Objective        To determine the effect of collapsin response mediator protein 2 (CRMP2) on the neuronal loss and neurogenesis in the rats after cerebral ischemia/reperfusion (I/R) injury and investigate its possible mechanisms.   Methods       A total of 60 adult male SD rats were divided into 4 groups

that is

sham operation group

cerebral I/R group (middle cerebral artery occlusion

MCAO)

cerebral ischemia with blank plasmid control group (MCAO+GFP group)

and cerebral ischemia with CRMP2 eukaryotic plasmid group (MCAO+CRMP2 group). In 1 d after the injection of corresponding plasmids

the cerebral I/R model was established. In 5 to 7 d after the operation

5ethinyl deoxidization uracil nucleoside 2′ (Edu) was injected intraperitoneally into these rats. Then the expression of MAP2

GFAP

Edu and Nestin/Edu was tested by immunofluorescence assay. The expression levels of CRMP2

brain derived neurotrophic factor (BDNF) and N-methyl-D-aspartate receptor 2B (NMDAR2B) were detected by Western blotting. The location of CRMP2 was tested by immunohistochemical staining. Neurological function was also evaluated.    Results        Compared with the sham group

cerebral I/R injury decreased the expression level of MAP2 (P0.05)

while increased that of GFAP (P0.05)

as well as the numbers of Edu (62.00±7.65

62.60±7.06) and Edu/Nestin (31.6±5.50

31.6±5.40) positive cells in the MCAO and MCAO+GFP groups (P0.05). Intervention of CRMP2 eukaryotic plasmid increased the expression of MAP2 (P0.05)

inhibited the expression of GFAP (P0.05)

and boosted the amounts of Edu (100.20±11.52) and Nestin/Edu (57.20±4.80) positive cells (P0.05). Compared with the sham group

the expression levels of BDNF and NMDAR2B were obviously increased in the MCAO and MCAO+ GFP groups (P0.05). After the intervention of CRMP2 eukaryotic plasmid

the expression of BDNF was further enhanced (P0.05)

and NMDAR2B was partly alleviated (P0.05). The neurological scores were improved significantly in the MCAO+CRMP2 groups than the other groups (P0.05).   Conclusion      CRMP2 may attenuate neuronal loss and promote the proliferation of the neural stem cells in rats after I/R injury

which might be due to the regulation of BDNF and NMDAR2B.