Preliminary Study On Somatosensory Cortex Plasticity After Focal Cerebral Ischemia In Rats

PARTâ… Focal cerebral ischemia in rats by photothrombosis of cortical microvesselsIschemic cerebral vascular disease is the main reason of people for death, and results in significant morbidity, mortality and disability. The systematic studies of the pathophysiology and treatment of stroke rely on the establishment of animal model with high similarity to human cerebral ischemia. The photothrombotic occlusion of cerebral microvessels is a thrombosis induced by endothelial injury through singlet oxygen produced by Rose Bengal injection and green light irradiation which is an effective and non-invasive method of simulating the ischemic stroke in humans. Optical intrinsic signal imaging (OISI) offers spatial and temporal resolution exceeding that achieved by most alternative imaging techniques for imaging cortical functional architecture or for monitoring local changes in cerebral blood volume or oxygen saturation. The infarction was verified by TTC staining and EB staining.AIM The aims of the present study are to establish a focal cerebral ischemia model in rat, and to investigate change of vessel and blood flow in infarction region by intrinsic optical imaging.METHODS Based on the principle of photochemical initiation of thrombosis, focal cortical was completely infracted. Intrinsic signals from irradiated region were recorded. The size of infarction and damage of blood brain barrier were investigated.RESULTS During illumination, clots flows were observed several times in illuminated region vessels, and vessels turned vague, which indicated occlusion is forming. The survival rate of ischemic rates was 100%. TTC staining showed infarction was reproducible and reliable. Evans blue leaked out at the edge of infarction. CONCLUSIONS The photochemical infarct model in rats is a reliable model with low mortality to study cerebral ischemia. Optical intrinsic signal imaging is an effective way to investigate changes in cerebral cortex during infarction.PARTâ…¡Effect of exercise on GFAP and GAP-43 Expression in Brain of Rats after Focal Cerebral InfarctionEvidence suggests that exercise has beneficial effects on brain recovery and function. Although behavioral improvements are well documented, little is known regarding the underlying mechanisms. The promotion of plasticity may be responsible for mediating these enhancements. During brain repair following injury, plastic changes are geared towards maximizing function in spite of the damaged brain. Glial fibrillary acidic protein (GFAP) and growth-associated protein-43 (GAP-43) are both related substance of plasticity. GFAP is a specific astrocyte marker participating in the formation of cytoskeletal filaments of glial cells. It is involved in many cellular functioning processes, such as cell structure and movement, cell communication, and the functioning of the blood brain barrier. GAP-43 appears to be permissive for neuro-axonal regeneration and synaptic remodeling. It is expressed at high levels in neuronal growth cones during development and axonal regeneration. This encoded protein is considered a crucial component of an effective regenerative response in the nervous systemAIM To investigate effects of exercise on GFAP and GAP-43 expression around infarction area in rats after focal cerebral infarction and on plasticity.METHODS 42 healthy male rats were randomly divided into group exercise (n=18), group resting (n=18), and control group with sham-operated (n=6). The rats in group exercise were subject to exercise on a treadmill for 30 min each day. The rats in group resting were fed without exercise. The rats in control group with sham-operated were just anaesthetized and sliced off scalp. The model of focal cerebral infarction was inducing by photothrombosis of cortical microvessels. The levels of GFAP and GAP-43 around the infarct area were observed at 7,14, and 21 d after infarction by using immunohistochemical staining.RESULTS The astrocytes with GFAP-positive have the plastic changes in shapes in the peri-infarct areas after focal cerebral infarcts. The expression of GFAP between group exercise and group model had no significant difference at 7 d. In group exercise, expression of GFAP was remarkable increased compared with group model and control group at 14, 21 d. In group model, expression of GFAP was remarkable increased compared with control group at 14, 21 d. The expression of GAP-43 was increased more remarkably in group exercise than in group model and control group at 7, 14 d. There was no significant difference at 21 d among three groups on expression of GAP-43.CONCLUSION The exercise training could improve synapse building and new contact of synapse by increasing expression of GFAP and GAP-43.