Effect of acetaminophen on relieving orthodontic pain with clear aligner based on GAD-7: A retrospective research.

Objectives: Patients may have uncomfortable feelings during orthodontic treatment, which can directly lead to dissatisfaction. So in order to improve the patient's sense of pleasure during the treatment, it would be of great benefit if orthodontic pain can be relieved. Materials and methods: We included 150 patients wearing clear aligners from 18 to 30 years old during 2018-2020. Then designed following groups to determine the effectiveness of both verbal behavior modification and combination therapy with acetaminophen in reducing treatment pain: Group A, generalized anxiety disorder 7 (GAD-7) scored 0-4; Group B, GAD-7 scored 5-9; Group C, GAD-7 scored 10-14; and Group D, GAD-7 scored 15-21. Results: There was a difference in the visual analog scale (VAS) between verbal behavior modification with and without a 300-mg acetaminophen tablet oral QD in Group A (received the intervention at 8 h and 1 d), Group B at 8 h and 1 d, Group C at 8 h, 1 d, 2 d, and 3 d, and Group D at 8 h, 1 d, 2 d, 3 d, and 4 d. After 8 h, 1 d, 2 d, 3 d, and 4 d in patients with verbal behavior modification, VAS was markedly increased in Group D compared with Group A, B and C. Furthermore, after 8 h and 1 d in patients with verbal behavior modification and 300-mg acetaminophen tablet oral QD, VAS was strongly enhanced in Group D. Conclusions: Dental anxiety is strongly associated with pain in orthodontic patients receiving clear aligners. Acetaminophen administration may be a benefit in orthodontic pain that results from clear aligners, especially in the group with more GAD-7.

Mechanistic insights of magnolol antimicrobial activity against Mycoplasma using untargeted metabolomic analyses.

The unreasonable use of antibiotics is one of the important causes of antimicrobial resistance (AMR) that poses a huge public health threat. Magnolol is a traditional Chinese medicine exhibiting antibacterial-, antifungal-, anti-inflammatory-, and antioxidant activities. However, it is unclear whether magnolol has an inhibitory effect on mycoplasma. This study found that magnolol showed excellent inhibitory activity against various mycoplasmas. Magnolol showed dose-dependent inhibition of Mycoplasma synoviae growth and biofilm formation in vitro. Magnolol caused severely sunken and wrinkled M. synoviae cell membranes at the minimum inhibitory concentration, and an enlarged cell diameter. The chicken embryo infection model showed that magnolol significantly reduced M. synoviae pathogenicity in vivo. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the citrate cycle, glycolysis/gluconeogenesis, and pyruvate metabolism were significantly disturbed at the minimum inhibitory concentration of magnolol. Interestingly, 41% of differential metabolites were in the categories of lipids and lipid-like molecules. Protegenin A was up-regulated 58752-fold after magnolol treatment. It belongs to fatty acyls, and destroys cell membrane integrity and cell activity. Ghosphatidylethanolamine, phosphatidylglycerol, phosphatidic acid, and phosphatidylserine related to membrane maintenance and stress response were widely down-regulated. Collectively, our results illustrate the feasibility of magnolol as a phytochemical compound to treat mycoplasma infection.

Photoelectrochemical UV Detector Based on High-Temperature Resistant ITO Nanowire Network Transparent Conductive Electrodes: Both the Response Range and Responsivity Are Improved.

UV transparent conductive electrodes based on transferable ITO nanowire networks were prepared to solve the problem of low UV light utilization in conventional photoelectrochemical UV detectors. The mutually cross-linked ITO nanowire network achieved good electrical conductivity and light transmission, and the novel electrode had a transmission rate of more than 80% throughout the near-UV and visible regions. Compared to Ag nanowire electrodes with similar functionality, the chemical stability of the ITO nanowire transparent conductive electrode ensured that the device worked stably in iodine-based electrolytes. More importantly, ITO electrodes composed of oxides could withstand temperatures above 800 °C, which is extremely critical for photoelectrochemical devices. After the deposition of a TiO2 active layer using the high-temperature method, the response range of the photoelectrochemical UV detector was extended from a peak-like response between 300-400 nm to a plateau-like response between 200-400 nm. The responsivity was significantly increased to 56.1 mA/W. The relationship between ITO nanowire properties and device performance, as well as the reasons for device performance enhancement, were intensively investigated.

