ABSTRACT
ObjectiveVentrolateral periaqueductal gray (vlPAG) locates in ascending reticular activating system, which plays a key role in the sleep-wake circle. However, the role of vlPAG in general anesthesia has not been identified. To investigate the effect of the dopamine receptor in vlPAG neurons on propofol anesthesia, we used real-time in vivo fiber photometry, microinjection and EEG.MethodsTo observe the alteration of neuronal activity in the vlPAG throughout propofol anesthesia, 10 Sprague-Dawley rats were used for calcium fiber photometry recording. 50 vlPAG bilateral microinjection models were established and assigned into five groups randomly, including D1R agonist group, D1R antagonist group, D2R agonist group, D2R antagonist group, and control group (n=10). Under propofol anesthesia, 1 μL of D1R agonist, D1R antagonist, D2R agonist, D2R antagonist, and isotonic saline were microinjected into the vlPAG of animals in the corresponding groups, respectively. The induction time, recovery time and the changes in electroencephalogram (EEG) before and after microinjection were recorded and analyzed.ResultsThe neuronal activity in the vlPAG was significantly inhibited during the induction period and markedly recovered during the recovery period from propofol anesthesia (P<0.05). Subsequently, the microinjection of D1R agonist into the vlPAG notably prolonged the induction time and reduced the emergence time of propofol anesthesia with a decrease of δ-band ratio. While the microinjection of D1R antagonist accelerated the induction time and prolonged the emergence time of propofol anesthesia with an increase of δ-band ratio and a decrease in β-band ratio in cortical EEG (P<0.05). The induction and recovery time of D2R agonist /antagonist group did not differ with those of control group. As well, EEG before and after microinjection in D2R agonist /antagonist group did not different.ConclusionThese results indicate that vlPAG modulates the process of propofol anesthesia via D1R.
ABSTRACT
Objective To clarify whether the +869T/C polymorphism in the transforming growth factor-β1 (TGF-β1) gene is associated with TGF-β1 expression,and involved in the severity of Graves disease(GD) and Hashimoto's thyroiditis(HT).Methods The TGF-β1+869T/C polymorphism was genotyped by using PCR-sequence specific primers(PCR-SSP) in genomic DNA samples in blood from 158 patients with HT who developed hypothyroidism before they were 45 years old (severe HT) and 125 untreated,euthyroid patients with HT who were older than 45(mild HT).Using the same method,129 euthyroid patients with GD who had been under treatment and were still positive for anti-thyrotropin receptor antibodies (intractable GD) and 130 euthyroid patients with GD in remission and 144 healthy controls were examined.Results It had no difference between GD,HT groups and control group (x2 =1.488,0.439; 0.626,0.005; all P ＞ 0.05 ).The frequency of the TT genotype and the T allele were higher in group with severe HT[34.81％(55/158),58.86％( 186/316)] than in those with mild HT[ 17.60％ (22/125),43.60％ (109/250); x2 =14.040,13.026,all P ＜ 0.05].In contrast,the frequency of the CC genotype was higher in group with intractable GD[ (21.03％(31/129),51.16％(132/258)] than in group with GD in remission[ 13.85％ (18/130),40.38％( 105/260); x2 =12.225,6.061,all P ＜ 0.05 ].TGF-β1 +869 T/C genotype had the correlation with severe groups of HT and GD.C allele would increase in severity of GD(OR =1.546,95％ CI =0.192 - 2.190),and T allele would increase in severity of HT(OR =1.851,95％ CI =1.323 - 2.589).Conclusion The +869T/C polymorphism in the TGF-β1 gene is associated with the severity and intractability of autoimmune thyroid disease.