A Cl- conductance activated by hyperpolarization in Aplysia neurones

Although many voltage-gated cation channels have been described and extensively studied in biological membranes, there are very few examples of voltage-gated anion channels. Chloride conductances activated by depolarization have been observed in skate electroplaque and in frog and chick skeletal muscle. A Cl- conductance activated by hyperpolarization has been suggested both for frog muscle treated with acid (pH 5) solutions, and for crayfish muscle where it could account for the fact that the pronounced inward-going rectification of the I-V curve disappears if the fibres have been soaked in a Cl(-)-free solution. More recently, voltage-dependent anion channels extracted from biological membranes have been incorporated into artificial membranes. I now report that in Aplysia neurones, and in particular those in which the internal Cl- concentration has been increased, a Cl- conductance can be observed which is slowly activated by hyperpolarization and shows a vary steep voltage dependence. This time- and voltage-dependent Cl- conductance probably exists also in many other cells. Its presence might explain why it is difficult when using KCl-filled microelectrodes to maintain prolonged hyperpolarizations. This Cl- conductance constitutes a new type of inward-going rectification distinct both from the classical "anomalous rectification' which involves selective K+ channels and from the current termed if in heart muscle that is presently attributed to a cationic conductance.     

Induction of increased calcium uptake in mouse T lymphocytes by concanavalin A and its modulation by cyclic nucleotides.

The binding of concanavqlin A to T but not B mouse spleen lymphocytes increases Ca-2+ uptake in these cells which is measurable by 45 s and complete by 1 min. Dibutyrl cyclic AMP, but not sodium azide inhibits induced Ca-2+ uptake, wheras dibutyryl cyclic GMP enhances it. B cell mitogens do not cause a similar Ca-2+ uptake in mouse B lymphocytes. The induction of increased Ca-2+ uptake by T cells is discussed in terms of gated membrane channels for Ca-2+.