D Y Ruan

University of Science and Technology of China, Hefei, Anhui Sheng, China

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Publications (13)34.63 Total impact

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    K Yu, D Y Ruan, S Y Ge
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    ABSTRACT: The conventional whole cell patch-clamp technique was used to measure the resting membrane conductance and membrane currents of nonstimulated cultured human umbilical vein endothelial cells (HUVECs) in different ionic conditions. Three electrophysiological phenotypes of cultured HUVECs (n = 122) were determined: first, 20% of cells as type I mainly displaying the inwardly rectifying potassium current (IKi); second, 38% of cells as type II in which IKi was super-posed on a TEA-sensitive, delayed rectifying current; third, 27% of cells as type III predominantly displaying the outwardly rectifying current which was sensitive to TEA and slightly inhibited by a chloride channel blocker niflumic acid (N.A.). In cells of type I, the mean zero-current potential (V0) was dependent on extracellular K+ ([K+]o) but not on Cl-, indicating major permeability to K+. Whereas V0 of type II was also affected by extracellular Cl- ([Cl-]o), indicating the contribution of an outward Cl- current in setting V0. The cells of type III were not sensitive to decrease of [Cl-]o and the outward current was activated in a relative stable voltage range. This varying phenotypic expression and multipotential behavior of HUVECs suggests that the electrical features of HUVEC may be primarily determined by embryonic origin and local effect of the microenvironment. This research provided the detailed electrophysiological knowledge of the endothelial cells.
    General Physiology and Biophysics 10/2002; 21(3):315-26. · 0.85 Impact Factor
  • M Wang, J -T Chen, D -Y Ruan, Y -Z Xu
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    ABSTRACT: Previous studies from our group have demonstrated that chronic aluminum exposure from parturition throughout life impairs both long-term potentiation (LTP) and long-term depression (LTD) of the excitatory postsynaptic potential (EPSP) slope and reduces the population spike (PS) amplitude in the rat dentate gyrus in vivo. The present study sought to extend these findings by evaluating the developmental periods critical for aluminum-induced impairment of synaptic plasticity. Rats were exposed to aluminum (gestational, lactational and postlactational) through drinking 0.3% aluminum chloride in water over different developmental intervals: (1) prenatal exposure; (2) beginning from birth and terminating at weaning; (3) beginning at weaning throughout life; (4) beginning at birth and continuing throughout life. As adults (postnatal day 80-100), field potentials were measured in the dentate gyrus of hippocampus in response to stimulation applied to the lateral perforant path. The results showed: (1) Prenatal aluminum exposure had no effect on the magnitude of LTP as measured by the EPSP slope and LTD as measured for the PS amplitude, while it had a small effect on the magnitude of LTP as measured for the PS amplitude and LTD as measured by the EPSP slope. (2) Lactational, postlactational and throughout life exposure to aluminum impaired both LTP and LTD of the EPSP slope and PS amplitude, except that LTD of PS amplitude was not significantly changed in animals postlactationally exposed. (3) Aluminum exposure from parturition throughout life caused the greatest impairment of the range of synaptic plasticity, while prenatal aluminum exposure caused the least. From these results we conclude that the lactational period was the most susceptible to aluminum-induced impairment of synaptic plasticity and that chronic aluminum exposure from parturition throughout life is extremely disruptive to synaptic plasticity and should be avoided.