Association between lipid metabolism and periodontitis in obese patients: a cross-sectional study.

BACKGROUND: To investigate the association between clinical periodontal parameters of periodontitis, serum lipid metabolism markers and adipokines' levels in patients with obesity and periodontitis. METHODS: A total of 112 patients admitted to Hospital of Xi'an Jiaotong University were included in this study. They were divided into normal body weight group (18.5 < body mass index, BMI < 25, n = 36), overweight group (25 ≤ BMI < 30, n = 38), and obesity group (BMI ≥ 30, n = 38) accordingly. The diagnosis of periodontitis was based on the newest international classification of periodontitis. Full-mouth clinical periodontal measurements included: plaque index, periodontal pocket depth, clinical attachment level, and bleeding on probing. Gingival crevicular fluid samples were analyzed for: Interleukin-1ß, tumor necrosis factor-α, Interleukin-6 and C-reactive protein. Serum triglycerides, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and glycosylated hemoglobin levels were measured. Visfatin, leptin, resistin, and adiponectin levels in serum were also measured. RESULTS: The ratio of participants without periodontitis was significantly highest in normal weight group, and the proportion of severe periodontitis (stage III and IV) was highest in obesity group. The periodontal pocket depth, clinical attachment level, and the inflammatory cytokines in gingival crevicular fluid in obesity group and overweight group were higher than those in normal body weight group. The BMI and waist-to-hip ratio (WHR) were significantly positive correlated with periodontal pocket depth and clinical attachment level. Using a Multivariate logistic regression model, periodontitis correlates to BMI, WHR, serum levels of triglyceride, total cholesterol, low density lipoprotein, and adipokines such as visfatin, leptin, and resistin. CONCLUSIONS: Obesity is positively correlated with the aggravation of periodontitis. Obesity may aggravate the damage to periodontal tissue by regulating the secretion level of adipokines.

Aldosterone activates ERK phosphorylation in the nucleus tractus solitarius.

Sodium intake effect of aldosterone has attracted much attention. In our recent study, aldosterone can play a nongenomic regulatory role on rapid sodium intake in the NTS (nucleus tractus solitarius) by activating G protein-coupled estrogen receptor (GPER), and it exhibited an obvious time-dependent and concentration-dependent regulation. However, the molecular mechanism how aldosterone regulated sodium intake rapidly, is unclear. To determine the molecular mechanism of rapid sodium intake regulation of aldosterone, rats with a stainless-steel cannula in the NTS were used (n = 6 each subgroup), and were injected different concentrations of aldosterone/G1 (GPER agonist)/G15 (GPER antagonist) at different time points, then detected ERK1/2 protein expression. The results showed that aldosterone/G1 increased the ERK1/2 protein phosphorylation, and presented a time-dependent and concentration-dependent similar to sodium intake; Meanwhile, G15 partially blocked this effect at least. Taken together, we postulate that ERK1/2 protein may influence nongenomic sodium intake regulated by aldosterone at nucleus tractus solitarius level.

High Temperature-Resistant Transparent Conductive Films for Photoelectrochemical Devices Based on W/Ag Composite Nanonetworks.

The traditional Ag nanowire preparation means that it cannot meet the demanding requirements of photoelectrochemical devices due to the undesirable conductivity, difficulty in compounding, and poor heat resistance. Here, we prepared an Ag nanonetwork with superior properties using a special template method based on electrospinning technology. The transparent conductive films based on Ag nanonetworks have good transmittance in a wide range from ultraviolet to visible. It is important that the films have high operability and are easy to be compounded with other materials. After compounding with high-melting-point W metal, the heat-resistance temperature of the W/Ag composite transparent conductive films is increased by 100 °C to 460 °C, and the light transmission and electrical conductivity of the films are not significantly affected. All experimental phenomena in the study are analyzed theoretically. This research can provide an important idea for the metal nanowire electrode, which is difficult to be applied to the photoelectrochemical devices.

Study of Morphology, Rheology, and Dynamic Properties toward Unveiling the Partial Miscibility in Poly(lactic acid)-Poly(hydroxybutyrate-co-hydroxyvalerate) Blends.

