Regulation of beta-adrenergic receptors during exposure of astrocytoma cells to catecholamines.

Abstract

In conclusion, our data indicate that exposure of 1321N1 astrocytoma cells to catecholamines initiates a series of reactions that decreases cellular responsiveness to catecholamines and eventually results in a loss of functional beta AR from the cell. Whether the series of reactions depicted in Fig. 1 indeed represents a sequential process is not yet known. The molecular nature of the beta AR modifications responsible for uncoupling, internalization, and loss of binding also remains unknown. Nonetheless, these reactions are not restricted to the beta AR/AC system of 1321N1 astrocytoma or C62B glioma cells, since a number of investigators working with a variety of homogeneous cell systems have reported the occurrence of similar phenomena (2,7,8,13-16,19,21,28). Thus, the basic framework of catecholamine-induced modification of the properties of beta AR in astrocytoma cells is likely representative of the general phenomenon of agonist-specific desensitization of the beta AR-linked AC of mammalian cells.

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@article{Perkins1984RegulationOB, title={Regulation of beta-adrenergic receptors during exposure of astrocytoma cells to catecholamines.}, author={John P . Perkins and Myron L. Toews and T. Kendall Harden}, journal={Advances in cyclic nucleotide and protein phosphorylation research}, year={1984}, volume={17}, pages={37-46} }