137 results on '"Zoidl G"'
Search Results
2. Abstracts
- Author
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Beniac, D. R., Ridsdale, R. A., Luckevich, M. D., Tompkins, T. A., Harauz, G., Sedzik, J., Hjertén, S., Brekkan, E., Lundahl, P., Tropak, Michael B., Roder, John C., Giordano, F., Chang, B., La Ronde, A. M., Al-Sabbagh, A., Kretschmer, M., Asipu, A., Blair, G. E., Mak, B., Moscarello, M. A., Doucette, R., Gratto, K., Verge, V., Yeung, J., Nazarali, A., Murphy, P., Topilko, P., Schneider-Maunoury, S., Seitanidou, T., Evercooren, A. Baron-Van, Charnay, P., Lee, M. J., Brennan, A., Tabernero, A., Dong, Z., Blanchard, A., Zoidl, G., Jessen, K. R., Mirsky, R., Couve, E., Cabello, F., Krsulovic, J., Roncagliolo, M., Li, J., Hertzberg, E. L., Nagy, J. I., Neuberg, Dirk H.-H., Anzini, Patrizia, Nelles, Eric, Willecke, Klaus, Schachner, Melitta, Martini, Rudolf, Suter, Ueli, Ankerhold, R., Stuermer, C. A. O., Chandross, Karen J., Norton, W. T., Hudson, L. D., Cohen, R. I., Asakura, K., Hunter, S. F., Rodriguez, M., Bansal, Rashmi, Winkler, Susan, Pfeiffer, S. E., Oh., Y. S., Yong, V. W., Juurlink, B. H. J., Griebel, R. W., Devon, R. M., Khorchid, A., Almazan, G., Liu, H.-N., Konat, G. W., Jin, Gu, Wiggins, R. C., Thorburne, S. K., Bartnik, B. L., Marrif, H., Hertz, L., Jelinski, S. E., Yager, J. Y., Del Bigio, M. R., Kanfer, J. N., Weiner, H. L., Nelson, P. A., Dyer, J. K., Bourque, J., Steeves, J. D., Labes, Monika, Roach, Arthur, Andersen, Parker L., Schreyer, David J., Vanderluit, J. L., Peterson, A., Tetzlaff, W., Hanemann, C. O., Gabreëls-Festen, A., Mueller, H. W., Karchewski, L. A., Verge, V. M. K., Foldvari, M., Jaafari, M. R., Fedoroff, Sergey, editor, Burkholder, Gary D., editor, Juurlink, Bernhard H. J., editor, Devon, Richard M., editor, Doucette, J. Ronald, editor, Nazarali, Adil J., editor, Schreyer, David J., editor, and Verge, Valerie M. K., editor
- Published
- 1997
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3. Influence of elevated expression of rat wild-type PMP22 and its mutant PMP22 Trembler on cell growth of NIH3T3 fibroblasts
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Zoidl, G., D’Urso, D., Blass-Kampmann, S., Schmalenbach, C., Kuhn, R., and Müller, H. W.
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- 1997
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4. PERIPHERAL MYELIN PROTEIN 22kD (PMP22): STRUCTURE, FUNCTION AND ROLE IN DEMYELINATING HEREDITARY NEUROPATHIES
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Müller, H. W., D'Urso, D, Zoidl, G, and Hanemann, C O
- Published
- 1997
5. An alternative splice variant of zebrafish cx52.6 is expressed in retinal horizontal cells
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Greb, H, Klaassen, Lauw J, Schultz, K, Kamermans, M, Zoidl, G., Weiler, R, Janssen-Bienhold, U., Greb, H, Klaassen, Lauw J, Schultz, K, Kamermans, M, Zoidl, G., Weiler, R, and Janssen-Bienhold, U.
