Desensitization of carbachol-activated nonselective cationic currents in murine gastric myocytes is mediated by the PLC β1 pathway rather than intracellular Ca2+.
This is the authors' abstract. We don't add key points for this paper.
In murine gastrointestinal myocytes muscarinic stimulation activates nonselective cation channels via a G-protein and Ca2+-dependent pathway. We recorded inward cationic currents following application of car- bachol (ICCh) to murine gastric myocytes held at -60 mV, using the whole-cell patch-clamp method. The properties of the inward cationic currents were similar to those of the nonselective cation channels activated by muscarinic stimulation in other gastrointestinal smooth muscle cells. CCh-induced ICCh and spontaneous decay of ICCh (desensitization of ICCh) occurred. Unlike the situation in guinea pig gastric myocytes, desensitization was not affected by varying [EGTA]i. Pretreatment with the PLC inhibitor (U73122) blocked the activation of ICCh, and desensitization of ICCh was attenuated in PLC β1 knock-out mice. These results suggest that the desensitization of ICCh in murine gastric myocytes is not due to a pathway dependent on intracellular Ca2+ but to the PLC β1 pathway.
Answers are grounded in this paper and cite their sources.
Advances understanding of PLC β1 in rodent gastric myocyte currents; human relevance and clinical implications remain untested.
No takes yet. Share an insight, caveat, or question.
Kim et al. (2006) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: