| Objective To investigate the time dependent manner of glutamate concentration in brain tissues of rodent model in different postnatal days and its intervention study. Methods Total128neonatal SD rats were divided into4groups according to postnatal days (P):P2, P6, P12,P18(n=32). Each group were randomly divided into4groups:hypoxic-ischemic brain damage (HIBD) group (H), a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) group (A), GYKI52466group (G) and normal control group (N),(n=8). Standard HIBD models were set up according to Rice methods on rats of H, A, G groups. Rats of the A and G groups were injected drugs immediately after modeling. Brain tissue of all groups was collected to detect the glutamate concentration and observe the pathological changes. Results The results of this study showed that there was a negative correlation between glutamate concentrations and postnatal ages (r=-0.81, p<0.01). The glutamate concentration in brain tissues of P2group was the maximum and was dramatically higher than those of P6group, P12group and P18group, respectively [(670.2±139.4)μmol/gprot. vs.(576±139) μmol/gprot.;(670.2±139.4)μmol/gprot. vs.(441.9±114.9) μmol/gprot.; and (670.2±139.4) μmol/gprot. vs.(287.0±82.8)μmol/gprot.Q=3.88,9.41,15.80, P<0.05or0.01]. The glutamate concentration in brain tissues of G group was the minimum and there were significant differences compared with those of A, H and N groups [(348.6±128.5)μmol/gprot. vs.(608.6±176.7)μmol/gprot.;(348.6±128.5) μmol/gprot. vs.(554.2±206.2)μmol/gprot.;(348.6±128.5)μmol/gprot. vs.(463.8±167.1)μmol/gprot.,Q=10.72,8.49,4.75, P all<0.01]. Pathological changes were consistent with the changes of glutamate concentration in each group. Conclusion Glutamate concentration shows time dependent in brain tissue of different postnatal days represent to different developmental level of neonatal brain. There is a negative correlation between glutamate concentrations and postnatal days. Glutamate concentrations increase in HIBD cases and decrease with treatment of GYKI52466. Neuroprotective effect of GYKI52466is more obvious in relative early stage of gestational age. Early intervention with GYKI52466is expected to prevent and cure neonatal brain damage resulted from premature birth or asphyxia. |