    Neuroscience 02/2002; 113(2):411-9. · 3.12 Impact Factor
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    ABSTRACT: The effects of Fe(2+) on the properties of three types of ion channels were studied in acutely dissociated rat hippocampal pyramidal neurons from area CA1 at postnatal ages of 7-14 days using the whole cell patch clamp technique. The results indicated that: (1) in the existence of Fe(2+), the activation voltage threshold of transient outward K(+) currents (I(A)) was decreased. The normalized current-voltage curves of activation were well fitted with a single Boltzmann function, and the V(1/2) was 2.44+/-1.14 mV (n=15) in control, whereas 1.79+/-1.53 (n=15), -2.96+/-0.92 (n=14), -5.11+/-1.31 (n=13), -9.05+/-1.64 mV (n=12) in 1, 10, 100 and 1000 microM Fe(2+), respectively. Differences between two groups were significant (P<0.05, n=12-15), except for that between the control and 1 microM (P>0.05, n=15). (2) Fe(2+) caused a left shift of the current-voltage curves of steady-state inactivation of I(A) in a concentration-dependent manner. The curves were well fitted with a single Boltzmann function with similar slope (P>0.05, n=10-13). The V(1/2) were -70.71+/-1.23 (n=13), -71.14+/-1.37 (n=13), -78.21+/-1.17 (n=11), -84.61+/-1.34 (n=12), and -89.68+/-2.59 mV (n=10) in control, 1, 10, 100 and 1000 microM Fe(2+), respectively. Fe(2+) also shifted the current-voltage curves of Na(+) channel steady-state inactivation to more negative depolarization potentials in parallel, with V(1/2), -67.37+/-1.33 mV (n=12) in control, and -67.52+/-1.28 mV (n=12), -68.24+/-1.61 mV (n=10), -71.58+/-1.45 mV (n=10), -76.65+/-1.76 mV (n=9) in 1, 10, 100 and 1000 microM Fe(2+) solutions, respectively. (3) In Fe(2+) solutions, the recovery from inactivation of I(A) was slowed. (4) With application of different concentrations of Fe(2+), the voltage threshold of activation of delayed rectified outward K(+) currents (I(K)) was decreased, while Fe(2+) showed a little inhibition at more positive depolarization. Briefly, the results demonstrated that Fe(2+) is a dose- and voltage-dependent, reversible modulator of I(A), I(K) and Na(+) channels. The results will be helpful to explain the mechanism of Fe(2+) physiological function and Fe(2+) intoxication in the central nervous system.
    Food and Chemical Toxicology 12/2001; 39(12):1271-8. · 3.01 Impact Factor
  • M Wang, J T Chen, D Y Ruan, Y Z Xu
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    ABSTRACT: Aluminum (Al), an important neurotoxin, contributes to a variety of cognitive dysfunction and mental diseases. Previous studies have demonstrated that Al impairs hippocampal long-term potentiation (LTP) in vitro and in vivo. In the present study, both LTP and LTD (long-term depression) were recorded in the same animal to investigate the Al-induced impairment of synaptic plasticity. Another aim of the present research was to verify whether the impairment of synaptic plasticity induced by Al could be reversed by vasopressin (VP) treatment. Neonatal Wistar rats were exposed to Al from parturition through adulthood (pre- and post-weaning) by the drinking of 0.3% aluminum chloride (AlCl(3)) solution. The input-output (I/O) function, paired-pulse reaction (PPR), excitatory postsynaptic potential (EPSP) and population spike (PS) amplitude were measured in the dentate gyrus (DG) of adult rats (60-90 days) in response to stimulation applied to the lateral perforant path. The results showed: (1) Al reduced the amplitudes of both EPSP LTP (control: 132+/-7%, n=7; Al-exposed: 115+/-10%, n=8, P<0.05) and PS LTP (control: 242+/-18%, n=7; Al-exposed: 136+/-7%, n=8, P<0.01) significantly. The amplitudes of EPSP LTD (control: 82+/-6%, n=7; Al-exposed: 92+/-7%, n=8, P<0.05) and PS LTD (control: 81+/-4%, n=7; Al-exposed: 98+/-5%, n=8, P<0.05) were also decreased by Al treatment. The Al-induced impairments of PS LTP and PS LTD were more serious than that of EPSP LTP and EPSP LTD. (2) In control rats, VP had an increase in the PS LTP amplitude (control: 242+/-18%, n=7; control+VP: 358+/-23%, n=6, P<0.01), while it had no significant effects on PS LTD (control: 81+/-4%, n=7; control+VP: 76+/-7%, n=6, P>0.05). (3) In Al-exposed rats, VP had a significant increase in the amplitudes of both PS LTP (Al-exposed: 136+/-7%, n=8, Al-exposed+VP: 255+/-16%, n=6, P<0.01) and PS LTD (Al-exposed: 98+/-5%, n=8; Al-exposed+VP: 81+/-6%, n=6, P<0.05). After the application of VP, the range of synaptic plasticity (PS LTP+PS LTD) in Al-exposed rats increased from 38% to 174%, which surpassed that in control rats (161%). It was suggested that VP could reverse Al-induced impairment of synaptic plasticity and might be an effective medicine to cure Al-induced neurological disorders.