- Abstract
Retinal horizontal cells (HCs) are inhibitory neurons, which modulate the transmission of light-elicited signals from photoreceptors to bipolar cells in the outer retina. HCs of the same physiological type are extensively coupled via gap junctions. In the zebrafish retina, the population of HCs comprises up to four morphologically distinct subtypes. Four different connexins (Cx52.6, Cx52.7, Cx52.9 and Cx55.5) were detected in these cells with overlapping expression patterns. In this study, we show that Cx52.6 is alternatively spliced in the retina, resulting in an additional isoform, designated as Cx53.4, which differs from the originally described Cx52.6 only by the final C-terminal peptide (12 vs. 4 aa). Further protein sequence alignments revealed that Cx53.4 represents the counterpart of alternatively spliced mouse Cx57 and human Cx62. RT-PCR analyses of mRNA expression in different adult zebrafish tissues showed that Cx53.4 is expressed exclusively in the retina. The localization of Cx53.4 protein within the retina was analyzed using a specific antibody. Immunofluorescence analyses demonstrated that the expression of Cx53.4 is restricted to HCs of all four subtypes. Further, immunoelectron microscopy confirmed the presence of Cx53.4 in gap junctions between HC dendrites and between their axon terminals.
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- 2018
6. An Alternative Splice Variant of Zebrafish Cx52.6 is Expressed in Retinal Horizontal Cells
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Greb, H., primary, Klaassen, L.J., additional, Schultz, K., additional, Kamermans, M., additional, Zoidl, G., additional, Weiler, R., additional, and Janssen-Bienhold, U., additional
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- 2018
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7. Complexity of gap junctions between horizontal cells of the carp retina
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Greb, H., primary, Hermann, S., additional, Dirks, P., additional, Ommen, G., additional, Kretschmer, V., additional, Schultz, K., additional, Zoidl, G., additional, Weiler, R., additional, and Janssen-Bienhold, U., additional
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- 2017
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8. Pannexin1 channel proteiins in the zebrafish retina have shared and unique properties
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Kurtenbach, S., Prochnow, N., Kurtenbach, S.T., Klooster, J., Zoidl, C., Dermietzel, R., Kamermans, M., Zoidl, G., and Netherlands Institute for Neuroscience (NIN)
- Published
- 2013
9. Synaptic transmission from horizontal cells to cones is impaired by loss of connexin hemichannels
- Author
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Klaassen, L.J., Sun, Ziyi, Steijaert, M.N., Bolte, P., Fahrenfort, I., Sjoerdsma, T., Klooster, J., Claassen, Y., Shields, C.R., Eikelder, ten, H.M.M., Janssen-Bienhold, U., Zoidl, G., McMahon, D.G., Kamermans, M., Klaassen, L.J., Sun, Ziyi, Steijaert, M.N., Bolte, P., Fahrenfort, I., Sjoerdsma, T., Klooster, J., Claassen, Y., Shields, C.R., Eikelder, ten, H.M.M., Janssen-Bienhold, U., Zoidl, G., McMahon, D.G., and Kamermans, M.
- Abstract
In the vertebrate retina, horizontal cells generate the inhibitory surround of bipolar cells, an essential step in contrast enhancement. For the last decades, the mechanism involved in this inhibitory synaptic pathway has been a major controversy in retinal research. One hypothesis suggests that connexin hemichannels mediate this negative feedback signal; another suggests that feedback is mediated by protons. Mutant zebrafish were generated that lack connexin 55.5 hemichannels in horizontal cells. Whole cell voltage clamp recordings were made from isolated horizontal cells and cones in flat mount retinas. Light-induced feedback from horizontal cells to cones was reduced in mutants. A reduction of feedback was also found when horizontal cells were pharmacologically hyperpolarized but was absent when they were pharmacologically depolarized. Hemichannel currents in isolated horizontal cells showed a similar behavior. The hyperpolarization-induced hemichannel current was strongly reduced in the mutants while the depolarization-induced hemichannel current was not. Intracellular recordings were made from horizontal cells. Consistent with impaired feedback in the mutant, spectral opponent responses in horizontal cells were diminished in these animals. A behavioral assay revealed a lower contrast-sensitivity, illustrating the role of the horizontal cell to cone feedback pathway in contrast enhancement. Model simulations showed that the observed modifications of feedback can be accounted for by an ephaptic mechanism. A model for feedback, in which the number of connexin hemichannels is reduced to about 40%, fully predicts the specific asymmetric modification of feedback. To our knowledge, this is the first successful genetic interference in the feedback pathway from horizontal cells to cones. It provides direct evidence for an unconventional role of connexin hemichannels in the inhibitory synapse between horizontal cells and cones. This is an important step in resolving a lo
- Published
- 2011
10. Synaptic transmission from horizontal cells to cones is impaired by loss of connexin hemichannels.
- Author
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Klaassen, L., Sun, Z., Steijaert, M.N., Bolte, P., Fahrenfort, I., Sjoerdsma, T., Klooster, J., Claassen, Y., Shields, C., Ten Eikelder, H.M.M., Janssen-Bienhold, U., Zoidl, G., McMahon, D., Kamermans, M., Klaassen, L., Sun, Z., Steijaert, M.N., Bolte, P., Fahrenfort, I., Sjoerdsma, T., Klooster, J., Claassen, Y., Shields, C., Ten Eikelder, H.M.M., Janssen-Bienhold, U., Zoidl, G., McMahon, D., and Kamermans, M.
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- 2011
11. Pannexin1 in the outer retina of the zebrafish, Dani rerio.
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Prochnow, N., Hoffman, S., Vroman, R., Klooster, J., Bunse, S., Kamermans, M., Dermietzel, R., Zoidl, G., Prochnow, N., Hoffman, S., Vroman, R., Klooster, J., Bunse, S., Kamermans, M., Dermietzel, R., and Zoidl, G.
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- 2009
12. Saturday, 17 July 2010
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Dimova, I., primary, Hlushchuk, R., additional, Makanya, A., additional, Djonov, V., additional, Theurl, M., additional, Schgoer, W., additional, Albrecht, K., additional, Beer, A., additional, Patsch, J. R., additional, Schratzberger, P., additional, Mahata, S., additional, Kirchmair, R., additional, Didie, M., additional, Christalla, P., additional, Rau, T., additional, Eschenhagen, T., additional, Schumacher, U., additional, Lin, Q., additional, Zenke, M., additional, Zimmmermann, W., additional, Hoch, M., additional, Fischer, P., additional, Stapel, B., additional, Missol-Kolka, E., additional, Erschow, S., additional, Scherr, M., additional, Drexler, H., additional, Hilfiker-Kleiner, D., additional, Diebold, I., additional, Petry, A., additional, Kennel, P., additional, Djordjevic, T., additional, Hess, J., additional, Goerlach, A., additional, Castellano, J., additional, Aledo, R., additional, Sendra, J., additional, Costales, P., additional, Badimon, L., additional, Llorente-Cortes, V., additional, Dworatzek, E., additional, Mahmoodzadeh, S., additional, Regitz-Zagrosek, V., additional, Posa, A., additional, Varga, C., additional, Berko, A., additional, Veszelka, M., additional, Szablics, P., additional, Vari, B., additional, Pavo, I., additional, Laszlo, F., additional, Brandenburger, M., additional, Wenzel, J., additional, Bogdan, R., additional, Richardt, D., additional, Reppel, M., additional, Hescheler, J., additional, Terlau, H., additional, Dendorfer, A., additional, Heijman, J., additional, Rudy, Y., additional, Westra, R., additional, Volders, P., additional, Rasmusson, R., additional, Bondarenko, V., additional, Ertas Gokhan, M. D., additional, Ural Ertan, M. D., additional, Karaoz Erdal, P. H. D., additional, Aksoy Ayca, P. H. D., additional, Kilic Teoman, M. D., additional, Kozdag Guliz, M. D., additional, Vural Ahmet, M. D., additional, Ural Dilek, M. D., additional, Poulet, C., additional, Christ, T., additional, Wettwer, E., additional, Ravens, U., additional, Van Der Pouw Kraan, C., additional, Schirmer, S., additional, Fledderus, J., additional, Moerland, P., additional, Leyen, T., additional, Piek, J., additional, Van