Possible role of cyclic nucleotides in regulation of noradrenaline release from rat pineal through presynaptic adrenoceptors

Abstract

PRESYNAPTIC α-adrenoceptors on noradrenergic nerve endings have been shown to mediate a negative feedback mechanism which leads to inhibition of transmitter release during depolarisation induced by nerve stimulation or potassium^1–3. On the other hand, it is known that in some tissues activation of presynaptic β-adrenoceptors both in vitro and in vivo leads to an increase in transmitter release^4–8. The α-adrenoceptors seem to operate by restricting the calcium available for the excitation–secretion coupling, and the facilitating effect of β-agonists on transmitter release seems to be mediated through an increase in the levels of cyclic AMP in noradrenergic nerve endings^7,8. Recent reports^9,10 have provided electrophysiological evidence for a prejunctional role of cyclic nucleotides in neurotransmission. In the rat pineal gland a calcium-dependent presynaptic mechanism for the generation of cyclic GMP has been reported which might be linked to an α-adrenergic-like receptor¹¹. In addition, there is evidence in this gland for an α-adrenergic presynaptic mechanism regulating noradrenaline release elicited by potassium¹². Consequently, we decided to examine and report here our finding of a role of cyclic nucleotides in noradrenaline release from the rat pineal gland and the possible involvement of these substances in the regulatory mechanisms mediated through the α and β presynaptic adrenoreceptors.