ABSTRACT
Objective:To evaluate the role of basolateral amygdala (BLA)-prelimbic cortex (PL) brain-derived neurotrophic factor (BDNF) in perioperative neurocognitive disorders (PND) and its relationship with tyrosine kinase B (TrkB) receptors in mice.Methods:Forty-eight clean-grade healthy C57BL/6J mice, aged 6 months, weighing 25-30 g, were divided into 4 groups ( n=12 each) using a random number table method: control group (group C), surgery group (group S), BDNF overexpression in BLA group (group B) and BDNF overexpression in BLA+ ANA-12 injection in PL group (group A). In group S, at 30 min after the end of training session of fear conditioning system, exploratory laparotomy was performed.In group B, recombinant adenovirus 0.3 μl was injected in BLA, fear conditioning test was performed 3 weeks later, and exploratory laparotomy was performed at 30 min after the end of the training session of fear conditioning system.In group A, recombinant adenovirus 0.3 μl was injected in BLA, catheterization was performed in PL, the fear conditioning test used performed 3 weeks later, TrkB receptor antagonist ANA-12 0.25 μg was given in PL starting from 30 min before training session, and exploratory laparotomy was performed at 30 min after training session.Test session was started at 24 h after the end of training session of fear conditioning system, and the percentage of time spent freezing was calculated in all groups.At 30 min after the end of the behavioral test, the expression of BDNF in brain areas, phosphorylated TrkB (p-TrkB) and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERKl/2) was determined by Western blot, and the expression BDNF mRNA in BLA was detected using reverse transcription fluorescence quantitative polymerase chain reaction assay. Results:Compared with group C, the percentage of time spent freezing was significantly decreased, and expression of BNDF protein and its mRNA in BLA and BDNF, p-TrkB and p-ERK1/2 in PL was down-regulated in group S ( P<0.05). Compared with group S, the percentage of time spent freezing was significantly increased, and expression of BNDF protein and its mRNA in BLA and BDNF, p-TrkB and p-ERK1/2 in PL was up-regulated in group B ( P<0.05). Compared with group B, the percentage of time spent freezing was significantly decreased, and expression of p-TrkB and p-ERK1/2 in PL was down-regulated in group A ( P<0.05). Conclusion:The mechanism of PND is probably related to reduction of BDNF secretion from BLA to PL caused by down-regulation of BDNF expression in BLA, and decreasing of post-synaptic phosphorylation of TrkB receptors in mice.
ABSTRACT
Objective T o analyse the genetic polym orphism s of 66 biallelic genetic m arkers on Y chro-m osom e in E astern C hinese H an population, and evaluate their values in forensic application. Methods G enotyping of 66 biallelic genetic m arkers on Y chrom osom e w as studied in 205 unrelated m ales of E astern C hinese H an population by m ultiplex PC R com bined m atrix-assisted laser desorption/ionization tim e-of-flight m ass spectrom etry (M A L D I-T O F-M S ). T he allele frequencies on the loci to be tested w ere calculated by direct counting m ethod, and the gene diversity (G D ) and haplotype diversity (H D ) w ere calculated by corresponding form ulas. T he haplotypes of this system w ere tested by softw are A rlequin v3.5.2.2 and the com parison of population genetics w ere analyzed. Results A total of 60 biallelic genetic m arkers on Y chrom osom e w ere polym orphic in m ales of E astern C hinese H an population, and the ranges of G D w ere from 0.0385 to 0.5019. E ighty-five different haplotypes w ere observed and the H D w as 0.9703. T he differences of partial SN P loci betw een the H an population of E astern C hina and that of X injiang and G uangdong w ere statistically significance. Conclusion Sixty biallelic genetic m arkers and the detection system can com plem entally provide genetic inform ation in kinship testing and individual identification. T he M A L D I-T O F-M S technology is able to type biallelic genetic m arkers.