    Brain Research 04/2001; 899(1-2):193-200. · 2.88 Impact Factor
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    ABSTRACT: Chronic developmental lead exposure is known to be associated with cognitive dysfunction in children. Previous studies have demonstrated that chronic lead exposure could impair the induction and maintenance of long-term potentiation induced by high-frequency stimulation (HFS-LTP). In area CA1 of rat hippocampus, long-term potentiation could also be induced following temporary replacement of 10 mM 2-deoxy-D-glucose (2-DG) for 10 mM glucose in the normal perfusate (artificial cerebrospinal fluid). The present study was carried out to investigate whether chronic lead exposure affected long-term potentiation induced by 2-DG (2-DG-LTP). Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams whose drinking water contained 0.2% lead acetate. Field excitatory postsynaptic potentials (EPSPs) in area CA1 of hippocampus were recorded on postnatal days 25-30. 2-DG application was followed by an increase in EPSP slopes in a time-course-dependent manner in both control and lead-exposed rats, while the amplitude of 2-DG-LTP in the lead-exposed rats (225.9+/-19.0%, n=12) was significantly greater than that in controls (155.2+/-9.8%, n=12). In contrast to the effects of lead exposure on 2-DG-LTP, the amplitude of HFS-LTP in the lead-exposed rats (121.5+/-13.7%, n=12) was significantly less than that in controls (183.9+/-18.6%, n=12). These results indicate that chronic lead exposure had opposite effects on the two types of LTP induced by HFS and 2-DG. This would suggest that the effects of lead on HFS-LTP and 2-DG-LTP are the result of different sites of lead toxicity.
    Neurotoxicology and Teratology 01/2001; 23(5):481-7. · 3.18 Impact Factor
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    Li Sui, D Y Ruan
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    ABSTRACT: Previous studies have demonstrated that chronic lead exposure may impair neuronal process underlying synaptic plasticity via a direct interaction with N-methyl-D-aspartate (NMDA) receptors. The present study was carried out to investigate the effects of lead exposure on non-NMDA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, AMPA/kainate) receptors of rat hippocampus. Ca2+-permeable AMPA/kainate receptors in organotypic slice cultures were evaluated by using cobalt uptake, a histochemical method that identifies cells expressing Ca2+-permeable non-NMDA receptors. Ten mM L-glutamate-induced cobalt accumulation was enriched in area CA1, area CA3 and in dentate gyrus, which was totally blocked by 100 microM DL-2-amino-5-phosphonovaleric acid (AP5) and 100 microM 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX). Three hundred microM NMDA-induced cobalt accumulation was in area CA1, area dentate gyrus and was blocked by AP5 or CNQX. One hundred microM AMPA had effects in area CA1, area CA3 and in dentate gyrus, which were blocked by CNQX, not by AP5. Furthermore, cobalt accumulations induced by NMDA and AMPA in the lead-exposed rats decreased significantly than those in the controls. The results indicate that AMPA receptors enriched in area CA1, area CA3, area dentate gyrus and kainate receptors enriched in area CA1, area dentate gyrus are impaired by lead exposure.
    Pharmacology &amp Toxicology 12/2000; 87(5):204-10.
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    ABSTRACT: Chronic developmental lead (Pb) exposure to the rat has been reported to impair the long-term potentiation (LTP) in area CA1 and DG of the hippocampus. The present study was performed to investigate the effects of chronic Pb exposure on homosynaptic short-term depression (STD) and long-term depression (LTD) of population spikes (PS) in area CA1 of the rat hippocampus in vivo. Neonatal Wistar rats were exposed to Pb from parturition to weaning via the milk of dams fed with 0.2% lead acetate solution. The input/output (I/O) function, paired-pulse reaction (PPR), the PS were measured in the area CA1 in response to low frequency stimulation (LFS). The results showed that the homo-STD amplitude of PS depotentiation in Pb-exposed rats (87.48 +/- 7.44%, n = 14) was less significant than that in control rats (72.34 +/- 6.05%, n = 18, P<0.05), and the homo-LTD amplitude of PS depotentiation in Pb-exposed rats (72.80 +/- 5.86%, n = 14) was even less significant than that in control rats (47.80 +/- 5.03%, n = 18, P<0.01). The results suggest that chronic Pb exposure in neonatal rats caused impairments in the STD and LTD of area CA1 of hippocampus.
