Voltage-dependent chloride conductance of the squid axon membrane and its blockade by some disulfonic stilbene derivatives.

Abstract

When giant axons of squid, Sepioteuthis, were bathed in a 100 mM Ca-salt solution containing tetrodotoxin (TTX) and internally perfused with a solution of 100 mM tetraethylammonium-salt (TEA-salt) or tetramethylammonium-salt (TMA-salt), the membrane potential was found to become sensitive to anions, especially Cl-. Membrane currents recorded from those axons showed practically no time-dependent properties, but they had a strong voltage-dependent characteristic, i.e., outward rectification. Cl- had a strong effect upon the voltage-dependent membrane currents. The nonlinear property of the currents was almost completely suppressed by some disulfonic stilbene derivatives applied intracellularly, such as 4-acetoamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) and as 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), which are blockers of chloride transport. On the basis of these experimental results, it is concluded that a voltage-dependent chloride-permeable channel exists in the squid axon membrane. The chloride permeability (PCl) is a function of voltage, and its value at the resting membrane (Em = -60 mV) is calculated, using the Goldman-Hodgkin-Katz equation, to be 3.0 X 10(-7) cm/s.

Guanosine 3',5'‐cyclic monophosphate regulates calcium channels in neurones of rabbit vesical pelvic ganglia.

“…4 C). 4-Acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) has been reported to block chloride current (Inoue, 1985;Gray & Ritchie, 1986;Bader, Bertrand & Schlichter, 1987;Akasu et al 1990a). Addition of SITS (500 gM) to the calcium-free solution completely inhibited the calcium-insensitive component of the inward current (Fig.…”

The Reserpine-Treated Rat as an Experimental Animal Model for Cystic Fibrosis: Abnormal Cl Transport in Pancreatic Acinar Cells

“…The results of our experiments with control acini can be interpreted as lending support to this model, as these inhibitors reduced C1 accumulation in both resting and acetylcholine-stimulated cells. Stilbene derivatives also inhibit, however, C1 conductances in several epithelial and non-epithelial cells (26)(27)(28)(29) and acetylcholine activates a C1 conductance pathway of fairly high permeability in pancreatic acinar cells (30). In general, the anion exchanger is sensitive to lower doses of these inhibitors (i.e.…”

A chloride channel from lobster walking leg nerves. Characterization of single-channel properties in planar bilayers.

“…Since this preparation is enriched in TIX-binding sites, it is likely that the C1-channel we observe originates from the axon plasma membrane; however, it is also possible that it may derive from Schwann cell membranes. To our knowledge, C1-channels have not been previously described in crustacean axons, although a macroscopic Cl-current has been documented in squid giant axons (Inoue, 1985), and single Cl-channels have been characterized in cultured vertebrate neurons (Franciolini and Nonner, 1987;Franciolini and Petris, 1988), Schwann cells (Gray et al, 1984), and oligodendrocytes (Barres et al, 1988). Several of the functional characteristics of the lobster C1-channel described in this paper are similar to those of small conductance C1-channels from various vertebrate tissues, including epithelia.…”