Effects of psychological stress on performances in open-field test of rats and tyrosine's modulation / 中国应用生理学杂志

<p><b>AIM</b>To explore the effects of different doses of tyrosine modulation on behavioral performances in open field test of psychological stress rats.</p><p><b>METHODS</b>The animal model of psychological stress was developed by restraint stress for 21 days. Wistar rats were randomly assigned to five groups (n = 10) as follows: control group (CT), stress control group (SCT), low, medium and high-doses of tyrosine modulation stress groups (SLT, SMT and SIT). The changes of behavioral performances were examined by open-field test. Serum levels of cortisol, norepinephrine and dopamine were also detected.</p><p><b>RESULTS</b>The levels of serum cortisol were all increased obviously in the four stress groups, and their bodyweight gainings were diminished. The behavioral performances of SCT rats in open-field test were changed significantly in contrast to that of CT rats. However, The behavioral performances of SMT and SHT rats were not different from that of CT rats. In addition, the serum levels of norepinephrine and dopamine were downregulated obviously in SCT and SLT groups, and no differences were observed in other groups.</p><p><b>CONCLUSION</b>Psychological stress can impair body behavioral performances, and moderate tyrosine modulation may improve these abnormal changes. The related mechanisms may be involved with the changes of norepinephrine and dopamine.</p>

The impairment of homocysteine on neurons and the related mechanisms / 中国应用生理学杂志

<p><b>AIM</b>To observe the impairment of homocysteine (Hcy) on neurons in vitro and the related mechanisms.</p><p><b>METHODS</b>We examined the consequences of treatment of cultured rat cortical and hippocampal neurons with Hcy and detected the neurons' apoptosis, calcium influx, DNA damage and oxidative injury.</p><p><b>RESULTS</b>Primary cortical and hippocampal neurons were treated with Hcy (250 micromol/L) for 4 h resulted in apoptosis time-dependently. S-adenosyl methionine (SAM) could significantly, but MK-801, an NMDA receptor inhibitor, couldn't repress the Hcy induced neuron apoptosis. Hcy could induce neuron calcium overload through activating the NMDA receptors. The DNA of neurons was damaged by Hcy because the methylation reactions were inhibited. Hcy treatment also induced MDA level significantly increased, but did not affect the neurons' T-AOC.</p><p><b>CONCLUSION</b>These findings indicate that Hcy compromises neuronal homeostasis by multiple, divergent routes, including DNA damage, neuron exitotoxicity, and oxidative injury. Hcy mediated neuron apoptosis was mainly due to DNA damage.</p>

Effects of zinc on the expression of metallothionein isoforms in stressed hippocampal neurons in vitro / 中国应用生理学杂志

<p><b>AIM</b>To evaluate the effects of different doses of zinc on the expression of metallothionein isoforms in stressed hippocampal neurons in vitro.</p><p><b>METHODS</b>The cell stress model was developed by corticosterone. The cultured hippocampal neurons were assigned to seven groups as follows: control group, zinc deficiency group, and their corresponding stressed groups, as well as three different levels of zinc complementarity groups.</p><p><b>RESULTS</b>In zinc deficiency group, the expressions of metallothionein and MT-1 mRNA, MT-3 mRNA were downregulated. On the other hand, inductions of metallothionein and it's mRNAs in stressed zinc complementarity group were increased. In addition, the levels of supernatant IL-6 and NO were increased clearly in zinc deficiency group and corticosterone stressed groups.</p><p><b>CONCLUSION</b>Our results suggest that zinc deficiency may decrease while zinc complementarity increase the expressions of metallothioneins and MT-1 mRNA, MT-3 mRNA in stressed hippocampal neurons in vitro.</p>

