Effects of muscarine on K +-channel currents in the C-cells of bullfrog sympathetic ganglion

Abstract

The effects of muscarine on small, putative C-cells and large, putative B-cells dissociated from bullfrog paravertebral sympathetic ganglia were studied by whole cell and single channel recording techniques. The dominant action of muscarine was to activate an inwardly-rectifying K + current ( I K(G) in C-cells and to suppress M-current ( I M) in B-cells. However, both I M and I K(G) were affected by muscarine in 5 out of 78 putative C-cells and in 8 others only I M was affected. By contrast, I K(G) was only activated in 1 out of 105 B-cells. This predicts that the muscarinic slow IPSP, which can be evoked by preganglionic stimulation, occurs exclusively in C-cells. 6% of these cells could, however, generate a muscarinic slow EPSP in addition to a slow IPSP and 10% could generate a slow EPSP without a slow IPSP. The rectification associated with I K(G) was neither a direct consequence of the direction of movement of K + ions nor a simple consequence of channel block by intracellular Mg 2+ or Na + ions. The fit of the activation curve by a Boltzmann equation suggests that the conductance underlying I K(G) is controlled by a voltage-dependent gating charge (valency ≈ − 2). Muscarine activated no new channels in outside-out or cell-attached patches but increased the opening probability of two types of K + channels (unitary conductances ≈ 20 pS and ≈ 55 pS). The possible role of these channels in the generation of I K(G) is discussed.