    Chemosphere 08/2000; 41(1-2):165-71. · 3.14 Impact Factor
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    ABSTRACT: Chronic developmental lead exposure is known to be associated with cognitive dysfunction in children. Impairment of the induction of long-term depression (LTD) has been reported in area CA1 and dentate gyrus (DG) of rat hippocampus following chronic lead exposure. The present study was carried out to investigate age-related alterations of LTD in area CA1 and DG of rat hippocampus following developmental lead exposure in vitro. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in hippocampal slices at various postnatal ages: postnatal day (PND) 17-23, 27-33, and 57-63. Following low-frequency stimulation (LFS, 900 pulses/1 Hz), the average magnitude of LTD is age related. In the controls, LTD magnitude in area CA1 decreased with age, whereas in DG it increased with age. In the lead-exposed groups, the magnitude of LTD declined during development in both area CA1 and DG. The differences of LTD magnitude between the control and lead-exposed rats were 27.26 +/- 9.15% (PND 17-23), 21.59 +/- 12.93% (PND 27-33), and 16.96 +/- 9.33% (PND 57-63) in area CA1, and were 6.95 +/- 9.26%, 17.60 +/- 3.91%, and 33.63 +/- 10.47% in DG, respectively. These results demonstrated that the lead-induced impairment of LTD magnitude was an age-related decline in area CA1 and an age-related increase in area DG of rat hippocampus. Published by Elsevier Science Inc.
    Neurotoxicology and Teratology 01/2000; 22(3):381-7. · 3.18 Impact Factor
  • L Sui, D Y Ruan, S Y Ge, X M Meng
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    ABSTRACT: Previous studies have demonstrated that low-level lead exposure can impair the induction of long-term depression (LTD) in area CA1 and dentate gyrus (DG) of rat hippocampus in vitro and in vivo. The induction of LTD in area CA1 and DG has been shown to associate with N-methyl-D-aspartate receptors (NMDARs) and voltage-gated calcium channel (VGCC). In this study, the relative contributions of NMDARs-dependent and VGCC-dependent components in the induction of LTD in the hippocampus and the impairments of these two components of LTD by chronic low-level lead exposure were investigated. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in area CA1 and DG before and after two 15-min trains of 1-Hz low-frequency stimulation (LFS) (2x900 pulses). In area CA1, the amplitude of NMDARs-dependent LTD (NMDA-LTD), in the presence of 10 microM nimodipine (a blocker of L-type Ca(2+) channels), was 80.05+/-2.54% (n=8) and 94.58+/-10.57% (n=8) in the control and lead-exposed rats, respectively. The amplitude of VGCC-dependent LTD (VGCC-LTD), in the presence of 50 microM (-)-2-amino-5-phosphonopentanoic acid (AP5), was 80.36+/-4.08% (n=10) and 93.91+/-7.85% (n=10) in the control and lead-exposed rats, respectively. In area DG the amplitude of NMDA-LTD, with both 50 microM Ni(2+) (a blocker of T-type Ca(2+) channels) and 10 microM nimodipine present, in the control rats (79. 97+/-4.30%, n=8) was significantly larger than that in the lead-exposed rats (91.24+/-11.08%, n=10, P<0.001). The amplitude of VGCC-LTD, with 50 microM AP5 present, was significantly larger in the control rats (70.80+/-3.64%, n=9) than that in the lead-exposed rats (87.60+/-9.00%, n=10, P<0.001). The results suggested that chronic lead exposure affected two components of LTD induction in area CA1 and DG. Furthermore, the impairment of two components by lead exposure might be similar in area CA1, while the impairment of VGCC-LTD might be more serious in DG of hippocampus.
