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Activation of protein kinase C potentiates isoprenaline-induced cyclic AMP accumulation in rat pinealocytes

Nature volume 314, pages 359–361 (1985)Cite this article

Abstract

The pineal gland has proven to be an excellent model for the study of adrenergic control systems1. Noradrenaline, released from sympathetic nerve terminals in the pineal gland, regulates a large nocturnal increase in melatonin synthesis by stimulating the activity of arylalkylamine N-acetyltransferase (NAT, EC 2.3.1.87) 30–70-fold1,2. An essential step in both the induction and maintenance of high NAT activity is an increase in intracellular cyclic AMP3,4. Noradrenaline acts via β-adrenoceptors to increase pineal cyclic AMP by activating adenylate cyclase5, and the activation of pineal α1-adrenoceptors6 potentiates β-adrenergic stimulation not only of NAT7,8 but of both cyclic AMP and cyclic GMP9–11. Here we describe investigations designed to test whether α1-adrenergic potentiation of β-adrenergic stimulation of pineal cyclic AMP involves protein kinase C. Our results suggest that kinase activation is involved and the data provide the first demonstration of a synergistic interaction between Ca2+-phospholipid-dependent protein kinase (protein kinase C) and neurotransmitter-dependent stimulation of cyclic AMP.

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Authors and Affiliations

  1. Section on Neuroendocrinology, Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, Bethesda, Maryland, 20205, USA

    David Sugden, Jiri Vanecek & David C. Klein

  2. Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland, 20205, USA

    Thomas P. Thomas & Wayne B. Anderson

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  1. David Sugden
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  2. Jiri Vanecek
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  3. David C. Klein
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  4. Thomas P. Thomas
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  5. Wayne B. Anderson
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Sugden, D., Vanecek, J., Klein, D. et al. Activation of protein kinase C potentiates isoprenaline-induced cyclic AMP accumulation in rat pinealocytes. Nature 314, 359–361 (1985). https://doi.org/10.1038/314359a0

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