MODULATION OF NEURAL ATP RELEASE THROUGH PRESYNAPTIC RECEPTORS

Neural release of ATP can be elicited through or modulated through pre synaptic receptors, as is known for classical transmitter substances. Activation of presynaptic nicotinic and serotonin receptors induces AT P release from postganglionic sympathetic axons. Inhibition of depolar ization-evoked ATP release from these axons is mediated by, e.g. alpha (2)- and beta(2)-adrenoceptors, adenosine A(1)-receptors and receptors for prostaglandin E(2), neuropeptide Y and atrial natriuretic peptide . Enhancement of release is mediated by receptors for angiotensin and endothelin-3. Whether presynaptic beta(2)-purinoceptors affect neural ATP release is unknown. A(1)-Receptors mediate an inhibition of ATP re lease also from cholinergic axons. Activation of some (e.g. neuropepti de Y) receptors causes an identical change in cotransmitter release. I n other cases there is evidence for a differential modulation. A(1)-Re ceptors, for example affect ATP release more markedly than noradrenali ne release. The mechanisms causing differential modulation of cotransm itter release remain to be identified. (C) 1996 Academic Press Ltd