Figure 3.

Schematic representation of an agmatinergic synapse: L-arginine enters the nerve ending via a transporter and is decarboxylated by the mitochondrial arginine decarboxylase (ADC) to agmatine (AGM), which is stored in vesicles and metabolized to putrescine (PUT) by agmatinase (AGMase). Agmatine inhibits NO synthase (NOS) as well as monoamine oxidase (MAO) since it was demonstrated that I₂-binding site (I₂-BS) is a regulative binding site of MAO. After agmatine is released from the neuron it is subject for a specific uptake or it interacts with various pre- and postsynaptic receptors including the I₁-binding site (I₁-BS), α₂ adrenoceptor (α₂-R), NMDA, nicotinic cholineric (NIC), 5−HT₃ (via the sigma-2 binding site) receptor. Furthermore, agmatine enters postsynaptic neurons via nicotinic and possibly NMDA ion channels. Whether such released agmatine represents a source for serum agmatine has not yet been determined. Peripheral effects of agmatine on blood pressure and cell growth are also a matter of debate. Released agmatine binds to presynaptic imidazoline binding sites and α₂ adrenoceptors and in this way is involved in the regulation of catecholamines. Agmatine penetrates glial cells where it also modulates the expression and activity of iNOS.