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

Nature. 1985 Mar 28-Apr 3;314(6009):359-61. doi: 10.1038/314359a0.


The pineal gland has proven to be an excellent model for the study of adrenergic control systems. 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 30-70-fold. An essential step in both the induction and maintenance of high NAT activity is an increase in intracellular cyclic AMP. Noradrenaline acts via beta-adrenoceptors to increase pineal cyclic AMP by activating adenylate cyclase, and the activation of pineal alpha 1-adrenoceptors potentiates beta-adrenergic stimulation not only of NAT but of both cyclic AMP and cyclic GMP. Here we describe investigations designed to test whether alpha 1-adrenergic potentiation of beta-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.

MeSH terms

  • Animals
  • Calcium / physiology
  • Cyclic AMP / metabolism*
  • Diglycerides / pharmacology
  • Drug Synergism
  • Female
  • Isoproterenol / pharmacology
  • Phenylephrine / pharmacology
  • Phorbol Esters / pharmacology
  • Pineal Gland / metabolism*
  • Protein Kinase C
  • Protein Kinases / physiology*
  • Rats
  • Rats, Inbred Strains


  • Diglycerides
  • Phorbol Esters
  • Phenylephrine
  • Cyclic AMP
  • Protein Kinases
  • Protein Kinase C
  • Isoproterenol
  • Calcium