Neuroprotective effects of receptor imidazoline 2 and its endogenous ligand agmatine.
- Author:
Wei-Wen QIU
1
;
Rong-Yuan ZHENG
Author Information
1. Department of Neurology, the First Affiliated Hospital of Wenzhou Medical College, Wenzhou 325000, China.
- Publication Type:Journal Article
- From:
Neuroscience Bulletin
2006;22(3):187-191
- CountryChina
- Language:English
-
Abstract:
Receptor imidazoline 2 (I₂) is one of the imidazoline receptors with high affinity for [³H]-idazoxan. Receptor I₂, being classified into I(₂A) and I(₂B) subtypes, is mainly localized to the outer membrane of mitochondria in liver, kidney and brain. Receptor I₂, displaying high similarity of sequence with monoamine oxidase-B (MAO-B), is structurally related to MAO-B, but the I₂ imidazoline binding site (I₂BS) with ligand is distinct from the catalytic site of MAO-B. Agmatine is the endogenous ligand of receptor I₂. Accumulating evidence have revealed that the activation of receptors I₂ 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.
