梅岩艾
神经递质和生物活性肽受体激活后对细胞膜离子通道的调控及其有关的跨膜信号转导机制;细胞膜离子通道在神经元和心血管等细胞的发育、增殖、迁移和凋亡中的变化规律及其作用;中枢神经元突触传递机制研究。
个性化签名
- 姓名:梅岩艾
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博士生导师
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学科领域:
生物物理学
- 研究兴趣:神经递质和生物活性肽受体激活后对细胞膜离子通道的调控及其有关的跨膜信号转导机制;细胞膜离子通道在神经元和心血管等细胞的发育、增殖、迁移和凋亡中的变化规律及其作用;中枢神经元突触传递机制研究。
梅岩艾,1980年上海第二医科大学医疗系毕业,留校任教。1983上海第二医科大学生理学专业硕士研究生。1986年获生理学专业硕士学位,后晋升讲师。1991年赴法国留学,在巴黎第十二大学生理系进修,学习膜片箝技术。1991至1995年在法国鲁昂大学的国家医学研究院所属细胞和分子神经内分泌实验室攻读生物学神经生物专业博士研究生,1995年获博士学位后回母校工作,同年晋升为副教授。1996年调入复旦大学生理学和生物物理学系,于1999年晋升为教授。2000年起担任复旦大学生命科学学院科研副院长至今;2001年评为生物物理学、神经生物学专业博士生导师博士生导师。
目前主要从事的研究内容为:神经递质和生物活性肽受体激活后对细胞膜离子通道的调控及其有关的跨膜信号转导机制;细胞膜离子通道在神经元和心血管等细胞的发育、增殖、迁移和凋亡中的变化规律及其作用;中枢神经元突触传递机制研究.回国十年来,已完成涉及细胞膜离子通道的调控及其生物学作用方面科研项目七项,目前仍在研三项。在国内外学术刊物共发表论文四十多篇,其中SCI收录的研究论文39篇,他人引用率超过 200次。指导学生完成各类毕业论文近二十篇。
目前担任的学术职务有:中国生物物理学会常务理事、上海生物物理学会常务理事、上海神经科学会理事。并担任中国生理学报、中国药理学报和中国生物物理学报编委等职。
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梅岩艾, Lin-Yun Liu, Xiao-Wei Fei, Zhao-Ming Li, Zhi-Hong Zhang, Yan-Ai Mei*
Neuropharmacology 48(2005)918-926,-0001,():
-1年11月30日
Diclofenac, a nonsteroidal anti-inflammatory drug (NSAID), has been widely investigated in terms of its pharmacological action, but less is known about its direct effect on ion channels. Here, the effect of diclofenac on voltage-dependent transient outward KC currents (IA) in cultured rat cerebellar granule cells was investigated using the whole-cell voltage-clamp technique. At concentrations of 10 5e10 3 M, diclofenac reversibly increased the IA amplitude in a dose-dependent manner and significantly modulated the steady-state inactivation properties of the IA channels, but did not alter the steady-state activation properties. Furthermore,diclofenac treatment resulted in a slightly accelerated recovery from IA channel inactivation.Intracellular application of diclofenac could mimic the effects induced by extracellular application, although once the intracellular response reached a plateau, extracellular application of diclofenac could induce further increases in the current. These observations indicate that diclofenac might exert its effects on the channel protein at both the inner and outer sides of the cell membrane. Our data provide the first evidence that diclofenac is able to activate transient outward potassium channels in neurons. Although further work will be necessary to define the exact mechanism of diclofenac-induced IA channel activation, this study provides evidence that the nonsteroidal anti-inflammatory drug, diclofenac, may play a novel neuronal role that is worthy of future study.
