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Related Experiment Videos

Carbachol-induced decrease in thyroid cell adenylyl cyclase activity is independent of calcium and phosphodiesterase

D Pasquali1, C S Rani, W J Deery

  • 1Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.

Molecular Pharmacology
|January 1, 1992
PubMed
Summary

Carbachol desensitizes adenylyl cyclase in dog thyroid cells by inhibiting thyrotropic hormone (TSH) stimulation. This effect occurs downstream of TSH receptor binding, potentially involving the Gs protein, and is independent of calcium or phosphodiesterase activity.

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Area of Science:

  • Endocrinology
  • Cell Signaling
  • Molecular Pharmacology

Background:

  • Thyroid-stimulating hormone (TSH) activates adenylyl cyclase in thyroid cells.
  • Carbachol stimulates polyphosphoinositide hydrolysis via muscarinic receptors.
  • Understanding adenylyl cyclase regulation is crucial for thyroid function.

Purpose of the Study:

  • To elucidate the mechanism of adenylyl cyclase desensitization induced by carbachol in dog thyroid cells.
  • To investigate the specific molecular targets and pathways involved in carbachol-mediated inhibition.

Main Methods:

  • Cultured dog thyroid cells were incubated with carbachol.
  • Adenylyl cyclase activity was measured in membrane preparations following stimulation with TSH, cholera toxin, guanosine 5'-O-(3-thio)triphosphate, and forskolin.

Related Experiment Videos

  • Pertussis toxin and H-7 were used to assess the roles of Gi protein and protein kinase, respectively.
  • Cholera toxin-mediated AD[32P]-ribosylation of Gs was analyzed.

    • Main Results:

    • Carbachol pretreatment (2-4 hr) reduced TSH-stimulated adenylyl cyclase activity by ~40%, an effect reversible by atropine.
    • The inhibition was independent of extracellular calcium and not mimicked by ionophore A23187.
    • Inhibition was not prevented by phosphodiesterase or protein kinase inhibitors and was unaffected by pertussis toxin.
    • Carbachol reduced stimulation by TSH, cholera toxin, GTPγS, and forskolin, and decreased cholera toxin-mediated Gs ribosylation, indicating a post-receptor, Gs-related mechanism.

    Conclusions:

    • Carbachol induces a long-lasting desensitization of adenylyl cyclase activity in dog thyroid cells.
    • The inhibition occurs downstream of TSH receptor binding, implicating the stimulatory G protein (Gs) as a potential site of action.
    • This carbachol-mediated adenylyl cyclase inhibition does not involve calcium or phosphodiesterase activation.