ArticleNaunyn-Schmiedeberg's archives of pharmacology1996
Chloride current in toad skeletal muscle and its modification by the histidine-modifying reagent diethylpyrocarbonate.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 1 citations in OpenAlex.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cl- currents were measured in short fibres in the toad lumbricalis muscle with a two-microelectrode voltage clamp. Membrane Cl- conductance increased markedly when external pH was raised. At pH 7 or higher, the Cl- current fell during a hyperpolarizing voltage pulse and the rate of inactivation was directly proportional to the voltage change. The histidinemodifying reagent diethylpyrocarbonate (DEPC, 1 mM) which carbethoxylates histidil residues in proteins, suppressed the inactivation of Cl- currents at pH 7.5. On the other hand, no apparent changes in the kinetics of the currents at pH 5 were seen. No3- currents, which are independent of the extracellular pH and time, were not affected by DEPC. Our results support the notion that the inactivation of Cl- currents at pH 7.5 represents a membrane permeability change and that DEPC interferes with this process. Protonation of histidine groups associated with Cl- channels may be the controlling reaction for the pH -dependent Cl- response.
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