Neurological recovery in diabetic rats following spinal cord injury

Tariq, Mohammad, Morais, Christudas, Kishore, Puli Nanda, Biary, Nabil, Al Deeb, Saleh and Al Moutaery, Khalaf (1998) Neurological recovery in diabetic rats following spinal cord injury. Journal of Neurotrauma, 15 4: 239-251. doi:10.1089/neu.1998.15.239


Author Tariq, Mohammad
Morais, Christudas
Kishore, Puli Nanda
Biary, Nabil
Al Deeb, Saleh
Al Moutaery, Khalaf
Title Neurological recovery in diabetic rats following spinal cord injury
Journal name Journal of Neurotrauma   Check publisher's open access policy
ISSN 0897-7151
1557-9042
Publication date 1998-04
Sub-type Article (original research)
DOI 10.1089/neu.1998.15.239
Volume 15
Issue 4
Start page 239
End page 251
Total pages 13
Place of publication New Rochelle, NY, United States
Publisher Mary Ann Liebert
Language eng
Abstract This study was designed to assess the effect of spinal cord injury on neurobehavioral, electrophysiological, structural, and biochemical changes in normal and diabetic rats. Experimental diabetes was induced in Sprague–Dawley male rats (weighing 250–280 g) with streptozotocin (50 mg/kg IP). Eight weeks after the treatment with streptozotocin the animals were anaesthetized with chloral hydrate and laminectomy was performed at T 7–8 level leaving the dura intact. A compression plate (2.2 × 5.0 mm) loaded with a weight of 35 g was placed on the exposed spinal cord for 5 min. Post-operative neurological function was assessed using inclined plane test, modified Tarlov score, and vocal and sensory score daily for 10 days. Electrophysiological changes were assessed using somatosensory and corticomotor evoked-potentials. The animals were sacrificed at different time intervals and injured site of the spinal cord was analyzed for changes in vitamin E and glutathione levels (as markers of oxidative stress). Pathological changes in spinal cord were also studied using light microscopy. The data on neurobehavioral study clearly indicated that the compression of spinal cord produced highly significant neurological deficit and poor recovery in diabetic rats as compared to nondiabetic rats. Our histopathological and electrophysiological results also confirmed that diabetic animals are more susceptible to compressive spinal cord injury as compared to nondiabetic animals. A higher depletion of antioxidant defense markers (vitamin E and glutathione) was observed in diabetic rats as compared to nondiabetic rats. These results point toward the role of free radicals in poor recovery in diabetic rats following neurotrauma. Further studies are warranted to assess the neuroprotective potential of antioxidants to retard the secondary pathophysiological events following neurotrauma and to enhance the recovery.
Keyword Diabetes
Electrophysiology
Glutathione
Oxidative stress
Spinal cord injury
Vitamin E
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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Created: Mon, 20 Dec 2010, 13:59:03 EST