ABSTRACT
<p><b>BACKGROUND</b>The molarless condition has been reported to compromise learning and memory functions. However, it remains unclear how the molarless condition directly affects the central nervous system, and the functional consequences on the brain cortex and hippocampus have not been described in detail. The aim of this study was to find the molecular mechanism related with learning and memory deficit after a bilateral molarless condition having been surgically induced in senescence-accelerated mice/prone 8 (SAMP8) mice, which may ultimately provide an experimental basis for clinical prevention of senile dementia.</p><p><b>METHODS</b>Mice were either sham-operated or subjected to complete molar removal. The animals' body weights were monitored every day. Learning ability and memory were measured in a water maze test at the end of the 1st, 2nd, and 3rd months after surgery. As soon as significantly prolonged escape latency in the molarless group was detected, the locomotor activity was examined in an open field test. Subsequently, the animals were decapitated and the cortex and hippocampus 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.</p><p><b>RESULTS</b>Slightly lower weights were consistently observed in the molarless group, but there was no significant difference in weights between the two groups (P > 0.05). Compared with the sham group, the molarless group exhibited lengthened escape latency in the water maze test three months after surgery, whereas no difference in locomotor activity was observed. Meanwhile, in the cortex and hippocampus, BDNF levels were significantly decreased in the molarless group (P < 0.05); but the expression of its receptor, TrkB, was not significantly affected.</p><p><b>CONCLUSION</b>These results suggested that the molarless condition impaired learning and memory abilities in SAMP8 mice three months after teeth extraction, and this effect was accompanied by significantly reduced BDNF expression in the cortex and hippocampus.</p>