Diclofenac, KC channel, Cerebellar granule neurons
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【期刊论文】Inhibition of Na+ channel currents in rat myoblasts by 4-aminopyridine
梅岩艾, Bo-Xun Lu, Lin-Yun Liu, Lei Liao, Zhi-Hong Zhang, Yan-Ai MeiT
Toxicology and Applied Pharmacology 207(2005)275-282,-0001,():
-1年11月30日
Our previous study revealed that 4-aminopyridine (4-AP), a specific blocker of A-type current, could also inhibit inward Na+ currents (INa) with a state-independent mechanism in rat cerebellar granule cells. In the present study, we report an inhibitory effect of 4-AP on voltage-gated and tetrodotoxin (TTX)-sensitive INa recorded from cultured rat myoblasts. 4-AP inhibited INa amplitude in a dose-dependent manner between the concentrations of 0.5 and 10 mM without significant alteration in the activation or inactivation kinetics of the channel. By comparison to the 4-AP-induced inhibitory effect on cerebellum neurons, the inhibitory effect on myoblasts was enhanced through repetitive pulse and inflected by changing frequency. Specifically, the lower the frequency of pulse, the higher the inhibition observed, suggesting that block manner is inversely use-dependent. Moreover, experiments adding 4-AP to the intracellular solution indicate that the inhibitory effects are localized inside the cell. Additionally, 4-AP significantly modifies the properties of steady-state activation and inactivation kinetics of the channel. Our data suggest that the K+ channel blocker 4-AP inhibits both neuron and myoblast Na+ channels via different mechanisms. These findings may also provide information regarding 4-AP-induced pharmacological and toxicological effects in clinical use and experimental research.
4-Aminopyridine, Na+, current, Myoblasts
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梅岩艾, Y A Mei, D. Vaudry, M.Basille, H Castel, A FOurnier, H Vaudryalqd B.J.Gonzalez
European Joumal of Neuroscience, Vol. 19, pp. 1446-1458.2004,-0001,():
-1年11月30日
Activation of potassium(K+)cu rrents plays a critical role in the control of prog rammed cell death Because pituitary adenylate cyclase-activating polypeptide(PACAP)has been shown to inhibit the apoptotic cascade in the cerebellar cortex du ring development, we hav einvestigated the effect of PACAP on K’cu rrents in cultu red cerebellar g ranule cells using the patch-clamp technique in the whole-cell configu ration Two types of outward K_cu rrents, a transient K+cu rrent(k)and a delayed rectifier K’cu rrent(/K)were characterized using two different voltage protocols and specific inhibitors of K’channels Application of PACAP induced a reversible reduction of the /K amplitude, but did not affect/A, while the PACAP-related peptide vasoactive intestinal polypeptide had no effect on either types of K+ cu rrents Repeated applications of PACAP induced g radual attenuation of the electrophysiological response In the presence of guanosine 5'-rthio1rlphosphate(GTPh, S), PACAP provoked a marked and i rreversible/K depression, whereas cell dialysis with guanosine 5'-bthiodiphosphate GDPl3S totally abolished the effect of PACAR P re-treatment of the cells with pertussis toxin did not modify the effect of PACAP on/K In contrast, cholera toxin suppressed the PACAP-induced inhibition of/K Exposu re of g ranule cells to dibutyryl cyclic adenosine monophosphate(dbcAMP)mimicked the inhibitory effect of PACAP on/K Addition of the specific protein kinaseAinhibitorH89inthepatch pipettesolution preventedthe reductionof/Kinducedbyboth PACAPand dbcAMR PACAPprovoked a sustainedincreaseofthe restingmembranepotentialin cerebellarg ranule cells cultu red eitherin high orlowKCI-containingmedium, and this long-ferm depolarizing effect of PACAP was mimicked by the/K specific blocker tetraethylammonium chloride fTEA)In addition, pre-incubation of g ranule cellswithTEA suppressedthe effect of PACAP on resting membrane potential TEAmimickedthe neu roprotective effect of PACAP against ethanol-induced apoptotic cell death, and the increase of caspase-3 activity observed after exposu re of g ranule cells to ethanol was also significantly inhibited by TEA Taken together, the present results demonstrate that, in rat cerebellar g ranule cells, PACAP reduces the delayed outward rectifier K’cu rrent by activating a type 1 PACAP(PACl)receptorcoupledtothe adenylyl cyclase/protein kinaseApathwayth rougha choleratoxin-sensitiveGsprotein Our dataalso showthat PACAP and TEA induce long-term depolarization of the resting membrane potential promote cell su rvival and inhibit caspase-3 activity, suggesting that PACAP-evoked inhibition of/K contributes to the anti-apoptotic effect of the peptide on cerebellar granule cells
