ABSTRACT
Objective:To evaluate the role of the sodium leak channel (NALCN) in the hippocampal dentate gyrus (DG) in the social behavior of mice.Methods:Thirty-nine male wild-type C57BL/6 mice, aged 6-8 weeks, weighing 18-22 g, were used in this study. Three mice were sacrificed to verify the expression and co-expression of NALCN with neuronal nuclear antigen (NeuN) in the hippocampal DG using the immunofluorescent staining. The remaining 36 mice were divided into 2 groups ( n=18 each) by the random number table method: control group (group C) and NALCN gene knockdown group (group KO). NALCN-shRNA virus was injected in group KO, and scrambled-shRNA virus was injected in group C. The three box social test and open field test were performed at 3 weeks after the virus injection. Mice were sacrificed under anesthesia after the behavioral test, hippocampal tissues were collected, and the injection location of the virus was verified with a fluorescence microscope, and the NALCN protein and mRNA expression in the hippocampal DG was detected by Western blot and real-time polymerase chain reaction, respectively. Results:NALCN and NeuN co-expressed a lot on the same neuron in the hippocampal DG of mice, indicating that NALCN was widely expressed on the neurons in the hippocampal DG. Compared with group C, the expression of NALCN and mRNA in the hippocampal DG was significantly down-regulated, and the social novelty preference disappeared ( P<0.05), and no significant change was found in the social ability and each parameter in the open field test in group KO ( P>0.05). Conclusions:NALCN in the hippocampal DG is involved in the regulation of social memory in mice, and the down-regulated expression of NALCN can lead to the loss of social novelty preference in mice.
ABSTRACT
Objective:To evaluate the relationship between Na + leak current channel (NALCN) in hippocampal dentate gyrus (DG) region and cognitive function in mice. Methods:Thirty-nine male wild type C57BL/6 mice, aged 6-8 weeks, weighing 18-22 g, were studied.Three mice were sacrificed to verify the expression of NALCN co-localized with neuronal nuclear antigen (NeuN) in the hippocampal DG region through immunofluorescence technique.The remaining 36 mice were divided into 2 groups ( n=18 each) by the random number table method: control group (group C) and NALCN gene knockout group (group KO). NALCN-shRNA virus was injected in hippocampal DG region in group KO, and scrambled-shRNA virus was injected in group C. Three weeks after virus injection, behavioral tests (Y maze test and open field test) were performed, then the animals were sacrificed, and the hippocampal tissues were removed for determination of the expression of NALCN protein and mRNA using Western blot and real-time polymerase chain reaction. Results:NALCN and NeuN colocalized a lot on the same neuron in the hippocampal DG region of mice, and NALCN was widely expressed in the hippocampal DG region.Compared with group C, the expression of NALCN protein and mRNA was significantly down-regulated, the times of entering the new arm were reduced, the duration of staying at the new arm was shortened ( P<0.05), and no significant change was found in the parameters mentioned above in the open field test in group KO ( P>0.05). Conclusions:NALCN in the hippocampal DG region is involved in the regulation of cognitive function in mice, and the down-regulation of NALCN may lead to cognitive decline.
ABSTRACT
Objective:To systematically compare the efficacy of different drugs in alleviating remifentanil-induced hyperalgesia.Methods:Databases such as PubMed, Cochrane Library, EMBASE, Web of Science, CNKI, Wanfang Data and CBM were searched using computers from inception to May 2020.The randomized controlled trials comparing the efficacy of different intervention measures for alleviating remifentanil-induced hyperalgesia were searched.After independently identifying the literature, the two reviewers conducted data extraction and evaluated the bias of the included studies, and Stata 14.0, ADDIS 1.16.5 and R4.0.2 softwares were used to analyze the data.Results:Thirty randomized controlled trials were included in our study.Compared with placebo, 3 out of 6 drugs could alleviate remifentanil-induced hyperalgesia, and the probability order for the effect was as follows: butorphanol with MD value (95% CI)-1.50 (-2.80, -0.24), dexmedetomidine with MD value (95% CI)-1.20 (-2.40, -0.09) and ketamine with MD value (95% CI) -0.88 (-1.60, -0.16). After sensitivity analysis, the efficacy of butorphanol remained to be verified.Two drugs could decrease the dosage of opioids within 24 h after operation, and the probability order for the effect was as follows: dexmedetomidine with MD value (95% CI) -14.00 (-28.00, -0.19) and ketamine with MD value (95% CI) -9.20 (-18.00, -0.08). One drug could decrease the incidence of postoperative nausea and vomiting within 24 h after operation: dexmedetomidine with RR value (95%CI) 0.28 (0.16, 0.22). Conclusion:The results of network meta-analyses show that dexmedetomidine has the best efficacy in alleviating remifentanil-induced hyperalgesia.