The purpose of the present work was to gain a fundamental understanding of how the composition and physico-chemical properties affect the rheology, morphology, miscibility, and thermal stability of poly(lactic acid) (PLA)-poly(hydroxybutyrate-co-hydroxyvalerate) (PHBV) biopolymer blends obtained by melt mixing. First, restricted processing conditions were chosen, due to the inherent thermal degradation of PHBV, as proven by rheological dynamic time sweep (DTS) measurements and size-exclusion chromatography (SEC). Based on this, the composition dependence of the blends was investigated using small-amplitude oscillatory shear rheology (SAOS), and the results were confirmed by scanning electron microscopy (SEM) analysis. Subsequently, the changes in glass transition temperatures (Tgs) from the molten to the solid state, as observed by DMA and DSC, were verified by coupling SAOS to dielectric relaxation spectroscopy (DRS). Herein, the thermo-rheological complexity of PLA/PHBV blends in the melt was revealed, especially for PLA-rich blends. Irregularly structured morphologies, caused by highly mismatched viscoelastic properties, illustrated the degree of partial miscibility. Moreover, the thermo-rheological complexity appeared in the molten state of the asymmetric PLA-rich phases could be correlated to the crystal-amorphous interfacial MWS polarization, because of the locally-induced phase separation and heterogeneity, and owing to the differences in their crystallization properties during cooling. The miscibility also suffered from the lower thermal stability of PLA and the even more unstable PHBV. Nevertheless, the melt-induced degradation process of the PLA/PHBV blends seemed to be responsible for some of the in situ self-compatibilization and plasticization mechanisms. As a result, the miscibility and thermo-rheological simplicity were improved for the intermediate and PHBV-rich compositions at low temperatures, since their properties were, to a large extent, governed by the significant degradation of PHBV. The present findings should increase the understanding of morphological changes in PLA/PHBV blends and help control their micro/nanostructure.

The role of central amygdaloid nucleus in regulating the nongenomic effect of aldosterone on sodium intake in the nucleus tractus solitary.

OBJECTIVE: The central nucleus of the amygdala (CeA) has dense downward fiber projections towards the nucleus tractus solitary (NTS) and can modulate the activity of NTS taste neurons. However, whether CeA affects the nongenomic role of aldosterone (ALD) in regulating sodium intake at the NTS level remains unclear. METHODS: First, 40 adult male Sprague Dawley rats were divided into five groups, referring to different concentrations of ALD, to observe the sodium intake pattern compared with the vehicle (n = 8). ALD, the mineralocorticoid receptor antagonist spironolactone (SPI), and ALD + SPI were injected into the NTS. Then, the rats were divided into four groups (n = 16): bilateral/unilateral CeA electrolytic lesions, bilateral/unilateral CeA sham lesions. After recovery, one stainless steel 23-gauge cannula with two tubes was implanted into the rat NTS, and all rats underwent a recovery period of 7 days. Then, each group was divided into two subgroups that received aldosterone or control solution injection, and the cumulative intake of 0.3 mol/L NaCl solution was recorded within 30 min. RESULTS: Bilateral CeA lesion eliminated the increased 0.3 mol/L NaCl intake induced by aldosterone microinjected into the NTS (CeA lesion: 0.3 ± 0.04 ml/30 min vs. sham lesion: 1.3 ± 0.3 ml/30 min). Unilateral CeA lesion reduced the increased NaCl intake induced by aldosterone microinjected into the NTS compared with the control group (p < .05) in the first 15 min but not in 15-30 min (p > .05). In sham lesion rats, aldosterone (5 ng/0.1 µl) still induced a significant increase in NaCl intake (aldosterone: 1.3 ± 0.3 ml/30 min vs. control: 0.25 ± 0.02 ml/30 min) (p < .05). CONCLUSION: The results verified that the complete CeA may play an important role in aldosterone to regulate the nongenomic effect on rapid sodium intake.

Arthroscopic versus open treatment for femoroacetabular impingement: A systematic review and meta-analyses.

