Carbachol-induced desensitization of PLC-b pathway in rat myometrium: downregulation of Gqa/G11a

نویسندگان

  • SANDRINE LAJAT
  • ZAHRA TANFIN
چکیده

Lajat, Sandrine, Simone Harbon, and Zahra Tanfin. Carbachol-induced desensitization of PLC-b pathway in rat myometrium: downregulation of Gqa/G11a. Am. J. Physiol. 275 (Cell Physiol. 44): C636–C645, 1998.—In the estrogentreated rat myometrium, carbachol increased the generation of inositol phosphates by stimulating the muscarinic receptorGq/G11-phospholipase C-b3 (PLC-b3) cascade. Exposure to carbachol resulted in a rapid and specific (homologous) attenuation of the subsequent muscarinic responses in terms of inositol phosphate production, PLC-b3 translocation to membrane, and contraction. Refractoriness was accompanied by a reduction of membrane muscarinic binding sites and an uncoupled state of residual receptors. Protein kinase C (PKC) altered the functionality of muscarinic receptors and contributed to the initial period of desensitization. A delayed phase of the muscarinic refractoriness was PKC independent and was associated with a downregulation of Gqa/G11a. Atropine failed to induce desensitization as well as Gqa/G11a downregulation, indicating that both events involve active occupancy of the receptor. Prolonged exposure to AlF4 2 reduced subsequent A lF4 2 as well as carbachol-mediated inositol phosphate responses and similarly induced downregulation of Gqa/G11a. Data suggest that a decrease in the level of Gqa/G11a is subsequent to its activation and may account for heterologous desensitization.

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تاریخ انتشار 1998