This paper reports that lesions of the medial frontal cortex (MFC) caused behavioral deficit in rats and that this deficit could be attenuated by a well formulated treatment with Org2766, an analog of ACTH- (4-9). Wis...This paper reports that lesions of the medial frontal cortex (MFC) caused behavioral deficit in rats and that this deficit could be attenuated by a well formulated treatment with Org2766, an analog of ACTH- (4-9). Wistar rats were distributed in 3 groups: MFC lesion treated with saline (M-N); MFC lesion treated with Org2766 (MO);and sham-operation treated with saline (S). Repeated Org2766 or saline injection commenced from the day of surgery and lasted for 1 3 days. After surgery. the rats were trained in a passive avoidance task and then in an active avoidance task. MFC lesions were found to be strongly associated with behavioral deficits. The M-N group rats displayed poor retention of the passive avoidance response and showed much slower learning of the active avoidance task as compared to S group rats. The result showed that chronic Org2766 administration improved the behavioral performance of both tasks in MFC lesioned rats. The also revealed that the superoxide dismutase (SOD)activity was significantly increased in the M-O group as compared to the M-N group 15 days after surgery. The possible mechanisms related to the beneficial effect of Org2766 on cortex damage are discussed.展开更多
文摘This paper reports that lesions of the medial frontal cortex (MFC) caused behavioral deficit in rats and that this deficit could be attenuated by a well formulated treatment with Org2766, an analog of ACTH- (4-9). Wistar rats were distributed in 3 groups: MFC lesion treated with saline (M-N); MFC lesion treated with Org2766 (MO);and sham-operation treated with saline (S). Repeated Org2766 or saline injection commenced from the day of surgery and lasted for 1 3 days. After surgery. the rats were trained in a passive avoidance task and then in an active avoidance task. MFC lesions were found to be strongly associated with behavioral deficits. The M-N group rats displayed poor retention of the passive avoidance response and showed much slower learning of the active avoidance task as compared to S group rats. The result showed that chronic Org2766 administration improved the behavioral performance of both tasks in MFC lesioned rats. The also revealed that the superoxide dismutase (SOD)activity was significantly increased in the M-O group as compared to the M-N group 15 days after surgery. The possible mechanisms related to the beneficial effect of Org2766 on cortex damage are discussed.
