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Carbachol‐induced oscillations in membrane potential and [Ca 2+ ] i in guinea‐pig ileal smooth muscle cells
Author(s) -
Kohda M.,
Komori S.,
Unno T.,
Ohashi H.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.559bh.x
Subject(s) - carbachol , membrane potential , biophysics , chemistry , depolarization , thapsigargin , stimulation , membrane , electrophysiology , endocrinology , medicine , biochemistry , intracellular , biology
1 Cytosolic free Ca 2+ concentration ([Ca 2+ ] i ) and membrane potential were simultaneously recorded from single smooth muscle cells of guinea‐pig ileum, using a combination of nystatin‐perforated patch clamp and fura‐2 fluorimetry techniques. 2 Carbachol (CCh, 2 μM) produced oscillatory changes in [Ca 2+ ] i and membrane potential which coincided well in time with each other, and peaks of membrane potential oscillations reached a saturated level of around −7 mV. Thapsigargin (1 μM) abolished these effects of 2 μM CCh. La 3 + (3 μM) immediately prevented the discharge of spike potentials, but allowed both on‐going oscillatory responses to persist for a while. 3 CCh (0.25‐0.75 μM) caused membrane potential and [Ca 2+ ] i to oscillate in some 20 % of cells studied. Every membrane potential oscillation was preceded by the discharge of single or multiple spike potentials. The effects of CCh were readily abolished by La 3 + (3 μM). 4 In cells exhibiting no oscillatory response to 0.25‐0.75 μM CCh, an electrically evoked action potential usually generated changes in [Ca 2+ ] i and membrane potential similar to those following spontaneously evoked action potentials, and sometimes it did so only after [Ca 2+ ] i or Ins P 3 had been slightly elevated by repeatedly evoking action potentials or by increasing CCh concentration in the bath medium. 5 The results suggest that in ileal smooth muscle cells, the oscillations of [Ca 2+ ] i and membrane potential arising from muscarinic stimulation result from release of Ca 2+ from internal stores and that there is a Ca 2+ ‐induced potentiation of coincidently elicited cation channel openings. Under weak muscarinic stimulation, Ca 2+ entry upon action potential discharge can trigger such a release of stored Ca 2+ , resulting in synchronous generation of a large rise in [Ca 2+ ] i and a slow, large membrane depolarization.