AIMS: The aim of this study is to determine the role of nitric oxide (NO) in neuropathic pain and the effect of embryonic neural stem cell (ENSC) transplantation on NO content in rat spinal cord neurons following spinal cord injury (SCI). MAIN METHODS: Ninety adult male Sprague-Dawley rats were divided into 3 groups (n=30, each): control (laminectomy), SCI (hemisection at T12-T13 segments) and SCI+ENSC. Each group was further divided into sub-groups (n=5 each) based on the treatment substance (L-NAME, 75 mg/kg/i.p.; L-arginine, 225 mg/kg/i.p.; physiological saline, SF) and duration (2h for acute and 28 days for chronic groups). Pain was assessed by tail flick and Randall-Selitto tests. Fos immunohistochemistry and NADPH-d histochemistry were performed in segments 2 cm rostral and caudal to SCI. KEY FINDINGS: Tail-flick latency time increased in both acute and chronic L-NAME groups and increased in acute and decreased in chronic L-arginine groups. The number of Fos (+) neurons decreased in acute and chronic L-NAME and decreased in acute L-arginine groups. Following ENSC, Fos (+) neurons did not change in acute L-NAME but decreased in the chronic L-NAME groups, and decreased in both acute and chronic L-arginine groups. NADPH-d (+) neurons decreased in acute L-NAME and increased in L-arginine groups with and without ENSC transplantation. SIGNIFICANCE: This study confirms the role of NO in neuropathic pain and shows an improvement following ENSC transplantation in the acute phase, observed as a decrease in Fos(+) and NADPH-d (+) neurons in spinal cord segments rostral and caudal to injury.
AIMS: The aim of this study is to determine the role of nitric oxide (NO) in neuropathic pain and the effect of embryonic neural stem cell (ENSC) transplantation on NO content in rat spinal cord neurons following spinal cord injury (SCI). MAIN METHODS: Ninety adult male Sprague-Dawley rats were divided into 3 groups (n=30, each): control (laminectomy), SCI (hemisection at T12-T13 segments) and SCI+ENSC. Each group was further divided into sub-groups (n=5 each) based on the treatment substance (L-NAME, 75 mg/kg/i.p.; L-arginine, 225 mg/kg/i.p.; physiological saline, SF) and duration (2h for acute and 28 days for chronic groups). Pain was assessed by tail flick and Randall-Selitto tests. Fos immunohistochemistry and NADPH-d histochemistry were performed in segments 2 cm rostral and caudal to SCI. KEY FINDINGS: Tail-flick latency time increased in both acute and chronic L-NAME groups and increased in acute and decreased in chronic L-arginine groups. The number of Fos (+) neurons decreased in acute and chronic L-NAME and decreased in acute L-arginine groups. Following ENSC, Fos (+) neurons did not change in acute L-NAME but decreased in the chronic L-NAME groups, and decreased in both acute and chronic L-arginine groups. NADPH-d (+) neurons decreased in acute L-NAME and increased in L-arginine groups with and without ENSC transplantation. SIGNIFICANCE: This study confirms the role of NO in neuropathic pain and shows an improvement following ENSC transplantation in the acute phase, observed as a decrease in Fos(+) and NADPH-d (+) neurons in spinal cord segments rostral and caudal to injury.