Neuroscience 2001 Abstract
| Presentation Number: | 210.12 |
|---|---|
| Abstract Title: | Aminoguanidine attenuates fluid-percussive brain injury in rats. A combined magnetic resonance imaging and histopathologic studies. |
| Authors: |
Lu, J.*1
; Shirhan, M.1
; Moore, S.3
; Kaur, C.2
; Ling, E. A.2
; Wong, M. C.3
; Teo, A. L.1
; Tan, M. H.1
; Moochhala, S.1
1Defence Medical Research Institute, Singapore, Singapore 2Anatomy, National University of Singapore, Singapore, Singapore 3National Cancer Centre, Singapore, Singapore |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Trauma -- Brain |
| Session: |
210. Trauma: brain injury--treatment I Poster |
| Presentation Time: | Sunday, November 11, 2001 4:00 PM-5:00 PM |
| Location: | Exhibit Hall XX-26 |
| Keywords: | iNOS inhibitor, traumatic brain injury, apoptosis, MRI |
The present study examined the effects of a selective inducible nitric oxide synthase (iNOS) inhibitor on neuronal cell survival and post-traumatic recovery in rats following a lateral fluid percussion injury. Aminoguanidine at the dosage of 100 mg/kg or normal saline was injected intraperitoneally into rats 2 hours before or 30 minutes after the head injury. Animals were sacrificed at 4h, 1, 3 and 7 days post-injury. Treatment with iNOS inhibitor aminoguanidine significantly reduced lesion volumes in rats after fluid percussion, as evaluated by high-resolution magnetic resonance imaging (MRI). Immunohistochemical analysis showed a marked induction of iNOS expression in macrophages in the subarachnoid space and cerebral ventricles ipsilateral to the injury in rats killed at 1-day. In parallel with the appearance of iNOS positive macrophages, apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL). In rats receiving prophylactic or post-injury treatment of aminoguanidine, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection. The location and extent of these pathologic changes correlated with MRI findings. Present results showed that inhibition of iNOS synthesis by aminoguanidine improved histopathological outcomes. It is suggested that nitric oxide (NO) may be involved in stimulating neuronal apoptosis following brain injury.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2001 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2001. Online.
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