More to the point, I've been looking into agmatine supplementation (agmatine sulfate), and found an abstract i shall share:
Recent evidence suggests that agmatine, which is an intermediate in polyamine biosynthesis, might be an important neurotransmitter in mammals. Agmatine is synthesized in the brain, stored in synaptic vesicles in regionally selective neurons, accumulated by uptake, released by depolarization, and inactivated by agmatinase. Agmatine binds to alpha2-adrenoceptors and imidazoline binding sites, and blocks NMDA receptor channels and other ligand-gated cationic channels. Furthermore, agmatine inhibits nitric oxide synthase, and induces the release of some peptide hormones. As a result of its ability to inhibit both hyperalgesia and tolerance to, and withdrawal from, morphine, and its neuroprotective activity, agmatine has potential as a treatment of chronic pain, addictive states and brain injury.
And also, 'Neuroprotective effects of receptor imidazoline 2 and its endogenous ligand agmatine' - here is the abstract:
Receptor imidazoline 2 (I(2)) is one of the imidazoline receptors with high affinity for [(3)H]-idazoxan. Receptor I(2), being classified into I(2A) and I(2B) subtypes, is mainly localized to the outer membrane of mitochondria in liver, kidney and brain. Receptor I(2), displaying high similarity of sequence with monoamine oxidase-B (MAO-B), is structurally related to MAO-B, but the I(2) imidazoline binding site (I(2)BS) with ligand is distinct from the catalytic site of MAO-B. Agmatine is the endogenous ligand of receptor I(2). Accumulating evidence have revealed that the activation of receptors I(2) may produce neuroprotective effects by increasing expression of glial fibrillary acidic protein (GFAP) in astrocytes, inhibiting activity of MAO, reducing calcium overload in cells. Agmatine exerts neuroprotection against ischemia-hypoxia, injury, glutamate-induced neurotoxicity by activating imidazoline receptors, blocking N-methyl-D-aspartate (NMDA) receptor, inhibiting all isoforms of nitric oxide synthase (NOS), and selectively blocking the voltage-gated calcium channels (VGCC). It would be expected that agmatine is one of the potential neuroprotective agents.