BACKGROUND: Femoroacetabular impingement (FAI) is a common cause of hip pain and restricted range of motion in young adults and athletes. This study aims to compare clinical results and complications between patients treated for FAI who underwent either arthroscopic or open treatment. METHODS: The 7 studies were acquired from PubMed, Medline, Embase, and Cochrane Library. The data were extracted analyzed by RevMan5.3. Mean differences (MDs), odds ratios (ORs), and 95% confidence intervals (CIs) were calculated. The Newcastle-Ottawa Scale were used to assess risk of bias. RESULTS: Seven observational studies were assessed. The methodological quality of the trials indicated a low risk of bias. The pooled results of the modified Harris Hip Score (mHHS), the Non-Arthritic Hip Score (NAHS), the Visual Analogue Scale (VAS), and satisfaction rate showed that the differences were not statistically significant between arthroscopic treatment (AT) and open treatment (OT). The difference of postoperative alpha angle was statistically significant, and OT was more effective [MD = 3.08, 95% confidence interval (95% CI) = 1.45-4.70, P = .0002]. The difference of postoperative internal rotation angle was statistically significant, and OT had better internal rotation angle (MD = -3.21, 95% CI = -6.14 to -0.28, P = .03). However, the difference of complications was statistically significant and AT achieved better result than OT (OR = 0.41, 95% CI = 0.22-0.74, P =0.003). CONCLUSION: AT had comparable effect and lower complications than OT, but had less improvement in alpha angle and internal rotation angle.

Elevated osteogenic potential of stem cells from inflammatory dental pulp tissues by Wnt4 overexpression for treating bone defect in rats.

BACKGROUND: The osteogenic capacity of inflammatory dental pulp stem cells (DPSCs-IPs) is reported lower than that of normal dental pulp stem cells (DPSCs-NPs). Down-regulation of Wnt4 may be the key factor affecting the osteogenic ability of DPSCs-IPs. In order to prove that the restoration of Wnt4 expression could improve the osteogenic potential of DPSCs-IPs, Wnt4 overexpressed inflammatory dental pulp stem cells (Wnt4-DPSCs-IPs) were performed to reconstruct bone defects in rats. METHODS: Human DPSCs-IPs were cultured and transfected with Wnt4 overexpression lentiviral vector. Stem cell characterization was performed by flow cytometry and induction of multidirectional differentiation. Wnt4-DPSCs-IPs were loaded onto poly (hydroxybutyrate-co-valerate) (PHBV). The compounds were engrafted into artificially-created defect in alveolar bone. The effectiveness of Wnt4-DPSCs-IPs/PHBV in bone regeneration was assessed by micro-CT and immunohistochemical staining of osteocalcin, a representative osteogenic marker. RESULTS: Collecting data showed that Wnt4 overexpression didn't change stem cell characteristics of DPSCs-IPs. Wnt4-DPSCs-IPs retain osteogenic, adipogenic and chondrogenic differentiation abilities. Wnt4-DPSCs-IPs/PHBV were more effective than DPSCs-IPs/PHBV in repair of rat bone defects by 3 months' post-surgical reconstruction. CONCLUSIONS: Restoration of Wnt4 expression could improve the osteogenic potential of DPSCs-IPs. Wnt4 restored DPSCs-IPs may be a feasible resource of seed cells for bone regeneration in future clinical application.

MicroRNA­29a promotes the neural differentiation of rat neural stem/progenitor cells by targeting KLF4.

Neural stem/progenitor cells (NSPCs) remain in the mammalian brain throughout life, where they have the ability to self­renew and generate different types of cell in the central nervous system (CNS). Therefore, NSPCs may be a potential novel therapeutic strategy following damage to the CNS. Previous research has reported that microRNA (miR)­29a served an important role in regulating cell proliferation, differentiation and survival; however, to the best of our knowledge, little is known of the effect of miR­29a in neural differentiation. The present study aimed to investigate the effect of miR­29a on the differentiation of NSPCs, determined via RNA interference, immunostaining, reverse transcription-quantitative PCR and western blotting. The present study discovered that the expression levels of miR­29a were significantly upregulated in a time­dependent manner during neural differentiation. Immunostaining showed that overexpression of miR­29a promoted neural differentiation, which manifested in increased expression levels of neuron­specific class III ß­tubulin (Tuj1); however, miR­29a had no effect on neuroglial differentiation. The expression levels of Kruppel­like factor 4 (KLF4) were downregulated following overexpression of miR­29a, whereas the inhibition of miR­29a demonstrated the opposite effect. These results suggested that the overexpression of miR­29a may promote neural differentiation in cultured rat NSPCs by decreasing the expression levels of KLF4. Thus indicating that targeting KLF4, a crucial regulatory factor for the maintenance of stemness, may be a potential underlying mechanism of action for miR­29a. In conclusion, the findings of the present study identified a potential mechanism of action for miR­29a in NSPC differentiation and provided a novel insight into the treatment strategies for CNS damage.

