Reduced brain-derived neurotrophic factor expression in cortex and hippocampus involved in the learning and memory deficit in molarless SAMP8 mice

摘要

＜正＞ Background The molarless condition has been reported to compromise learning and memory functions. However, itremains unclear how the molarless condition directly affects the central nervous system, and the functionalconsequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to findthe molecular mechanism related with learning and memory deficit after a bilateral molarless condition having beensurgically induced in senescence-accelerated mice/prone8 （SAMP8） mice, which may ultimately provide an experimentalbasis for clinical prevention of senile dementia.Methods Mice were either sham-operated or subjected to complete molar removal. The animals’ body weights weremonitored every day. Learning ability and memory were measured in a water maze test at the end of the 1st, 2nd, and 3rdmonths after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, thelocomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex andhippocampus were dissected for Western blotting to measure the expression levels of brain-derived neurotrophic factor（BDNF） and the tropomyosin related kinase B （TrkB）, the high affinity receptor of BDNF.Results Slightly lower weights were consistently observed in the molarless group, but there was no significantdifference in weights between the two groups （P ＞0.05）. Compared with the sham group, the molarless group exhibitedlengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activitywas observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarlessgroup （P＜0.05）; but the expression of its receptor, TrkB, was not significantly affected.Conclusion These results suggested that the molarless condition impaired learning and memory abilities in SAMP8mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression inthe cortex and hippocampus.