Royen, N., additional, Horrevoets, A., additional, Fleissner, F., additional, Jazbutyte, V., additional, Fiedler, J., additional, Galuppo, P., additional, Mayr, M., additional, Ertl, G., additional, Bauersachs, J., additional, Thum, T., additional, Protze, S., additional, Bussek, A., additional, Li, F., additional, Hoo, R., additional, Lam, K., additional, Xu, A., additional, Subramanian, P., additional, Karshovska, E., additional, Megens, R., additional, Akhtar, S., additional, Heyll, K., additional, Jansen, Y., additional, Weber, C., additional, Schober, A., additional, Zafeiriou, M., additional, Noack, C., additional, Renger, A., additional, Dietz, R., additional, Zelarayan, L., additional, Bergmann, M., additional, Meln, I., additional, Malashicheva, A., additional, Anisimov, S., additional, Kalinina, N., additional, Sysoeva, V., additional, Zaritskey, A., additional, Barbuti, A., additional, Scavone, A., additional, Mazzocchi, N., additional, Crespi, A., additional, Capilupo, D., additional, Difrancesco, D., additional, Qian, L., additional, Shim, W., additional, Gu, Y., additional, Mohammed, S., additional, Wong, P., additional, Zafiriou, M., additional, Schaeffer, H., additional, Kovacs, P., additional, Simon, J., additional, Varro, A., additional, Athias, P., additional, Wolf, J., additional, Bouchot, O., additional, Vandroux, D., additional, Mathe, A., additional, De Carvalho, A., additional, Laurent, G., additional, Rainer, P., additional, Huber, M., additional, Edelmann, F., additional, Stojakovic, T., additional, Trantina-Yates, A., additional, Trauner, M., additional, Pieske, B., additional, Von Lewinski, D., additional, De Jong, A., additional, Maass, A., additional, Oberdorf-Maass, S., additional, Van Gelder, I., additional, Lin, Y., additional, Li, J., additional, Wang, F., additional, He, Y., additional, Li, X., additional, Xu, H., additional, Yang, X., additional, Coppini, R., additional, Ferrantini, C., additional, Ferrara, C., additional, Rossi, A., additional, Mugelli, A., additional, Poggesi, C., additional, Cerbai, E., additional, Rozmaritsa, N., additional, Voigt, N., additional, Dobrev, D., additional, Kienitz, M.-C., additional, Zoidl, G., additional, Bender, K., additional, Pott, L., additional, Kohajda, Z., additional, Kristof, A., additional, Virag, L., additional, Jost, N., additional, Trafford, A., additional, Prnjavorac, B., additional, Mujaric, E., additional, Jukic, J., additional, Abduzaimovic, K., additional, Brack, K., additional, Patel, V., additional, Coote, J., additional, Ng, G., additional, Wilders, R., additional, Van Ginneken, A., additional, Verkerk, A., additional, Xaplanteris, P., additional, Vlachopoulos, C., additional, Baou, K., additional, Vassiliadou, C., additional, Dima, I., additional, Ioakeimidis, N., additional, Stefanadis, C., additional, Ruifrok, W., additional, Qian, C., additional, Sillje, H., additional, Van Goor, H., additional, Van Veldhuisen, D., additional, Van Gilst, W., additional, De Boer, R., additional, Schmidt, K., additional, Kaiser, F., additional, Erdmann, J., additional, De Wit, C., additional, Barnett, O., additional, Kyyak, Y., additional, Cesana, F., additional, Boffi, L., additional, Mauri, T., additional, Alloni, M., additional, Betelli, M., additional, Nava, S., additional, Giannattasio, C., additional, Mancia, G., additional, Vilskersts, R., additional, Kuka, J., additional, Svalbe, B., additional, Liepinsh, E., additional, Dambrova, M., additional, Zakrzewicz, A., additional, Maroski, J., additional, Vorderwuelbecke, B., additional, Fiedorowicz, K., additional, Da Silva-Azevedo, L., additional, Pries, A., additional, Gryglewska, B., additional, Necki, M., additional, Zelawski, M., additional, Grodzicki, T., additional, Scoditti, E., additional, Massaro, M., additional, Carluccio, M., additional, Distante, A., additional, Storelli, C., additional, De