Abstract

Objective To study the hippocampal corticotropin releasing hormone (CRH) mRNA expression and neuroprotective mechanism of adrenocorticotropic hormore (ACTH) in immature rats after N-methyl-D-aspartate (NMDA)-induced spasm seizures. Methods Sixty 10-day-old Wistar rats were randomly divided into blank control group, NMDA-induced seizure group and ACTH treatment group (n=20). Rats in the blank control group did not give any treatment; rat models of infantile spasm in the NMDA-induced seizure group and ACTH treatment group were induced by intraperitoneal injection of NMDA (7 mg/kg) for a consecutive 7 d; 3 h after NMDA injection, intraperitoneal injection of ACTH 0.5 mg/(kg·d) was performed in the rats of ACTH treatment group, and NMDA-induced seizure group was given an equal volume of saline. By in situ hybridization (ISH), the mean optical density of CRH mRNA-positive neurons in the hippocampus was measured. Results In the ACTH treatment group, the latencies of epileptic seizures one week after treatment were significantly prolonged as compared with those before treatment, and the scores of epileptic seizures one week after treatment were significantly decreased as compared with those before treatment (P<0.05); the latencies of epileptic seizures were significantly prolonged and the scores of epileptic seizures were significantly decreased in the ACTH treatment group as compared with those in the NMDA-induced seizure group (P<0.05). The CRH mRNA expression in NMDA-induced seizure group was significantly increased as compared with that in the blank control group (P<0.05), and the CRH mRNA expression in the ACTH treatment group was significantly decreased as compared with that in the NMDA-induced seizure group (P<0.05). Conclusion Systemic ACTH has neuroprotective effect via down-regulating the hippocampal CRH mRNA expression. Key words: Infantile spasm; Corticotropin releasing hormone; Adrenocorticotropic hormore; Hippocampus

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