Abstract
Agmatine, an endogenous derivative of arginine, has been found to be effective in treating idiopathic pain, convulsion, stress-mediated behavior, and attenuate the withdrawal symptoms of drugs like morphine. In the early stages of ischemic brain injury in animals, exogenous agmatine treatment was found to be neuroprotective. Agmatine is also considered as a putative neurotransmitter and is still an experimental drug. Chemically, agmatine is called agmatine 1-(4-aminobutyl guanidine). Crystallographic study data show that positively-charged guanidine can bind to the protein containing Gly and Asp residues, and the amino group can interact with the complimentary sites of Glu and Ser. In this study, we blocked the amino end of the agmatine by conjugating it with FITC, but the guanidine end was unchanged. We compared the neuroprotective function of the agmatine and agmatine-FITC by treating them in neurons after excitotoxic stimulation. We found that even the amino end blocked neuronal viability in the excitotoxic condition, by NMDA treatment for 1 h, was increased by agmatine-FITC, which was similar to that of agmatine. We also found that the agmatine-FITC treatment reduced the expression of nitric oxide production in NMDA-treated cells. This study suggests that even if the amino end of agmatine is blocked, it can perform its neuroprotective function.
Highlights
Primary amine agmatine can be created naturally from α-amino l-arginine
We demonstrated the procedure of making a fluorescence agmatine by biding a fluorescein isothiocyanate (FITC) molecule at the amino end of the agmatine and the guanidine end remains active
Agmatine has two ends that consist of a guanidine moiety and an amino group [32]
Summary
Primary amine agmatine can be created naturally from α-amino l-arginine. The decarboxylation of l-arginine to produce agmatine occurs in the presence of the mammalian mitochondrial outer membrane enzyme arginine decarboxylase. Agmatine has been found in different organs of the body at lower concentrations, with enrichments in a few parts of the brain and spinal cord, packaged in the synaptic vesicles [1,2,3]. N the synaptic vesicles, agmatine is found to be co-localized with other classical neurotransmitters such as glutamate and vasopressin and can be released by calcium-dependent depolarization [4, 5]. Agmatine is believed to be a neuromodulator that can act as a neurotransmitter, and localized in the oxytocin and vasopressin neurons [6, 7]. Agmatine was found to be neuroprotective in different excitotoxic and ischemic neurological diseases. Agmatine has been reported to reduce vascular permeability in the brain; this induces gastric protection in ischemic-injury rats
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
