关键词: 轴突; 大脑梗死; 大鼠

Abstract: Objective To approach the course of secondary axonal degeneration in ipsilateral ventroposterior nucleus of the thalamus (VPN) after cerebral cortex infarction in hypertensive rats.Methods Experimental animals were divided into three groups: middle cerebral artery occlusion (MCAO) group, sham-operated group and normal control group. The model of MCAO was duplicated in the stroke-prone renovascular hypertensive rats (RHRSP) with occlusion of right distal middle cerebral artery (MCA). In the sham-operated group, the right MCA of RHRSP only exposed without occlusion. The matched healthy rats served as normal control group. At the end of 1,2 and 4 weeks of MCAO, the animals were killed and the brains were sectioned for Bielschowsky’s silver stainning and immunohistochemistry analysis of the expression of amyloid βA4 precursorprotein (APP), growth associated protein-43 (GAP-43), microtubule associated protein-2 (MAP-2) in the ipsilateral VPN.Results The positive neural fiber of silver stainning were decreased in MCAO group compared with in sham-operated group in ipsilateral VPN at the end of 4 weeks after ischemia (P <0.05). The expression of APP protein was beginning to increase in ipsilateral VPN at the end of 1 week afterischemia, then enhanced to a higher level from 2 through 4 weeks after ischemia (P <0.05). GAP-43,MAP-2 immunoreactivity were beginning to decrease in ipsilateral VPN at the end of 1 or 2 weekafter ischemia (P <0.05), then reduced to a lower level (P <0.05).Conclusion The immuno-detection of protein marker of axons was more sensitive than conventional silver staining which could find the pathological change of axons at the earlier time.Combined with silver staining, it could evaluate in detail the pathological course of axonal anddendritic destroy. This study proved that a long lasting, progressive axonal degeneration developed in ipsilateral VPN after MCAO.

Key words: Axons; Cerebral infarction; Rats