Acute treatment with MgSO4 attenuates long-term hippocampal tissue loss after brain trauma in the rat
✍ Scribed by Kevin D. Browne; Matthew J. Leoni; Akira Iwata; Xiao-Han Chen; Douglas H. Smith
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 385 KB
- Volume
- 77
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Previous studies have shown that magnesium salts and the noncompetitive N‐methyl‐D‐aspartate (NMDA) receptor antagonist, NPS 1506, attenuated short‐term cognitive deficits and histopathological changes associated with traumatic brain injury (TBI). We evaluated the long‐term effects of both therapies after brain trauma. Young adult rats were subjected to parasagittal fluid‐percussion brain injury and received either MgSO~4~ (125 μmol/400 g rat; n = 12) 15 min post‐injury, NPS 1506 (1.15 mg/kg; n = 12) 15 min and 4 hr post‐injury, or vehicle (n = 9) 15 min post‐injury. Uninjured animals (sham) received vehicle (n = 10). Learning function in these animals was evaluated using a water maze paradigm 8 months after injury or sham treatment, and the brains were examined for cortical and hippocampal tissue loss. Compared to sham animals, injured vehicle‐treated animals displayed a substantial learning dysfunction, indicated by an increased latency to find a hidden platform in the water maze (P < 0.001). No improvements in learning, however, were found for injured animals treated with NPS 1506 or MgSO~4~. Injury induced >30% loss of tissue in the ipsilateral cortex in vehicle‐treated animals that was not reduced in animals treated with either NPS 1506 or MgSO~4~. Treatment with MgSO~4~ significantly reduced progressive tissue loss in the hippocampus (P < 0.001). These findings are the first to demonstrate long‐term neuroprotection of hippocampal tissue by an acute treatment in a TBI model. These data also show that the previously reported broad efficacy of MgSO~4~ or NPS 1506 observed shortly after brain trauma could not be detected 8 months post‐injury. © 2004 Wiley‐Liss, Inc.