Effects of zinc deficiency on bone mineralization and its mechanism in rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the influence of zinc deficiency on bone mineralization.</p><p><b>METHODS</b>Thirty Wistar rats were randomly divided into three groups with ten in each group, i.e., zinc-deficient group (ZD), control group, and pair-fed group. Histomorphological changes of bone mineralization, bone mineral content and bone density, bone contents of zinc, calcium, phosphorus, magnesium, manganese, copper and hydroxyproline, and serum levels of parathyroid hormone, calcitonin and osteocalcin in the rats were measured.</p><p><b>RESULTS</b>The results showed that the mineral deposit rate and bone contents of zinc, phosphorus and hydroxyproline, and serum levels of calcitonin and osteocalcin lowered significantly in ZD group, as compared with those in the control and pair-fed groups, with (3.26 +/- 0.34) micro m/d, (64.54 +/- 2.34) g/kg, (54.4 +/- 9.5) mg/kg, (9.28 +/- 1.62) g/kg, (41.2 +/- 13.5) micro g/L, (82 +/- 30) micro g/L in ZD group; (5.37 +/- 0.53) micro m/d, (69.01 +/- 4.05) g/kg, (117.4 +/- 8.0) mg/kg, (11.31 +/- 1.30) g/kg, (68.3 +/- 14.4) micro g/L, (131 +/- 46) micro g/L in the control group; and (5.45 +/- 0.30) micro m/d, (67.81 +/- 3.56) g/kg, (106.7 +/- 8.4) mg/kg, (10.88 +/- 1.47) g/kg, (63.7 +/- 12.0) micro g/L, (120 +/- 52) micro g/L in the pair-fed group, respectively. While the time for mineralization lag and osteoid maturation obviously prolonged, (1.08 +/- 0.19) d and (7.12 +/- 2.30) d in ZD group, (0.39 +/- 0.06) d and (2.21 +/- 1.12) d in the control group, and (0.40 +/- 0.06) d and (2.12 +/- 0.58) d in the pair-fed group, respectively. In addition, bone mineral content and bone density and serum parathyroid hormone in ZD group decreased significantly and were lower than those in the control group, but not significantly different from those in the pair-fed group. There were no significant difference in femoral contents of calcium, magnesium, manganese and copper between the ZD group and the control and pair-fed groups.</p><p><b>CONCLUSIONS</b>Zinc deficiency could lower the contents of parathyroid hormone and calcitonin in blood circulation affecting bone mineral deposit and causing defect in bone mineralization.</p>

Effects of stress on hippocampal Glu-NMDAR pathway in rats and mechanism of zinc protection / 中国应用生理学杂志

<p><b>AIM</b>To observe the effects of stress on Glu uptake and NMDAR of hippocampus synaptosome in rats with different zinc status.</p><p><b>METHODS</b>Stress model was established by photoelectric stimulus. The behaviors of rats were tested in open-field case. 3H-L-Glu was taken as radioligand to detect the NMDAR binding. Glu uptake was determined with radioimmunoassay.</p><p><b>RESULTS</b>Compared with CT rats, ZD rats performed less movement in open-field test, both Bmax of NMDAR and 3H-L-Glu uptake of hippocampus in these rats were significantly decreased. Compared with corresponding non-stressed groups, the stressed groups appeared longer latency and less movement in open-field test. Increased Bmax of NMDAR and decreased 3H-L-Glu uptake were observed in all stressed rats, but only in SZD rats these indices showed statistical difference.</p><p><b>CONCLUSION</b>Abnormal behaviors of rats induced by photoelectric stress were observed in open-field test, which was more serious in zinc deficiency rats. It is supposed that the Glu-NMDAR pathway is involved in the process of stress reaction. As it shows in our experiment, the changes of Bmax of NMDAR and 3H-L-Glu uptake of hippocampus synaptosome seems to be a part of the mechanisms of stress action.</p>

Effect of zinc on the corticosterone-induced injury of primary cultured rat hippocampal neurons / 生理学报

The effect of zinc on the damage of primary cultured hippocampal neurons induced by corticosterone (CORT) was studied. Neuronal injury and expression of NMDA receptor subunits (NR1,NR2A,NR2B) mRNA were detected by using in situ staining and RT-PCR, respectively. Neurons treated with 5 micromol/L CORT for 24 h showed decreased survival rates and increased apoptotic rates compared with the controls; co-application of CORT and 10 or 100 micromol/L Zn(2+) attenuated apoptotic rates while 250 micromol/L Zn(2+) worsened CORT-induced neuronal injury. Expression of NR1, NR2B mRNA in neurons treated by 5 micromol/L CORT for 24 h was significantly increased, while those concurrently added with 10 or 100 micromol/L Zn(2+) showed no changes. No statistic difference in NR2A mRNA was obtained under any treatment. These results suggest that zinc can bilaterally regulate neuronal injuries induced by CORT, among while NMDA receptors probably play an important role.