Maternal low protein exposure alters glucose tolerance and intestinal nutrient-responsive receptors and transporters expression of rat offspring.

AIMS: Maternal protein malnutrition during perinatal period has long-term consequences on the offspring's metabolic phenotype. Here we determined the effects of maternal protein-restricted (PR) diet on offspring's metabolism in 3- and 12-week-old. MAIN METHODS: Sprague-Dawley rats were fed with standard chow diet or PR diet during pregnancy and lactation. Food intake and body weight of offspring were measured weekly. The oral glucose tolerance tests were underwent, the pancreases were collected for histochemical staining, and the duodenum, jejunum and ileum were collected for gene and protein expression analysis in 3- and 12-week-old offspring. KEY FINDINGS: PR offspring had significant lower body weight and persisted till 12-week-old. From 3- to 12-week-old, PR offspring presented considerably impaired glucose tolerance, while no marked change was shown in control rats. Additionally, the average islet size of PR offspring decreased significantly in 12-week-old. The mRNA and protein expression of nutrient-responsive receptors and transporters T1R3, SGLT1 and GLUT2 increased significantly in the intestine of 3-week-old PR offspring. And from 3- and 12-week-old, the increase tendency of expression subdued. SIGNIFICANCE: These results suggest that maternal PR diet during critical developmental windows influences offspring metabolism, which may be subdued partially, but not be reversed completely by chow diet after weaning.

The central nucleus of the amygdala lesion attenuates orthodontic pain during experimental tooth movement in rats.

INTRODUCTION: Orthodontic pain is the most common adverse side effect reported in the context of tooth movement. Given its central role in processing pain and negative emotion, the central nucleus of the amygdala (CeA) is thought to be a key site involved in orthodontic pain sensation. METHODS: In the present study, we therefore explored whether the CeA is involved in contributing to orthodontic pain in a rat model of tooth movement. For this study, we utilized adult male rats with bilateral sham or electrolytic CeA lesions (400 µA; 25 s), and then we analyzed face grooming behavior as a measure of pain sensation. RESULTS: Through this approach, we found that there were time- and force-dependent factors influencing pain levels in these rats. We further found that bilateral CeA lesions markedly reduced tooth movement-induced orofacial pain and that unilateral CeA lesions did so to a lesser extent. CONCLUSIONS: As such, these results suggest the CeA is a key area of orthodontic pain, with the results of this study highlighting potential avenues for achieving pain relief in those suffering from orthodontic pain.

miR­29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway.

Neural stem/progenitor cells (NSPCs) are self­renewing, multipotent cells and remain in the human brain throughout an individual's lifetime. NSPCs are activated by brain damage and contribute towards repair and motor function recovery in the central nervous system (CNS). It was previously reported that miR­29 was involved in regulating proliferation, differentiation and survival in hepatocellular carcinoma, and osteoblast and mantle cell lymphoma; however, the effects of miR­29 on NSPCs remain unclear. In the present study, it was demonstrated via Cell Counting Kit­8 assays that overexpression of miR­29 promoted the viability of NPSCs, and downregulated the expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) protein. Additionally, treatment with a PTEN­specific inhibitor (VO­OHpic trihydrate) abolished the effects of the miR­29 inhibitor on PTEN expression, as determined via western blotting. Flow cytometry and 5­bromo­2­deoxyuridine (BrdU) staining revealed that overexpression of miR­29 further promoted the proliferation of NSPCs; however, knocking down miR­29 inhibited cell proliferation. VO­OHpic trihydrate reversed the effects of miR­29 knockdown on cell proliferation. Furthermore, it was observed that overexpression of miR­29 increased the phosphorylation levels of AKT. Collectively, the results indicated that overexpression of miR­29 promoted the proliferation of cultured rat NSPCs and decreased the expression of PTEN protein, and that the activation of Akt may be a potential underlying mechanism. The present findings may provide novel insight for the development of strategies for stem cell­mediated treatment of CNS diseases.

