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

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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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