Caterina, R., additional, Kocgirli, O., additional, Valcaccia, S., additional, Dao, V., additional, Suvorava, T., additional, Kumpf, S., additional, Floeren, M., additional, Oppermann, M., additional, Kojda, G., additional, Leo, C., additional, Ziogas, J., additional, Favaloro, J., additional, Woodman, O., additional, Goettsch, W., additional, Marton, A., additional, Goettsch, C., additional, Morawietz, H., additional, Khalifa, E., additional, Ashour, Z., additional, Rupprecht, V., additional, Scalera, F., additional, Martens-Lobenhoffer, J., additional, Bode-Boeger, S., additional, Li, W., additional, Kwan, Y., additional, Leung, G., additional, Patella, F., additional, Mercatanti, A., additional, Pitto, L., additional, Rainaldi, G., additional, Tsimafeyeu, I., additional, Tishova, Y., additional, Wynn, N., additional, Kalinchenko, S., additional, Clemente Lorenzo, M., additional, Grande, M., additional, Barriocanal, F., additional, Aparicio, M., additional, Martin, A., additional, Hernandez, J., additional, Lopez Novoa, J., additional, Martin Luengo, C., additional, Kurlianskaya, A., additional, Denisevich, T., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Wang, Y., additional, Gabrielsen, A., additional, Ripa, R., additional, Jorgensen, E., additional, Kastrup, J., additional, Arderiu, G., additional, Pena, E., additional, Kobus, K., additional, Czyszek, J., additional, Kozlowska-Wiechowska, A., additional, Milkiewicz, P., additional, Milkiewicz, M., additional, Madonna, R., additional, Montebello, E., additional, Geng, Y., additional, Chin-Dusting, J., additional, Michell, D., additional, Skilton, M., additional, Dixon, J., additional, Dart, A., additional, Moore, X., additional, Ehrbar, M., additional, Reichmuth, P., additional, Heinimann, N., additional, Hewing, B., additional, Stangl, V., additional, Stangl, K., additional, Laule, M., additional, Baumann, G., additional, Ludwig, A., additional, Widmer-Teske, R., additional, Mueller, A., additional, Stieger, P., additional, Tillmanns, H., additional, Braun-Dullaeus, R., additional, Sedding, D., additional, Troidl, K., additional, Eller, L., additional, Benli, I., additional, Apfelbeck, H., additional, Schierling, W., additional, Troidl, C., additional, Schaper, W., additional, Schmitz-Rixen, T., additional, Hinkel, R., additional, Trenkwalder, T., additional, Pfosser, A., additional, Globisch, F., additional, Stachel, G., additional, Lebherz, C., additional, Bock-Marquette, I., additional, Kupatt, C., additional, Seyler, C., additional, Duthil-Straub, E., additional, Zitron, E., additional, Scholz, E., additional, Thomas, D., additional, Gierten, J., additional, Karle, C., additional, Fink, R., additional, Padro, T., additional, Lugano, R., additional, Garcia-Arguinzonis, M., additional, Schuchardt, M., additional, Pruefer, J., additional, Toelle, M., additional, Pruefer, N., additional, Jankowski, V., additional, Jankowski, J., additional, Zidek, W., additional, Van Der Giet, M., additional, Fransen, P., additional, Van Hove, C., additional, Michiels, C., additional, Van Langen, J., additional, Bult, H., additional, Quarck, R., additional, Wynants, M., additional, Alfaro-Moreno, E., additional, Rosario Sepulveda, M., additional, Wuytack, F., additional, Van Raemdonck, D., additional, Meyns, B., additional, Delcroix, M., additional, Christofi, F., additional, Wijetunge, S., additional, Sever, P., additional, Hughes, A., additional, Ohanian, J., additional, Forman, S., additional, Ohanian, V., additional, Gibbons, C., additional, Vernia, S., additional, Das, A., additional, Shah, V., additional, Casado, M., additional, Bielenberg, W., additional, Daniel, J., additional, Daniel, J.