Abstract
The intracellular free calcium concentration, [Ca 2+] i, has been measured in dog thyroid cells using the fluorescent Ca 2+-indicator, quin2. Acetylcholine or its non-hydrolyzable analog, carbamylcholine rapidly increased [Ca 2+] i by 40 ± 4% (mean ± SE) over the basal level of 81 ± 2 nM. This increase was totally abolished by atropine, a muscarinic cholinergic receptor blocker, but was not influenced by verapamil, a voltage dependent-calcium channel blocker. Depletion of extracellular Ca 2+ by the addition of EGTA, diminished but did not abolish the response to carbamylcholine. These data suggest that cholinergic effectors increase [Ca 2+] i by mobilization of Ca 2+ from intracellular stores rather than from an influx of Ca 2+. Addition of TSH, isoproterenol, phorbol ester, dibutyryl cyclic GMP or cyclic AMP did not elicit any change in [Ca 2+] i suggesting that their action may not involve any mobilization of intracellular Ca 2+. These data provide direct evidence that in the thyroid cell, cholinergic agents act via their receptors to cause a rapid increase in [Ca 2+] i, which may mediate their metabolic effects.
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