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目的:研究砷暴露对不同发育阶段仔鼠海马脑源性神经营养因子（BDNF）和酪氨酸激酶受体B（TrkB）水平的影响，探讨砷暴露引起仔鼠学习记忆能力损伤的可能机制。方法:将24只妊娠昆明种小鼠采用随机数字表法分为对照（蒸馏水）组和15、30、60 mg/L亚砷酸钠（NaAsOn 2）组，每组6只。从妊娠第1天至仔鼠断乳前经母鼠染砷，仔鼠断乳至出生后40 d（PND 40）继续染砷，染砷方式为自由饮水。对PND 40仔鼠进行水迷宫实验以检测其学习记忆能力，分别对PND 10、20、40仔鼠称量体重，取脑组织并分离海马，采用实时荧光定量PCR（Real-time PCR）法检测仔鼠海马BDNF和TrkB mRNA表达水平。n 结果:对照组，15、30、60 mg/L NaAsOn 2组PND 20仔鼠体重组间比较差异有统计学意义[（14.42 ± 1.88）、（13.50 ± 1.38）、（13.00 ± 1.14）、（11.75 ± 0.82）g，n F = 4.000，n P < 0.05]，其中60 mg/L NaAsO n 2组仔鼠体重显著低于对照组（n P < 0.05）；PND 40仔鼠体重组间比较差异有统计学意义[（38.58 ± 2.35）、（37.17 ± 1.78）、（35.67 ± 1.69）、（33.83 ± 1.47）g， n F = 7.248，n P < 0.05]，其中30和60 mg/L NaAsO n 2组仔鼠体重显著低于对照组，60 mg/L NaAsOn 2组仔鼠体重显著低于15 mg/L NaAsOn 2组（n P均< 0.05）。水迷宫实验训练的第3、4、5天仔鼠寻找平台潜伏期组间比较差异有统计学意义（n F = 3.380、6.788、7.240，n P均< 0.05），训练的第4、5天，15、30、60 mg/L NaAsOn 2组仔鼠寻找平台潜伏期[（67.76 ± 6.45）、（71.47 ± 12.19）、（73.96 ± 10.42），（58.63 ± 9.24）、（60.20 ± 3.74）、（67.96 ± 15.41）s]均明显长于对照组[（52.83 ± 8.33）、（43.39 ± 8.98）s，n P均< 0.05]；空间探索实验，撤台后仔鼠在第Ⅱ象限停留时间组间比较差异有统计学意义（n F = 5.709，n P < 0.05），与对照组[（24.48 ± 3.18）s]比较，30和60 mg/L NaAsO n 2组仔鼠停留时间[（18.85 ± 3.97）、（16.90 ± 1.62）s]显著减少（n P均< 0.05）。PND 20仔鼠海马BDNF mRNA水平（1.00 ± 0.05、0.98 ± 0.06、0.85 ± 0.06、0.68 ± 0.03）组间比较差异有统计学意义（n F = 9.368，n P < 0.05），其中60 mg/L NaAsO n 2组显著低于对照组，15和30 mg/L NaAsOn 2组（n P均< 0.05）；PND 40仔鼠海马BDNF mRNA水平（1.00 ± 0.03、0.75 ± 0.02、0.76 ± 0.03、0.73 ± 0.06）组间比较差异有统计学意义（n F = 3.998，n P < 0.05），其中各砷暴露组显著低于对照组（ n P均< 0.05）。PND 20仔鼠海马TrkB mRNA水平（1.00 ± 0.08、0.71 ± 0.02、0.73 ± 0.02、0.68 ± 0.09）组间比较差异有统计学意义（n F = 16.158，n P < 0.05），其中各砷暴露组显著低于对照组（ n P均< 0.05）。n 结论:砷暴露可使仔鼠海马BDNF和TrkB mRNA水平降低，进而可能影响学习记忆能力。“,”Objective:To investigate the possible mechanism of learning and memory damage induced by arsenic exposure through studying the effects of arsenic exposure on levels of brain-derived neurotrophic factor (BDNF) and tyrosine kinases B (TrkB) in hippocampus of offspring mice at different developmental stages.Methods:Twenty-four pregnant Kunming mice were divided into control (distilled water) group and 15, 30 and 60 mg/L sodium arsenite (NaAsOn 2) groups according to random number table method, six mice in each group. The pregnant mice were exposed to NaAsOn 2 until weaning. After weaning, the offspring mice were still exposed to NaAsOn 2 through drinking water till postnatal day (PND) 40. Morris water maze was used to determine the effects of arsenic exposure on learning and memory ability in PND 40 mice. The body weight of the mice was measured at PND 10, 20 or 40, and brain tissues were taken after the mice were sacrificed and the hippocampus was isolated. The levels of BDNF and TrkB mRNA in the hippocampus of offspring mice were measured