cAMP cerebellar g ranule cell PACl receptor potassium cu rrents protein kinase phosphorylation
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梅岩艾, Mi-ou Zhou, Song Jiao, Zheng Liu, Zhi-hong Zhang, Yan-ai Mei*
Brain Research 970(2003)169-177,-0001,():
-1年11月30日
The inhibitory effect of the melatonin receptor antagonist luzindole on voltage-activated transient outward K current (I) was K(A) investigated in cultured rat cerebellar granule cells using the whole cell voltage-clamp technique. At the concentration of 1 mM to 1 mM,luzindole reversibly inhibited I in a concentration-dependent manner. In addition to reducing the current amplitude of I,luzindole K(A) K(A) accelerated the fast inactivation of I channels and shifted the curves of voltage-dependent steady-state activation and inactivation of K(A) I by 16.6 mV and 27.0 mV, respectively. The inhibitory effect of luzindole was neither use-dependent nor voltage-dependent, K(A) suggesting that the binding affinity of luzindole to I channels is state-dependent. Including luzindole in the pipette solution, or K(A) extracellular application of 4 P-PDOT, an antagonist of melatonin receptors, did not change the luzindole-induced inhibitory effect on the I current, indicating that luzindole exerts its channel blocking inhibitory action at the extracellular mouth of the channel, and that the K(A)effect is not due to action of the melatonin receptors. Our data are the first demonstration that luzindole is able to block transient outward 1 K channels in rat cerebellar granule cells in a state-dependent manner, likely associated with extracellular interaction of the drug with the I inactivation gate.
Luzindole, K current, Cerebellar granule cell
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【期刊论文】Regulation of swelling-activated chloride channels in embryoic chick heart cells
梅岩艾, HUA WEI, , YAN AI MEI, JIA TING SUN, HAN QING ZHOU, ZHI HONG ZHANG, *
Cell Research (2003); 13(1): 21-28,-0001,():
-1年11月30日
Swelling-activated Cl? currents, I(Cl,swell), were measured during hyposmotic shock in white Leghorn embryonic chick heart cells using the whole-cell recording of patch-clamp technique. Genistein, an inhibitor of protein tyrosine kinase (PTK), suppressed I(Cl,swell). Under isosmotic condition phorbol 12-myristate 13-acetate (PMA), an activator of PKC, elicited the Cl? current similar to that in hyposmotic solution, whereas hyposmotic shock did not elicit I(Cl,swell) in chelerythrine chloride(an inhibitor of PKC)-treated cells. Confocal microscopy experiments using FITC-phalloidin as a fluorescent label of F-actin showed that the actin network was moved from cortical region of the cell to the center after hyposmotic shock as compared with the image under isosmotic condition. When the cells were treated with cytochalasin B (CB) or cytochalasin D (CD) under isosmotic condition the disruption of the F-actin integrity was observed, and I(Cl,swell) was not elicited. With combination treatment of CB with PMA, hyposmotic solution could not elicited I(Cl,swell). The results suggested that the role of PTK, probably receptor tyrosine kinase, for regulation of I(Cl,swell) appeared to be at upstream site related to the role of F-actin. Then PKC signal pathway was activated somehow and finally change in the polymerization state of cytoskeleton led to activate the swelling-activated Cl? channels. These results demonstrate clearly that PTK, PKC and F-actin are important factors for regulation of I(Cl,swell), in embryonic chick heart cells as compared with often controversial results reported in different cell types.
