Accelerated functional recovery and neuroprotection by agmatine after spinal cord ischemia in rats.
Treatment with agmatine, decarboxylated arginine, proved to be non-toxic and to exert neuroprotective effects in several models of neurotoxic and ischemic brain and spinal cord injuries. Here we sought to find out whether agmatine treatment would also prove beneficial in a rat spinal cord ischemia model (balloon occlusion of the abdominal aorta bellow the branching point of the left subclavian artery for 5 min). Agmatine was injected (100 mg/kg, i.p. ) 5 min after beginning of re-perfusion and again once daily for the next 3 post-operative days. Motor performance ('combined motor score') was recorded for up to 17 days post-operative and motoneuron cell counts (in representative spinal cord sections) performed on the 17th post-operative day. Agmatine treatment was found to accelerate recovery of motor deficits and to prevent the loss of motoneurons in the spinal cord after transient ischemia. Together, the present and previous findings demonstrate that agmatine is an efficacious neuroprotective agent and that this naturally occurring non-toxic compound should be tried for therapeutic use after neurotrauma and in neurodegenerative diseases.[1]References
- Accelerated functional recovery and neuroprotection by agmatine after spinal cord ischemia in rats. Gilad, G.M., Gilad, V.H. Neurosci. Lett. (2000) [Pubmed]
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