Abstract
The activation of a monovalent cation current was studied in rat megakaryocytes using patch clamp techniques combined with photometric measurements of intracellular concentrations of Ca2+ ([Ca2+]i) and Na+. ADP evoked a release of [Ca2+]i and transiently activated a monovalent cation-selective channel, which, at negative potentials and under physiological conditions, would be expected to carry an inward Na+ current. The single channel conductance, estimated by noise analysis from whole cell currents at -50 to -60 mV was 9 picosiemens. Thapsigargin-induced [Ca2+]i increases failed to stimulate the monovalent cation current, suggesting that neither [Ca2+]i nor the depletion of internal Ca2+ stores were activators of this conductance. However, buffering of [Ca2+]i changes with 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid showed that both activation and inactivation of the current were accelerated by a rise in [Ca2+]i. The monovalent cation conductance was activated by internal perfusion with inositol 1,4,5-trisphosphate, both in the presence and in the absence of a rise in [Ca2+]i. Internal perfusion with inositol 2,4,5-trisphosphate, the poorly metabolizable isomer of inositol trisphosphate, similarly activated the m...Continue Reading
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