Aim:To investigate the effect of gabapentin on neural [neuron-specific enolase(NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S 100B] in differ-ent brain regions of diabetic rats.Methods:Diabetes was induced by a singleintraperitoneal injection of streptozotocine (50 mg/kg body weight).Rats in onediabetic group received gabapentin (50 mg.kg~(-1).d~(-1)) and rats in the other diabeticgroup received vehicle only for 6 weeks.The levels of GFAP,S100B,and NSE weredetermined by immunoblotting in the hippocampus,cortex,and cerebellum.Lipidperoxidation (LPO as malondialdehyde+ 4-hydroxyalkenals) and glutathione (GSH)levels were also determined in the same brain parts.Results:Total and degradedGFAP content and S100B protein expression in different areas of brain tissuessignificantly increased in diabetic rats compared to control rats.Similarly,NSElevels were also significantly elevated in hyperglycemic rats.In addition,therewas a significant increase in LPO levels in the diabetic rat brain compared tocontrol rat brains.Pretreatment with gabapentin prevented the upregulation ofGFAP,S 100B,and NSE in all brain regions of diabetic rats.The level of LPO wasreduced,but not completely halted,by treatment with gabapentin.Conclusion:These results suggest that diabetes causes glial and neuronal injury,possibly asa result of elevated oxidative stress,and that gabapentin protects neurons andglial cells.Thus,we predict that gabapentin treatment will attenuate the hippo-campal and cortical neurodegeneration observed during diabetes mellitus in rats. Aim: To investigate the effect of gabapentin on neural [neuron-specific enolase (NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S 100B] in differ-ent brain regions of diabetic rats. Methods: Diabetes was induced by a single intraperitoneal injection of streptozotocine (50 mg / kg body weight). Rats in onediabetic group received gabapentin (50 mg.kg -1 (d)) and rats in the other diabetic group received vehicle only for 6 weeks The levels of GFAP, S100B, and NSE were identified by immunoblotting in the hippocampus, cortex, and cerebellum. Lipid proroxidation (LPO as malondialdehyde + 4-hydroxyalkenals) and glutathione (GSH) levels were also determined in the same brain parts. Results: Total and degradedGFAP content and S100B protein expression in different areas of brain tissuessignificantly increased in diabetic rats compared to control rats.Similarly, NSElevels were also significantly elevated in hyperglycemic rats. In addition, therewas a significant increase in LPO levels in the di abetic rat brain compared tocontrol rat brains. Treatment with gabapentin prevented the upregulation of GFAP, S 100B, and NSE in all brain regions of diabetic rats. level of LPO wasreduced, but not completely halted, by treatment with gabapentin. Contact: These results suggest that diabetes causes glial and neuronal injury, possibly asa result of elevated oxidative stress, and that gabapentin protects neurons and glial cells .hus, we predict that gabapentin treatment will attenuate the hippo-campal and cortical neurodegeneration observed during diabetes mellitus in rats.