TY - JOUR
T1 - Exposure of dog thyroid slices to acetylcholine induces refractoriness to its subsequent stimulation of glucose oxidation
AU - Arem, Ridha
AU - Chayoth, Reuben
AU - Shenkenberg, Todd D.
AU - Miller, Samuel I.
AU - Chou, Margaret C.Y.
AU - Field, James B.
N1 - Funding Information:
This work was supported by United States Public Health Service Grants AM 26088 and AM 27685 and Training Grant Am 07348. The authors would like to thank Mrs. Barbara Smine for her secretarial assistance in the preparation of this manuscript.
PY - 1983/1/1
Y1 - 1983/1/1
N2 - An initial incubation of dog thyroid slices with 0.1 or 1 μm acetylcholine (ACH) for at least 2 h decreases its subsequent stimulation of [1-14C]glucose oxidation. Refractoriness persists for as long as 6 h in the absence of ACH. While new protein synthesis is essential for recovery, it is not necessary for its induction. Refractoriness is prevented when 25 μm tropicamide, an atropine-like drug, is present from the beginning of the initial incubation, but not when it is added after 2 h of incubation of slices with ACH, indicating that at this time ACH is no longer necessary for refractoriness. During refractoriness induced by ACH, stimulation of glucose oxidation by thyroid-stimulating hormone, prostaglandin E1, dibutyryl cyclic AMP, and cholera toxin, but not menadiol, is also significantly diminished. Incubation of thyroid slices with ACH does not modify its stimulation of iodide organification or 32Pi incorporation into phospholipids. These results suggest that the desensitization is not due to changes in the ACH receptor but rather to intracellular metabolic effects. This phenomenon may be important in the regulation of cholinergic effects on the thyroid.
AB - An initial incubation of dog thyroid slices with 0.1 or 1 μm acetylcholine (ACH) for at least 2 h decreases its subsequent stimulation of [1-14C]glucose oxidation. Refractoriness persists for as long as 6 h in the absence of ACH. While new protein synthesis is essential for recovery, it is not necessary for its induction. Refractoriness is prevented when 25 μm tropicamide, an atropine-like drug, is present from the beginning of the initial incubation, but not when it is added after 2 h of incubation of slices with ACH, indicating that at this time ACH is no longer necessary for refractoriness. During refractoriness induced by ACH, stimulation of glucose oxidation by thyroid-stimulating hormone, prostaglandin E1, dibutyryl cyclic AMP, and cholera toxin, but not menadiol, is also significantly diminished. Incubation of thyroid slices with ACH does not modify its stimulation of iodide organification or 32Pi incorporation into phospholipids. These results suggest that the desensitization is not due to changes in the ACH receptor but rather to intracellular metabolic effects. This phenomenon may be important in the regulation of cholinergic effects on the thyroid.
UR - https://www.scopus.com/pages/publications/0020620543
U2 - 10.1016/0003-9861(83)90007-3
DO - 10.1016/0003-9861(83)90007-3
M3 - Article
AN - SCOPUS:0020620543
SN - 0003-9861
VL - 225
SP - 66
EP - 74
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
IS - 1
ER -