-M., additional, Hersemeyer, K., additional, Schmidt-Woell, T., additional, Kaetzel, D., additional, Tillmans, H., additional, Kanse, S., additional, Tuncay, E., additional, Kandilci, H., additional, Zeydanli, E., additional, Sozmen, N., additional, Akman, D., additional, Yildirim, S., additional, Turan, B., additional, Nagy, N., additional, Acsai, K., additional, Farkas, A., additional, Papp, J., additional, Toth, A., additional, Viero, C., additional, Mason, S., additional, Williams, A., additional, Marston, S., additional, Stuckey, D., additional, Dyer, E., additional, Song, W., additional, El Kadri, M., additional, Hart, G., additional, Hussain, M., additional, Faltinova, A., additional, Gaburjakova, J., additional, Urbanikova, L., additional, Hajduk, M., additional, Tomaskova, B., additional, Antalik, M., additional, Zahradnikova, A., additional, Steinwascher, P., additional, Jaquet, K., additional, Muegge, A., additional, Wang, G., additional, Zhang, M., additional, Tesi, C., additional, Ter Keurs, H., additional, Kettlewell, S., additional, Smith, G., additional, Workman, A., additional, Lenaerts, I., additional, Holemans, P., additional, Sokolow, S., additional, Schurmans, S., additional, Herchuelz, A., additional, Sipido, K., additional, Antoons, G., additional, Wehrens, X., additional, Li, N., additional, Respress, J. R., additional, De Almeida, A., additional, Van Oort, R., additional, Lohmann, H., additional, Saes, M., additional, Messer, A., additional, Copeland, O., additional, Leung, M., additional, Matthes, F., additional, Steinbrecher, J., additional, Salinas-Riester, G., additional, Opitz, L., additional, Hasenfuss, G., additional, Lehnart, S., additional, Caracciolo, G., additional, Eleid, M., additional, Carerj, S., additional, Chandrasekaran, K., additional, Khandheria, B., additional, Sengupta, P., additional, Riaz, I., additional, Tyng, L., additional, Dou, Y., additional, Seymour, A., additional, Dyer, C., additional, Griffin, S., additional, Haswell, S., additional, Greenman, J., additional, Yasushige, S., additional, Amorim, P., additional, Nguyen, T., additional, Schwarzer, M., additional, Mohr, F., additional, Doenst, T., additional, Popin Sanja, S., additional, Lalosevic, D., additional, Capo, I., additional, Momcilov Popin, T., additional, Astvatsatryan, A., additional, Senan, M., additional, Shafieian, G., additional, Goncalves, N., additional, Falcao-Pires, I., additional, Henriques-Coelho, T., additional, Moreira-Goncalves, D., additional, Leite-Moreira, A., additional, Bronze Carvalho, L., additional, Azevedo, J., additional, Andrade, M., additional, Arroja, I., additional, Relvas, M., additional, Morais, G., additional, Seabra, M., additional, Aleixo, A., additional, Winter, J., additional, Zabunova, M., additional, Mintale, I., additional, Lurina, D., additional, Narbute, I., additional, Zakke, I., additional, Erglis, A., additional, Marcinkevics, Z., additional, Kusnere, S., additional, Abolins, A., additional, Aivars, J., additional, Rubins, U., additional, Nassar, Y., additional, Monsef, D., additional, Hamed, G., additional, Abdelshafy, S., additional, Chen, L., additional, Wu, Y., additional, Wang, J., additional, Cheng, C., additional, Sternak, M., additional, Khomich, T., additional, Jakubowski, A., additional, Szafarz, M., additional, Szczepanski, W., additional, Mateuszuk, L., additional, Szymura-Oleksiak, J., additional, Chlopicki, S., additional, Sulicka, J., additional, Strach, M., additional, Kierzkowska, I., additional, Surdacki, A., additional, Mikolajczyk, T., additional, Balwierz, W., additional, Guzik, T., additional, Dmitriev, V., additional, Oschepkova, E., additional, Polovitkina, O., additional, Titov, V., additional, Rogoza, A., additional, Shakur, R., additional, Metcalfe, S., additional, Bradley, J., additional, Demyanets, S., additional, Kaun, C., additional, Kastl, S., additional, Pfaffenberger, S., additional, Huk, I., additional, Maurer, G., additional, Huber, K., additional, Wojta, J., additional, Eriksson, O., additional, Aberg, M., additional, Siegbahn, A., additional, Niccoli, G., additional, Sgueglia, G., additional, Conte, M., additional, Giubilato, S., additional, Cosentino, N., additional, Ferrante, G., additional, Crea, F., additional, Ilisei, D., additional, Leon, M., additional, Mitu, F., additional, Kyriakakis, E., additional, Philippova, M., additional, Cavallari, M., additional, Bochkov, V., additional, Biedermann, B., additional, De