Traumatic brain axonal injury produces sustained decline in intracellular free magnesium concentration.
Decline in brain intracellular free magnesium concentration following experimental traumatic brain injury has been widely reported in a number of studies. However, to date, these studies have been confined to focal models of brain injury and temporally limited to the immediate 8-h period post-trauma. Recently, a new model of impact-acceleration brain injury has been developed which produces nonfocal diffuse axonal injury more typical of severe clinical trauma. The present study has used phosphorus magnetic resonance spectroscopy and the rotarod motor test to characterise magnesium homeostasis and neurologic outcome over a period of 8 days after induction of severe impact-acceleration injury in rats. Severe impact-acceleration induced injury resulted in a highly significant and sustained decline in intracellular free magnesium concentration that was apparent for 4 days post-trauma with recovery to preinjury levels by day six. There were no significant changes in pH or ATP concentration at any time point post-injury. All animals demonstrated a significant neurologic deficit over the assessment period. The extended period of magnesium decline after severe diffuse brain trauma suggests that repeated administration may be required for pharmacotherapies targeted at restoring magnesium homeostasis.
Heath
D L
DL
Department of Physiology and Pharmacology, James Cook University, Townsville, Queensland, Australia.
Vink
R
R
D000818:Animals; D001369:Axons; D001930:Brain Injuries / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology; D006706:Homeostasis; D007425:Intracellular Membranes / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009420:Nervous System / Q000503:physiopathology; D009994:Osmolar Concentration; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D008274:Magnesium