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Objective::To investigate the effects of modified Buwangsan on the learning and memory ability of Alzheimer's disease (AD) model rats and the expression of NOD-like receptor 3 (NLRP3), cysteine-containing aspartate-specific proteases 1 (Caspase-1) and interleukin-1 beta (IL-1β) in NLRP3 inflammatory pathway in hippocampus of AD model rats, and exploring the underlying mechanism of modified Buwangsan. Method::The 52 eligible rats were randomly divided into sham control group, AD model group, low-dose modified Buwangsan group (1.5 g·kg-1) and high-dose modified Buwangsan group (3 g·kg-1). AD mouse model was established by bilateral hippocampus injection of Aβ1-425 μL (2 g·L-1). The rats in low-dose and high-dose modified Buwangsan group received low and high dose modified Buwangsan respectively within the next 4 weeks, once daily. The learning and memory ability was tested by Morris water maze. The expression of NLRP3, Caspase-1 and IL-1β mRNA was tested by quantitative PCR(Real-time PCR) and Western blot. Result::As compared with the sham group, the learning and memory ability of the rats were significantly impaired (P<0.05). Compared with AD model group, the learning and memory ability and the expression levels of NLRP3, Caspase-1, and IL-1β mRNA and protein were all no statistical differences in low-dose modified Buwangsan group, while the learning and memory ability of the rats were significantly improved and the expression of NLRP3, Caspase-1 and IL-1β mRNA in hippocampus of rats was significantly decreased in high-dose modified Buwangsan group (P<0.05). Conclusion::High-dose modified Buwangsan could attenuate neuroinflammation in the hippocampus of AD mouse model via inhibiting the expression of NLRP3, Caspase-1 and IL-1β, which may be the mechanisms of modified Buwangsan could be used to ameliorate the learning and memory ability of AD mouse model.
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<p><b>OBJECTIVE</b>To record the electrical activities of Antirior cingulate cortex (ACC) neurons by in vivo multi-channel recording methods using the model of complete freund's adjuvant (CFA) induced conditioned place avoidance (C-CPA), which has been set up in our previous studies.</p><p><b>METHODS</b>The electrode was self-made and the CPA responses were recorded by in vivo multi-channel recording method.</p><p><b>RESULTS</b>(1) The electrical activities of ACC neurons could be successfully recorded by the self-made electrode. (2) Before or after the injection of CFA, rats were respectively conditioned to the different place. The firing rates of ACC neurons in the CFA-paired place vs that in the non-CFA-paired place was (0.853 ± 1.377) imp/s vs (0.221 ± 0.971) imp/s (P < 0.05, n = 26). (3) The CPA responses in the CFA-paired place vs that in the non-CFA-paired place were (303.55 ± 61.77)s vs (140.32 ± 33.52)s(P < 0.05, n = 6).</p><p><b>CONCLUSION</b>The firing rates of rACC (rostral Anterior Cingulate Cortex) neurons were involved in the occurrence of the affective pain.</p>