    Neurotoxicology and Teratology 01/2000; 22(5):741-9. · 3.18 Impact Factor
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    ABSTRACT: Long-term potentiation (LTP) and long-term depression (LTD), two forms of synaptic plasticity, are believed to underlie the mechanisms of learning and memory. Previous studies have demonstrated that low-level lead exposure can impair the induction and maintenance of LTP in vivo and in vitro. The present study was carried out to investigate whether the low-level lead exposure affected the induction and maintenance of LTD. Neonatal Wistar rats were exposed to lead from parturition to weaning via milk of dams drinking 0.2% lead acetate solution. Field excitatory postsynaptic potentials (EPSPs) were recorded in hippocampal slices in adult rats (50-65 days) to study the alterations of LTD in area CA1 and dentate gyrus (DG) of hippocampus following chronic lead exposure. The input-output (I/O) curves before conditioning in both areas showed no evident alterations in basic synaptic transmission between the control and lead exposure groups. In area CA1, the mean amplitude of EPSP slope in control rats (61+/-11%, n=15) decreased significantly greater than that in lead-exposed rats (78+/-8%, n=8, P<0.05) following low frequency stimulation (LFS, 1 Hz, 15 min), which lasted at least 45 min. In area DG, with application of the same LFS, the LTD was induced in control rats (72+/-22%, n=8), while the LFS failed to induce LTD in lead-exposed rats (100+/-26%, n=8). These results showed that chronic lead exposure affected the induction of LTD in both area CA1 and DG. The effect of lead on synaptic plasticity in area CA1 was also investigated. The alteration of the amplitude of LTP in hippocampal slices caused by lead was reexamined in order to compare with that on LTD (control: 189+/-23, n=5; lead-exposed: 122+/-12, n=10). The result demonstrated that low-level lead exposure could reduce the range of synaptic plasticity, which might underlie the dysfunction of learning and memory caused by chronic lead exposure.
    Brain Research 02/1999; 818(1):153-9. · 2.88 Impact Factor
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    ABSTRACT: Neonatal rats were exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate solution. The alterations of long-term potentiation (LTP) and paired-pulse facilitation (PPF) of hippocampal dentate gyrus in adult rats (90-115 days) following developmental lead exposure were studied in vivo. Input/output (I/O) function, paired-pulse facilitation (PPF), excitatory postsynaptic potential (EPSP) and population spike (PS) amplitude were measured in the dentate gyrus (DG) in response to stimulation applied to the lateral perforant path. The results showed that LTP was induced in control rats with an average PS potentiation of 321.1+/-50.0% (n=18), which was significantly greater than the increase in PS potentiation (173.5+/-30.0%, n=17, p<0.001) in lead-exposed rats after tetanizing stimulation. The mean EPSP potentiation increased to 172.4+/-27.0% (n=18) in control and 138.8+/-21.4% (n=17) in lead-exposed rats after tetanizing stimulation. The lead-induced impairment of LTP of PS potentiation was more serious than that of EPSP potentiation. Following pairs stimulation of perforant fiber at 250 microA and an interpulse interval (IPI) of 10-1000 ms, the average peak facilitation of PS was 211.3+/-25.0% (n=13) in control and 187.7+/-23.0% (n=11) in lead-exposed rats. The average facilitation period duration of PS was 243.0+/-35.8 ms (n=13) in control and 138.0+/-24.4 ms (n=11) in lead-exposed rats. These results suggested that developmental lead exposure in neonatal rats caused impairments in LTP and PPF of hippocampal dentate gyrus.
    Brain Research 10/1998; 806(2):196-201. · 2.88 Impact Factor
  • Ruan D.-Y, Chen J, Zhao Y, Xu Y.-Z
    Toxicology Letters 06/1998; 95:128-128. · 3.15 Impact Factor
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    ABSTRACT: Neonatal Wistar rats were exposed to lead from parturition to weaning via the milk of dams drinking 0.2% lead acetate solution. The alterations in EPSPs in areas CA1 and CA3 of hippocampal slices of 60-day-old adult rats following developmental lead exposure were studied. The results demonstrate that lead exposure in neonatal rats causes a decrease in LTP in area CA1 and an increase in LTP in area CA3. The effects of exposure to NO-generating compound sodium nitroprusside (SNP) on LTP in areas CA1 and CA3 of control and lead-exposed rats were also tested. The data demonstrate that NO causes an increase in LTP in area CA1 and no different alterations in area CA3 of lead-exposed rats. The results also demonstrate that NO may be a messenger molecule in areas CA1 and CA3. It suggests that lead might selectively interfere with specific neurochemical pathways in the hippocampus.
    Neurotoxicology and Teratology 01/1998; 20(1):69-73. · 3.18 Impact Factor