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BACKGROUND: The functional role of brain-derived neurotrophic factor (BDNF) is enhanced following cerebral ischemic injury providing neurons with an important self-protection mechanism in early stage ischemia/hypoxia. OBJECTIVE: To investigate the expression pattern of BDNF in different rat hippocampal regions following focal cerebral ischemic injury. DESIGN, TIME AND SETTING: We performed a comparative and neurobiological study of animals in the Department of Histology and Embryology and the Central Laboratory, Hebei Medical University from March to December 2003. MATERIALS: Forty healthy Sprague Dawley rats were randomly divided into a cerebral ischemia group and a sham operation group, with 20 rats per group. METHODS: In the cerebral ischemia group, we occluded the right middle cerebral artery with a suture, threading it to a depth of 17–19 mm. In the sham operation group, the threading depth was approximately 10 mm. MAIN OUTCOME MEASURES: We analyzed the expression of BDNF in different hippocampal regions by immunohistochemical staining of brain sections taken on post-operative days 7, 14, 21 and 30. RESULTS: Sham operation group: We observed a number of a few BDNF-positive cells with light staining in the hippocampal CA1-CA4 regions and dentate gyrus. Cerebral ischemia group: compared with the sham operation group, BDNF increased on day 7, significantly increased on day 14, and reached a peak on day 21 (P < 0.05). Furthermore, immunologically reactive products were darkly stained, and neurons had long axons. BDNF was particularly highly expressed in the hippocampal CA3 and CA4 regions and dentate gyrus. CONCLUSION: Cerebral ischemic injury can damage hippocampal neurons. Neurons can increase their anti-ischemic capacity by increasing BDNF expression in the hippocampal CA3 and CA4 regions and dentate gyrus.
BACKGROUND: The functional role of brain-derived neurotrophic factor (BDNF) is enhanced following cerebral ischemic injury to neurons with an important self-protection mechanism in early stage ischemia / hypoxia. OBJECTIVE: To investigate the expression pattern of BDNF in different rat hippocampal regions following focal cerebral ischemic injury. DESIGN, TIME AND SETTING: We performed a comparative and neurobiological study of animals in the Department of Histology and Embryology and the Central Laboratory, Hebei Medical University from March to December 2003. MATERIALS: Forty healthy Sprague Dawley rats were randomly divided into a cerebral ischemia group and a sham operation group, with 20 rats per group. METHODS: In the cerebral ischemia group, we occluded the right middle cerebral artery with a suture, threading it to a depth of 17-19 mm. In the sham operation group, the threading depth was approximately 10 mm. MAIN OUTCOME MEASURES: We analyzed the expression of BDNF in dif ferent hippocampal regions by immunohistochemical staining of brain sections taken on post-operative days 7, 14, 21 and 30. RESULTS: Sham operation group: We observed a number of a few BDNF-positive cells with light staining in the hippocampal CA1-CA4 regions and dentate gyrus. Cerebral ischemia group: compared with the sham operation group, BDNF increased on day 7, significantly increased on day 14, and reached a peak on day 21 (P <0.05). Furthermore, immunologically reactive products were darkly stained, and Neurons had long axons. BDNF was particularly highly expressed in the hippocampal CA3 and CA4 regions and dentate gyrus. CONCLUSION: Cerebral ischemic injury can damage hippocampal neurons. Neurons can increase their anti-ischemic capacity by increasing BDNF expression in the hippocampal CA3 and CA4 regions and dentate gyrus.