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Objective: To investigate the influence of occupational aluminum exposure on cognitive function and glutamate receptor protein expression in peripheral blood lymphocytes in workers and the possibility of glutamate receptor being used as a biomarker for cognitive impairment in aluminum workers. Methods: From October to December, 2014, cluster sampling was performed to select 121 workers in aluminum electrolysis workshop as exposure group and 231 workers in thermoelectric workshop and logistics department as control group. Mini-Mental State Examination, clock drawing test, digit span test (DST) , verbal fluency test (VFT) , and Fuld Object-Memory (FOM) Evaluation were used to analyze cognitive function. Graphite furnace atomic absorption spectrophotometry was used to measure plasma aluminum level as an exposure indicator. Enzyme-linked immunosorbent assay was used to measure the content of glutamate receptor proteins in peripheral blood lymphocytes, including the subunits of N-methyl-D-aspartate receptor NR1, NR2A, and NR2B and metabotropic glutamate receptor 1 (mGluR1) . The correlation between cognitive function indices and the content of glutamate receptor proteins was analyzed. Results: There was no significant difference in plasma aluminum level between the control group and the exposure group (132.52±80.40 μg/L vs 182.88±72.32 μg/L, P >0.05) . According to the plasma aluminum level, the study subjects were divided into control group and low-, medium-, and high-level plasma aluminum groups, and there were significant differences in plasma aluminum level between these groups (all P <0.01) . The high-level plasma aluminum group had a significantly lower memory ability score than the control group and the low- and medium-level plasma aluminum groups (all P <0.05) . The high-level plasma aluminum group had lower DST and digital span forward (DSF) scores than the control group and the low-and medium-level plasma aluminum groups. The low-, medium-, and high-level plasma aluminum groups had lower digital span backward (DSB) scores than the control group. The medium-and high-level plasma aluminum groups had lower VFT scores than the control group and the low-level plasma aluminum group. The high-level plasma aluminum group had significantly lower expression of NR1 and NR2A proteins than the control group and the low-and medium-level plasma aluminum groups, and the medium- and high-level plasma aluminum groups had significantly higher expression of mGluR1 protein than the control group and the low-level plasma aluminum group (all P <0.05) . The expression of NR1 and NR2A proteins was negatively correlated with plasma aluminum level ( r =-0.475 and -0.692, both P <0.05) , andthe expression of mGluR1 protein was positively correlated with plasma aluminum level ( r =0.756, P <0.05) . The expression of NR1 protein was positively correlated with DSF, DSB, DST, and VFT scores ( r (s)=0.213, 0.249, 0.271, and 0.228, all P <0.05) , and the expression of NR2A protein was positively correlated with VFT score ( r (s)=0.206, P <0.05) . Conclusion: Occupational aluminum exposure may affect workers' memory function, and the expression of NR1 and NR2A in peripheral blood lymphocytes is correlated with cognitive function indices and can be used as biomarkers for cognitive impairment in aluminum workers.

Aim: To investigate the effects of free radicals (FRs) and amyloid beta protein (A beta 1-40) on the functions of expressed neurotransmitter receptors (NRs) from rat brains in Xenopus oocytes., Methods: Total RNA and Messenger RNA (mRNA) was prepared from 3-month-old Wistar rat brain tissues with Promega kits and microinjected into mature Xenopus oocytes (stage V - VI) with 50 nl (50 ng) for each oocyte for receptor expression and their currents were recorded with double electrode voltage clamp technique. Superoxide anion free radicals (SAFRs) and A beta 1-40 was added 12 h, 24 h, 96 h to incubation solution before recording., Results: The results showed that oocytes expressed mACh, glutamate, dopamine, serotonin and gamma-aminobutyric acid receptors. The current characteristics of these receptors were inward currents carried by chloride ion with their equilibrium potentials close to - 22 mV. A beta 1-40 and free radicals had a kind of inhibitory effect on the expressed GluR. When treated with 60 nmol/L A beta 1-40 over 24 h, the currents of GluR significantly decreased (25% off, P < :0.01). When oocytes were co-treated with 60 nmol/L A beta 1-40 and SAFRs over a period of 12 h, the currents of glutamate receptor significantly decreased (21% of P < 0.05), and the decreased percentage reached 52% over 24h co-treated with 60 nmol/L A beta 1-40 and SAFRs. Vitamin E had partial antagonistic effect against these effects., Conclusion: The result suggests that A beta has a kind of inhibitory effects upon glutamate receptor, which is similar to those of free radicals. Their effects can be antagonized by vitamin E. This implies that A beta may play roles via inhibiting receptor function in pathophysiology of Alzheimer's disease.