Product Module Network Modeling and Evolution Analysis.

Modular technology for product design and manufacturing is an effective way to solve mass customization problems. One difficulty in the application of modular technology is that the characteristics of mass customization, such as multi batch and small batch, easily increase the complexity of the module structure of the enterprise products. To address this problem, based on complex network theory, the enterprise products module is mapped as the vertex of the network, the number of modules used is mapped as the node weight, the dependency between the modules is mapped to the edge, and the product module network is established. The brittleness risk entropy of the product module network is put forward by considering the internal and external factors that influence the application of the enterprise module to determine the rationality of the required modules' organizational structures. Then, the stability uncertainty of the product module network can be determined by calculating the brittleness risk entropy, in which the subsystem that is the most brittle risk entropy can be identified. And the evolution of the product module network can be promoted by changing factors of the entropy maximum subsystem. To analyze the change in the product module network caused by module evolution, a BBV (Barrat-Barthelemy-Vespignani) model of the product module network is established to dynamically determine the brittle risk of the product module network. Finally, the modularity structure of a series of special vehicles is used as an example to verify the presented method, and the results confirm the rationality and effectiveness of the method.

Loss of Wnt4 expression inhibits the odontogenic potential of dental pulp stem cells through JNK signaling in pulpitis.

Dental pulp stem cell (DPSC)-based odontogenic regeneration in inflammatory conditions is important in the process of pulpitis. DPSCs have been reported to lose potential for odontogenic regeneration in inflammatory conditions. This study aims to determine the mechanism of impaired odontogenic differentiation of DPSCs in an inflammatory microenvironment. We regulated Wnt4 expression using recombinant lentiviral Wnt4 and Wnt4 siRNA. Alkaline phosphatase (ALP) and Alizarin red S (ARS) staining as well as Real-Time PCR were performed to evaluate the osteogenic differentiation potential of DPSCs with either upregulated or downregulated Wnt4. Furthermore, SP600125 was used to inhibit the potential downstream factor JNK1, and the osteogenic differentiation ability of DPSCs was evaluated. As shown, Wnt4 was downregulated in DPSCs under inflammatory conditions. Inhibition of Wnt4 expression in DPSCs negatively regulated odontogenic differentiation. Overexpression of Wnt4 in LPS-treated DPSCs promoted odontogenic differentiation. In addition, JNK1 was responsible for Wnt4-mediated odontogenic differentiation of DPSCs. Taken together, Wnt4 may function by affecting JNK signaling pathways in the process of impaired odontogenic regeneration by DPSCs under inflammatory conditions.

Inhibitory effects of peripheral administration of exendin-4 on food intake are attenuated by lesions of the central nucleus of amygdala.

The long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 suppresses food intake and decreases body weight. However, the mediating site(s) of action of the anorectic effects induced by peripheral administration of GLP-1R agonists are not well known. The present study investigated the effects of bilateral lesions of the central nucleus of the amygdala (CeA) on the suppression of chow and high-sucrose food intake by exendin-4 in rats. Adult male Sprague-Dawley rats with bilateral sham or electrolytic lesions (400 µA; 25 s) of the CeA were used for this experiment. No significant difference was found in the daily chow intake and high-sucrose food intake in rats with CeA lesion compared to sham-operated rats. Bilateral lesions of the CeA significantly attenuated the suppression of high-sucrose food intake by i.p. exendin-4, but not the suppression of chow intake. These results suggest that a mediating role of the CeA on the peripheral effects of exendin-4.

[Role of the central nucleus of the amygdala in regulating the nongenomic effect of aldosterone on sodium intake in rat nucleus tractus solitarius].

