Objective To study the changes of vitamin C（ VC） levels and sodium vitamin C transporter 2（ SVCT2） protein levels in cerebrospinal fluid（ CSF） and important brain regions of rats after 4 days of binge drinking and ethanol withdrawal. Methods A total of 30 healthy wistar rats were randomly divided into 5 groups： control group（ Group A）， binge drinking for 4 days（ Group B）， withdrawal 1 day after 4-day binge drinking（ Group C）， withdrawal 2 days after 4-day binge drinking（ Group D）， withdrawal 7 days after 4-day binge drinking（ group E）. There were 6 rats in each group. Rats in group B， C， D and E were given ethanol by gavage for 4 days at a concentration of 25% W/V and gavage once every 8 hours for 4 days. Group A was given equal-volume distilled water. Y maze experiment was used to evaluate the spatial working memory of rats. The concentration of intracellular VC in cerebrospinal fluid， prefrontal cortex， parietal cortex， temporal cortex and hippocampus of rats in each group was detected by HPLC combined with electrochemical detector（ HPLC-ECD）， and the protein level of SVCT2 in each brain area of rats was detected by Western blotting. Results In the Y maze experiment， the rate of spontaneous response alternations of rats in group C and D was（ 24.64±11.51）% and（ 41.48±13.01）%， respectively， which were significantly lower than that in group A（ 75.47±8.61）%. The rate of spontaneous response alternations of rats in group E（ 61.64±15.11）% was close to normal， and there is no statistically significant difference between group E and group A（ P＜ 0.05）. The content of VC in CSF of rats in group B was（ 204.54±25.51） μmol/L， which was significantly higher than that in group A（ 145.57±18.98） μmol/L. The CSF VC levels in group C and group D were（ 90.24±15.45）μmol/L and（ 86.93±14.53） μmol/L， respectively， lower than those in group A and group B， and the differences were statistically significant（ P ＜ 0.001）. The CSF VC level of group E was （135.80±17.16）μmol/L. There was no significant difference in the content of VC in CSF between group A and group E（ P＜ 0.05）. The VC levels in brain tissue homogenates（ intracellular） in prefrontal cortex， parietal cortex and hippocampus showed the same trend in group B， which were（ 1.18±0.13） μmol/g，（ 1.14±0.12） μmol/g， （1.20±0.20） μmol/g， respectively， and were all significantly lower than those in group A［ （1.64±0.11） μmol/g， （1.62±0.13） μmol/g，（ 2.06±0.27） μmol/g］. The VC levels in brain tissue homogenates（ intracellular） in prefrontal cortex， parietal cortex and hippocampus of group C after ethanol withdrawal［ （1.20±0.29） μmol/g， （1.05±0.06） μmol/g，（ 1.21±0.15） μmol/g， respectively］recovered to some extent， but still significantly lower than those of group A（ P＜ 0.01）. In group C， the level of VC in temporal cortex［ （1.37±0.04） μmol/g］ was significantly higher than that in parietal cortex（ P ＜ 0.05）. In group D， the level of VC in all brain regions increased， and the level of VC in prefrontal cortex was significantly higher than that in parietal cortex ［（1.63±0.24） μmol/g vs（ 1.26±0.16） μmol/g， P ＜ 0.05］. The levels of VC in prefrontal cortex， parietal cortex， temporal cortex and hippocampus in group E were（ 1.72±0.19） μmol/g，（ 1.43±0.22） μmol/g， （1.67±0.19） μmol/g and（ 1.86±0.22）μmol/g， respectively， significantly higher than those in group B（ all P ＜ 0.01）， and gradually returned to normal level. The level of VC in hippocampus was significantly higher than that in parietal cortex（ P＜0.05）. Western blot results showed that compared with group A， the protein of SVCT2 in prefrontal cortex， parietal cortex of group B， group C and group D， and in hippocampus of group C， group D and group E was significantly increased（ P＜0.05）. Conclusions Binge drinking for 4 days can cause brain damage in rats. The VC level in CSF and brain tissue homogenates of each brain region present a negative correlation dynamic change process after ethanol treatment. During ethanol treatment process， the expression of SVCT2 protein is up-regulated， which will help the VC in the CSF to be transported to the neurons in each brain region to play an antioxidant role.