Objective    To explore the protective effect of brain-derived neurotrophic factor (BDNF) on cultured rat cortical neurons against glutamate (Glu)-induced injury and its mechanism.     Methods    Cortical neurons were primarily cultured from 1-day-old newborn Sprague-Dawley rats and then cultured for 7 d. The cortical neurons were divided randomly into 3 groups: control group

Glu group and BDNF group after identified with neuron-specific enolase (NSE) immunostaining. The cells of BDNF were treated with 50 ng/ml BDNF on day 6 for 24 h followed by cultured with 50 μmol/L Glu for 0.5 h. While

the cells of Glu group were cultured with 50 μmol/L Glu for 0.5 h on day 7. The control cells received no such treatments. On day 8

cell viability were determined by the colorimetric MTT assay. The morphological features of the neuron cells were observed under AO/EB fluorescence microscopy. Expressions of p75NTR

JNK and ERK were observed using Western blot analysis.     Results    On day 8

the primary cortical neurons grew well. BDNF protected cortical neural cells from Glu injury. Cell viability of BDNF group was (1.14±0.06)

significantly higher than that of Glu group (0.72±0.10

P0.01)

though which was lower than that of the control group (1.26±0.06). More cell apoptosis was observed in Glu group than in BDNF group (P0.05). The expression of p75NTR was higher in Glu group (0.90±0.18) and BDNF group (0.78±0.09) than in normal control group (0.15±0.12

P0.05); the expression of JNK was lower in the BDNF group (0.56±0.16) than in the Glu group (0.95±0.06

P0.05); at the same time

the expression of ERK was opposite to that of JNK (0.83±0.16 in the BDNF group vs 0.57±0.08 in the Glu group

P0.05).     Conclusion    BDNF protects cultured rat cortical neurons from the injury induced by high-dose Glu

which may be through changing the proportion between p75NTR and TrkB

up-regulating ERK and down-regulating JNK to suppress cell apoptosis and improve cell viability.