swelling activation,, myocardium,, chloride current,, F-actin,, phosphorylation.,
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【期刊论文】Compartmentalized and Binary Behavior of Terminal Dendrites in Hippocampal Pyramidal Neurons
梅岩艾, Dong-Sheng Wei, Yan-Ai Mei, Ashish Bagal, Joseph P. Y. Kao, , Scott M. Thompson, Cha-Min Tang, *
SCIENCE VOL 293 21 SEPTEMBER 2001,-0001,():
-1年11月30日
The dendritic arbor of pyramidal neurons is not a monolithic structure.Weshow here that the excitability of terminal apical dendrites differs from that of the apical trunk. In response to ?uorescence-guided focal photolysis of caged glutamate, individual terminal apical dendrites generated cadmium-sensitive all-or-none responses that were subthreshold for somatic action potentials. Calcium transients produced by all-or-none responses were not restricted to the sites of photolysis, but occurred throughout individual distal dendritic compartments, indicating that electrogenesis is mediated primarily by voltagegated calcium channels. Compartmentalized and binary behavior of parallelconnected terminal dendrites can greatly expand the computational power of a single neuron.
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梅岩艾, Yan Ai Mei*, Ming Ming Wu, Chun Lei Huan, Jia Ming Sun, Han Qing Zhou, Zhi Hong Zhang
Brain Research 873(2000)46-53,-0001,():
-1年11月30日
The effects of 4-aminopyridine (4-AP), a specific blocker of outward K current, on voltage-activated transient outward K current 1(I) and inward Na current (I) were investigated on cultured rat cerebellar granule cells using the whole cell voltage-clamp K(A) Na 1technique. At the concentration of 1–5 mM, 4-AP inhibited both I and I. It reduced the amplitude of peak Na current without K(A) Na significant alteration of the steady-state activation and inactivation properties. The inhibitory effect was not enhanced by repeated 1depolarizing pulses (0.5 or 0.1 Hz), suggesting that the binding affinity of 4-AP on Na channels is state-independent. In contrast, the 1 effect of 4-AP on Na channels appeared to be voltage-dependent, the weaker inhibition occurred at more depolarization. Moreover, 4-AP 1 slowed both the activation and inactivation kinetics of Na current. These effects were similar to those induced by a-scorpion toxin and 1 sea anemone toxins on Na channels in other cell model. Our data demonstrate for the first time that 4-AP is able to block not only 11 1 A-type K channels, but also Na channels in rat cerebellar granule cells. It is concluded that the inhibition exerted by 4-AP on Na current likely differs from that provoked by local anesthetics. The possibility that the binding site of neurotoxin receptor 3 may be involved is discussed.
4-aminopyridine, Na current, Cerebellar granule cells
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梅岩艾, OLIVIER SORIANI, HUBERT VAUDRY, YAN AI MEI, FRANC, OIS ROMAN and LIONEL CAZIN
Vol.286, No.1 printect in U.S.A,-0001,():
-1年11月30日
We have investigated the effects of sigma ligands [1,3-di(2-tolyl)guanidine (DTG) and (1)-pentazocine] on the electrical activity of cultured frog pituitary melanotrope cells by using the patch-clamp technique. DTG and (1)-pentazocine (10 mM each) induced a reversible depolarization associated with an increase in membrane resistance and action potential firing. In voltage-clamp experiments, DTG and (1)-pentazocine elicited inward currents whose intensity augmented with membrane depolarization. The currents vanished or reversed between -90 and -100 mV, at values close to the K1 equilibrium potential(EK15 -102 mV). DTG (2–500 mM) and (1)-pentazocine (0.2-200 mM) reduced the outward delayed rectifier K1 current [IK(V)] in a dose-dependent manner with EC50 of 64 and 37 mM,respectively. In contrast, naloxone (50 mM) and pirenzepine (10mM) did not affect the sigma ligand-induced inhibition of IK (V).Addition of guanosine-59-O-(3-thiophosphate) in the pipettesolution irreversibly sustained the DTG-induced current whereas guanosine-59-O-(2-thiodiphosphate) virtually suppressed the response. Cholera toxin-pretreatment (1 mg/ml; 18hr) abolished the inward current and the inhibition of IK (V)induced by sigma ligands. In contrast, pretreatment with pertussis toxin (1 mg/ml; 18 hr) had no effect. Taken together, these data indicate that DTG and (1)-pentazocine activate the electrical activity of cultured frog melanotrope cells by reducing both a tonic K1 current and a voltage-dependent [IK (V)] K1conductance through the activation of a cholera toxin-sensitive G-protein.
