acid alters the stability of the membrane potential in cardiac muscle

Intracellular recording techniques and neuraminidase, an enzyme that specifically catalyzes the hydrolysis of sialic acid's glycosidic linkage in glycoproteins and glycolipids, were employed to investigate the role of sialic acid residues in maintaining a stabilized resting potential or rhythmic electrical activity in embryonic chick cardiac muscle. Free sialic acid was quantified by a fluorometric assay. Release of more than 25% of the sarcolemma-bound sialic acid from spheroidal aggregates of cultured heart cells resulted in a) depolarizing fluctuations in the membrane potential, b) initiation of spontaneous firing in the presence of tetrodotoxin, c) arrhythmic spontaneous activity, d) depolarization of the maximum diastolic potential, and e) a significant reduction in the plateau and duration of the action potential. Control experiments demonstrated that these effects were not caused by phospholipase contamination of the enzyme or by the sialic acid released during hydrolysis.