Aim and Methods: In 36 anesthetized spontaneously breathing Sprague-Dawley rats, the types of respiratory neurons and the state of neurotransmitters and receptors in nucleus paragigantocellularis lateralis (PGCL) were studied with extracellular recording technique and multibarrel microelectrode techniques., Results: At the caudal part of the PGCL(cPGCL) in 14 rats, a total of 39 respiratory neurons (RNs) were recorded including 24 inspiratory, 12 expiratory and 3 phase-spanning neurons. At the cPGCL in another 22 rats, we discovered that out of 14 RNs tested, 12 were excited by iontophoretic application of sodium glutamate (L-GLu), and all the 22 RNs tested were inhibited by gamma-aminobutyric acid (GABA). DL-2-amino-5-phosphonovaleric acid (AP5), an antagonist of N-methyl-D-aspartate (NMDA) receptor, and bicuculline (BIC), an antagonist of GABA(A) receptor, both showed three kinds of effects on the RNs discharge: excitatory, inhibitory and no-effect. AP5 could block partially the excitatory effect of L-GLu on a large part of RNs tested (6/9). BIC blocked, partially or completely, the inhibitory effect of GABA also on a large part of the RNs tested (9/11)., Conclusion: It is implied that PGCL is one of the important neural substrates responsible for the regulation of respiration. There might exist endogenous glutamate and GABA acting as neurotransmitters in the cPGCL area and excitatory amino acids (including NMDA and non- NMDA) and GABA(A)-receptors on cPGCL neurons. These neurotransmitters and receptors may mediate the regulatory action of cPGCL on respiration.

Effects of deltamethrin on the binding function of glutamate receptor of cerebral cortical synaptosomal membrane in rat were studied by radio-labeled ligand receptor binding assay. Results showed that deltamethrin could obviously increase the 3H-glutamate binding to synaptosomal membrane, by doses of 1 x 10(-8) to 1 x 10(-4) mol/L, with a dose-dependent relationship. Glutamate binding rate increased by 3.2 percent to 13.5 percent in deltamethrin treated group, as compared with dimethyl sulfoxide solvent controls. Binding dynamic analysis of receptor and ligand showed that an obvious synergistic action of deltamethrin and dimethyl sulfoxide. It indicated that neurotoxicity of deltamethrin could be related to the disturbance of central transmitter system of glutamate.

In order to probe into dexamethasone's effect on glutamate receptor (Glu R) in hypoxic-ischemic encephalopathy (HIE) of newborn, we established newborn pigs' model of HIE to investigate Glu R in their forebrain crude synaptic membrane and the effect of dexamethasone in different HIE times and different dosages on the changes of Glu R. This study included five groups: HIE group (no medication); dexamethasone treatment group (10 mg/kg before HIE); dexamethasone treatment group (10 mg/kg after HIE); dexamethasone treatment group (5 mg/kg before HIE); dexamethasone treatment group (5 mg/kg after HIE). The results showed that the mean receptor density (Bmax) of dexamethasone treatment group (10 mg/kg before HIE) was significantly lower than that of the other groups (P < 0.05), but there was no statistic difference in the affinity of Glu R between all the experimental groups. These findings suggested that the preventive use of dexamethasone in large dosage would reduce the binding of Glu, and could possibly protect the brain tissues from damage in HIE.