Libero, G., additional, Erne, P., additional, Resink, T., additional, Bakogiannis, C., additional, Antoniades, C., additional, Tousoulis, D., additional, Demosthenous, M., additional, Psarros, C., additional, Sfyras, N., additional, Channon, K., additional, Del Turco, S., additional, Navarra, T., additional, Basta, G., additional, Carnicelli, V., additional, Frascarelli, S., additional, Zucchi, R., additional, Kostareva, A., additional, Sjoberg, G., additional, Gudkova, A., additional, Semernin, E., additional, Shlyakhto, E., additional, Sejersen, T., additional, Cucu, N., additional, Anton, M., additional, Stambuli, D., additional, Botezatu, A., additional, Arsene, C., additional, Lupeanu, E., additional, Anton, G., additional, Patsch, J., additional, Huber, E., additional, Lande, C., additional, Cecchettini, A., additional, Tedeschi, L., additional, Trivella, M., additional, Citti, L., additional, Chen, B., additional, Ma, Y., additional, Yang, Y., additional, Ma, X., additional, Liu, F., additional, Hasanzad, M., additional, Rejali, L., additional, Fathi, M., additional, Minassian, A., additional, Mohammad Hassani, R., additional, Najafi, A., additional, Sarzaeem, M., additional, Sezavar, S., additional, Akhmedov, A., additional, Klingenberg, R., additional, Yonekawa, K., additional, Lohmann, C., additional, Gay, S., additional, Maier, W., additional, Neithard, M., additional, Luescher, T., additional, Xie, X., additional, Fu, Z., additional, Kevorkov, A., additional, Verduci, L., additional, Cremisi, F., additional, Wonnerth, A., additional, Katsaros, K., additional, Zorn, G., additional, Weiss, T., additional, De Rosa, R., additional, Galasso, G., additional, Piscione, F., additional, Santulli, G., additional, Iaccarino, G., additional, Piccolo, R., additional, Luciano, R., additional, Chiariello, M., additional, Szymanski, M., additional, Schoemaker, R., additional, Hillege, H., additional, Rizzo, S., additional, Basso, C., additional, Thiene, G., additional, Valente, M., additional, Rickelt, S., additional, Franke, W., additional, Bartoloni, G., additional, Bianca, S., additional, Giurato, E., additional, Barone, C., additional, Ettore, G., additional, Bianca, I., additional, Eftekhari, P., additional, Wallukat, G., additional, Bekel, A., additional, Heinrich, F., additional, Fu, M., additional, Briedert, M., additional, Briand, J., additional, Roegel, J., additional, Pilichou, K., additional, Korkmaz, S., additional, Radovits, T., additional, Pali, S., additional, Hirschberg, K., additional, Zoellner, S., additional, Loganathan, S., additional, Karck, M., additional, Szabo, G., additional, Pucci, A., additional, Pantaleo, J., additional, Martino, S., additional, Pelosi, G., additional, Matteucci, M., additional, Kusmic, C., additional, Vesentini, N., additional, Piccolomini, F., additional, Viglione, F., additional, L'abbate, A., additional, Slavikova, J., additional, Chottova Dvorakova, M., additional, Kummer, W., additional, Campanile, A., additional, Spinelli, L., additional, Ciccarelli, M., additional, De Gennaro, S., additional, Assante Di Panzillo, E., additional, Trimarco, B., additional, Akbarzadeh Najar, R., additional, Ghaderian, S., additional, Tabatabaei Panah, A., additional, Vakili, H., additional, Rezaei