Modulation of neural ATP release through presynaptic receptors

Abstract

Neural release of ATP can be elicited through or modulated through presynaptic receptors, as is known for classical transmitter substances. Activation of presynaptic nicotinic and serotonin receptors induces ATP release from postganglionic sympathetic axons. Inhibition of depolarization-evoked ATP release from these axons is mediated by, e.g. α₂- and β₂-adrenoceptors, adenosine A₁-receptors and receptors for prostaglandin E₂, neuropeptide Y and atrial natriuretic peptide. Enhancement of release is mediated by receptors for angiotensin and endothelin-3. Whether presynaptic P₂-purinoceptors affect neural ATP release is unknown. A₁-Receptors also mediate an inhibition of ATP release from cholinergic axons. Activation of some (e.g. neuropeptide Y) receptors causes an identical change in cotransmitter release. In other cases there is evidence for a differential modulation. A₁-Receptors, for example, affect ATP release more markedly than noradrenaline release. The mechanisms causing differential modulation of cotransmitter release remain to be identified.