OBJECTIVE: To reveal the nongenomic effect of aldosterone on the regulation of sodium intake in the nucleus tractus solitarius (NTS) and the role of central nucleus of the amygdala (CeA) in regulating this effect. METHODS: Adult male SD rats were divided into four groups and underwent operations to induce bilateral CeA electrolytic lesions (400 µA, 25 s; n=28), bilateral sham CeA lesions (n=28), unilateral CeA lesions (n=28), or unilateral sham CeA lesions (n=26). After 3 days of recovery, the rats received implantation of a stainless steel 23-gauge cannula wih two tubes into the NTS followed by a recovery period of 7 days. The rats in each group were then divided into two subgroups for microinjection of aldosterone (50 ng/µL) or control solution in the NTS, and the cumulative intake within 30 min of 0.3 mol/L NaCl solution was recorded for each rat. RESULTS: Bilateral CeA lesions (3 days) eliminated the increased 0.3 mol/L NaCl intake induced by aldosterone microinjected into the NTS (0.3±0.04 mL in CeA lesion group vs 1.3±0.3 mL in sham lesion group). Unilateral CeA lesion (3 days) reduced aldosterone-induced increase of NaCl intake in the first 15 min (P < 0.05) but not in 15-30 min (P > 0.05). In rats with sham lesions, aldosterone (50 ng/µL) still induced a significant increase in NaCl intake[1.3±0.3 mL vs 0.25±0.02 mL in the control group; F (3, 224)=24.0, P < 0.05]. CONCLUSIONS: The regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake.

The purinergic mechanism of the central nucleus of amygdala is involved in the modulation of salt intake in sodium-depleted rats.

The central nucleus of the amygdala (CeA) is a critical region in regulating sodium intake, and interestingly, purinergic receptors reportedly related to fluid balance, are also expressed in CeA. In this study, we investigated whether the purinergic mechanisms of CeA were involved in regulating sodium intake. Male Sprague-Dawley rats had cannulas implanted bilaterally into the CeA and were sodium depleted with furosemide (FURO 20 mg/kg) plus 24 h-sodium deficient food fed. Bilateral injections of the P2X purinergic agonist, α,ß-methyleneadenosine 5'-triphosphate (α,ß-methylene ATP 1.0, 2.0, 4.0 nmol, respectively) into the CeA region induced dose-related reductions in sodium intake without affecting water intake. Injection of P2X purinergic antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS 4.0 nmol/0.5 µl) into the CeA region did not alter sodium and water intake, however, prior injection of PPADS into the CeA area abolished the inhibitory effects on sodium intake by α,ß-methylene ATP. Interestingly, prior injection of γ-aminobutyric acid type A (GABAA) receptor antagonist, bicuculline (4.0 nmol/0.5 µl) into the CeA region partially reversed the deficit of sodium intake induced by α,ß-methylene ATP. These results suggest that purinergic receptors in the CeA are involved in the control of sodium intake in the sodium-depleted rats and this negative modulation may be, at least partly, mediated by the GABAA receptor.

Angiotensin II facilitates GABAergic neurotransmission at postsynaptic sites in rat amygdala neurons.

The central nucleus of the amygdala (CeA) is critical in the regulation of sodium appetite. Angiotensin II (Ang II) is important in the generation of sodium appetite and may function as a neurotransmitter or modulator to affect the synaptic transmission and the excitability of neurons. However, the role of Ang II in the CeA remains unclear. In this study, we determined the effects of Ang II on the excitatory and inhibitory synaptic inputs to the CeA neurons in brain slices with whole-cell patch-clamp recordings. Ang II (0.5-5 µM) significantly potentiated the amplitude of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) in a concentration-dependent manner. Ang II (2 µM) significantly increased the amplitude of miniature GABAergic inhibitory postsynaptic currents (mIPSCs) without affecting the frequency. This effect was blocked by Ang II type 1 (AT1) receptor antagonist, losartan. One mM guanosine 5'-O-(-2-thiodiphosphate) (GDP-ß-s) in the pipette internal solution eliminated the facilitatory effect of Ang II on GABAergic synaptic transmission. In contrast, Ang II had no effect on the spontaneous glutamatergic excitatory postsynaptic currents (EPSCs) and did not alter the frequency and amplitude of miniature EPSCs at concentrations that facilitated IPSCs. Furthermore, Ang II decreased the firing activity of CeA neurons, and this effect was abolished by losartan and GDP-ß-s. In addition, Ang II failed to inhibit CeA neurons in the presence of bicuculline. These data provide substantial new evidence that Ang II inhibits the CeA neurons by facilitation of GABAergic synaptic input efficacy through activation of postsynaptic AT1 receptors.