by Real-time PCR.n Results:There was significant difference in body weight of PND 20 offspring mice among the control, 15, 30 and 60 mg/L NaAsOn 2 groups [(14.42 ± 1.88), (13.50 ± 1.38), (13.00 ± 1.14), (11.75 ± 0.82) g, n F = 4.000, n P < 0.05], the body weight of offspring mice in 60 mg/L NaAsO n 2 group decreased significantly than that in control group(n P < 0.05); there was significant difference in body weight of PND 40 offspring mice among groups [(38.58 ± 2.35), (37.17 ± 1.78), (35.67 ± 1.69), (33.83 ± 1.47) g, n F = 7.248, n P < 0.05], the body weights of offspring mice in 30 and 60 mg/L NaAsO n 2 groups were significantly lower than that in control group, and the body weight of PND 40 offspring mice in 60 mg/L NaAsOn 2 group was significantly lower than that in 15 mg/L NaAsOn 2 group (n P < 0.05); the results of Morris water maze showed that there were significant differences in the escape latency of offspring mice among groups since 3 - 5 days of training ( n F = 3.380, 6.788, 7.240, n P < 0.05), the escape latency of offspring mice in NaAsO n 2 groups [(67.76 ± 6.45), (71.47 ± 12.19), (73.96 ± 10.42), (58.63 ± 9.24), (60.20 ± 3.74), (67.96 ± 15.41) s] was significantly longer than that in control group [(52.83 ± 8.33), (43.39 ± 8.98) s] since 4 - 5 days of training (n P < 0.05); on the other hand, in the probe trail, there was significant difference in time spent in the target quadrant of offspring mice among groups ( n F = 5.709, n P < 0.05), time spent in the target quadrant of offspring mice in 30 and 60 mg/L NaAsO n 2 groups [(18.85 ± 3.97), (16.90 ± 1.62) s] was significantly less than that in control group [(24.48 ± 3.18) s, n P < 0.05]; there was significant difference in BDNF mRNA levels (1.00 ± 0.05, 0.98 ± 0.06, 0.85 ± 0.06, 0.68 ± 0.03) of PND 20 mice among groups ( n F = 9.368, n P < 0.05), BDNF mRNA level of mice exposed to 60 mg/L NaAsO n 2 was significantly lower than that in control, 15 and 30 mg/L NaAsOn 2 groups (n P < 0.05); there was significant difference in BDNF mRNA levels (1.00 ± 0.03, 0.75 ± 0.02, 0.76 ± 0.03, 0.73 ± 0.06) of PND 40 mice among groups ( n F = 3.998, n P < 0.05), and that of PND 40 mice exposed to NaAsO n 2 decreased significantly than that in control group (n P < 0.05); there was significant difference in TrkB mRNA levels (1.00 ± 0.08, 0.71 ± 0.02, 0.73 ± 0.02, 0.68 ± 0.09) of PND 20 mice among groups ( n F = 16.158, n P < 0.05), and that of PND 20 mice exposed to NaAsO n 2 were significantly lower than that in control group (n P < 0.05).n Conclusion:Arsenic exposure could decrease the mRNA levels of BDNF and TrkB in the hippocampus of offspring mice, which may affect the ability of learning and memory.