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梅岩艾, Yan Ai Mei a, Olivier Soriani b, He?le`ne Castel b, Hubert Vaudry b, Lionel Cazin b, )
Brain Research 793 1998. 271-278,-0001,():
-1年11月30日
The effects of adenosine on the voltage-sensitive delayed-rectifier Kq I. currents and hyperpolarization-activated cationic inward K current Ih. were studied in cultured frog melanotrophs using the whole-cell configuration of the patch-clamp technique. The A1 receptor agonist R-N6-phenylisopropyl-adenosine R-PIA; 50 mM. reversibly increased I. Perfusion of dibutyryl-cAMP 1 mM. in the external K solution did not modify the R-PIA-induced enhancement of IK. Pretreatment of melanotrophs with pertussis toxin 1 mgrml; 12 h.totally abolished the R-PIA-evoked response. Application of hyperpolarizing voltage pulses from y60 to y120 mV to melanotrophs induced a two-component inward current corresponding to an I-like conductance. This conductance was characterized by a high Kq hselectivity and a low Naq permeability and was resistant to etrodotoxin 1 mM.. R-PIA had no effect on I. The present study hdemonstrates that in frog melanotrophs adenosine inhibits the electrical activity by activating IK through an A1 receptor subtype coupled to a pertussis toxin-sensitive pathway independent of the cAMPrPKA system. This study also demonstrates the existence of a Ih conductance in frog melanotrophs which is not modulated by A1 receptors. q1998 Elsevier Science B.V. All rights reserved.
Adenosine receptor, Kq current, Melanotroph
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【期刊论文】A-type potassium current modulated by A1 adenosine receptor in frog melanotrophs
梅岩艾, Yan Ai Mei, Estelle Louiset, Hubert Vaudry and Lionel Cazin *
Journal of Phy8iology (1995), 489.2, pp.431-442,-0001,():
-1年11月30日
1. Transient outward current was recorded in cultured frog melanotrophs with the whole-cell configuration of the patch-clamp technique. The ionic dependence, kinetics and pharmacological properties of the current were studied. The effects of the A1 adenosine receptor agonist R-N6 enylisopropyl-adenosine (R-PIA) on this current were also investigated. 2. In tetrodotoxin-and cobalt-containing solution, depolarization from -120 mV elicited both transient and delayed outward currents. Pulses from -60 mV activated only a sustained late current. 3. 4-Aminopyridine (4 mM) reduced the transient outward current much more than the delayed outward current. In contrast, tetraethylammonium (10-20 mM) selectively reduced the delayed current. 4. Tail current measurements showed a positive shift in the reversal potential when external K+ concentration was increased, indicating that K+ was the predominant charge carrier. 5. Steady-state inactivation was complete at potentials positive to -10 mV and removed by hyperpolarization. 6. Inactivation of the transient current was slowed and accelerated in oxidizing and reducing conditions, respectively, confirming the involvement of an inactivating 'ball and chain'peptide. 7. R-PIA increased the transient current. The steady-state inactivation curve was shifted towards more positive potentials without changing the activation kinetics. Pretreatment with pertussis toxin (1 jug ml-') blocked the response to R-PIA. 8. It is concluded that frog melanotrophs possess an A-type current that is likely to play an important role in excitability. This current, which is directly modulated by A, adenosine receptors through a Gi/Go protein, appears to be responsible for the inhibitory effects of adenosine on electrical activity.
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