These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Effects of muscarine on K(+)-channel currents in the C-cells of bullfrog sympathetic ganglion. Author: Kurenny DE, Chen H, Smith PA. Journal: Brain Res; 1994 Sep 26; 658(1-2):239-51. PubMed ID: 7834347. 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 (IK(G)) in C-cells and to suppress M-current (IM) in B-cells. However, both IM and IK(G) were affected by muscarine in 5 out of 78 putative C-cells and in 8 others only IM was affected. By contrast, IK(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 IK(G) was neither a direct consequence of the direction of movement of K+ ions nor a simple consequence of channel block by intracellular Mg2+ or Na+ ions. The fit of the activation curve by a Boltzmann equation suggests that the conductance underlying IK(G) is controlled by a voltage-dependent gating charge (valency approximately -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 approximately 20 pS and approximately 55 pS). The possible role of these channels in the generation of IK(G) is discussed.[Abstract] [Full Text] [Related] [New Search]