Farimani, A., additional, Rezaie, G., additional, Beigi Harchegani, A., additional, Hamdani, N., additional, Gavina, C., additional, Van Der Velden, J., additional, Niessen, H., additional, Stienen, G., additional, Paulus, W., additional, Moura, C., additional, Lamego, I., additional, Eloy, C., additional, Areias, J., additional, Bonda, T., additional, Dziemidowicz, M., additional, Hirnle, T., additional, Dmitruk, I., additional, Kaminski, K., additional, Musial, W., additional, Winnicka, M., additional, Villar, A., additional, Merino, D., additional, Ares, M., additional, Pilar, F., additional, Valdizan, E., additional, Hurle, M., additional, Nistal, J., additional, Vera, V., additional, Karuppasamy, P., additional, Chaubey, S., additional, Dew, T., additional, Sherwood, R., additional, Desai, J., additional, John, L., additional, Marber, M., additional, Kunst, G., additional, Cipolletta, E., additional, Attanasio, A., additional, Del Giudice, C., additional, Campiglia, P., additional, Illario, M., additional, Berezin, A., additional, Koretskaya, E., additional, Bishop, E., additional, Fearon, I., additional, Heger, J., additional, Warga, B., additional, Abdallah, Y., additional, Meyering, B., additional, Schlueter, K., additional, Piper, H., additional, Euler, G., additional, Lavorgna, A., additional, Cecchetti, S., additional, Rio, T., additional, Coluzzi, G., additional, Carrozza, C., additional, Conti, E., additional, Andreotti, F., additional, Glavatskiy, A., additional, Uz, O., additional, Kardesoglu, E., additional, Yiginer, O., additional, Bas, S., additional, Ipcioglu, O., additional, Ozmen, N., additional, Aparci, M., additional, Cingozbay, B., additional, Ivanes, F., additional, Hillaert, M., additional, Susen, S., additional, Mouquet, F., additional, Doevendans, P., additional, Jude, B., additional, Montalescot, G., additional, Van Belle, E., additional, Castellani, C., additional, Angelini, A., additional, De Boer, O., additional, Van Der Loos, C., additional, Gerosa, G., additional, Van Der Wal, A., additional, Dumitriu, I., additional, Baruah, P., additional, Kaski, J., additional, Maytham, O., additional, D Smith, J., additional, Rose, M., additional, Cappelletti, A., additional, Pessina, A., additional, Mazzavillani, M., additional, Calori, G., additional, Margonato, A., additional, Cassese, S., additional, D'anna, C., additional, Leo, A., additional, Silenzi, A., additional, Baca', M., additional, Biasucci, L., additional, Baller, D., additional, Gleichmann, U., additional, Holzinger, J., additional, Bitter, T., additional, Horstkotte, D., additional, Antonopoulos, A., additional, Miliou, A., additional, Triantafyllou, C., additional, Masson, W., additional, Siniawski, D., additional, Sorroche, P., additional, Casanas, L., additional, Scordo, W., additional, Krauss, J., additional, Cagide, A., additional, Huang, T., additional, Wiedon, A., additional, Lee, S., additional, Walker, K., additional, O'dea, K., additional, Perez Berbel, P., additional, Arrarte Esteban, V., additional, Garcia Valentin, M., additional, Sola Villalpando, M., additional, Lopez Vaquero, C., additional, Caballero, L., additional, Quintanilla Tello, M., additional, Sogorb Garri, F., additional, Duerr, G., additional, Elhafi, N., additional, Bostani, T., additional, Swieny, L., additional, Kolobara, E., additional, Welz, A., additional, Roell, W., additional, Dewald, O., additional, Kaludercic, N., additional, Takimoto, E., additional, Nagayama, T., additional, Chen, K., additional, Shih, J., additional, Kass, D., additional, Di Lisa, F., additional, Paolocci, N., additional, Vinet, L., additional, Pezet, M., additional, Briec, F., additional, Previlon, M., additional, Rouet-Benzineb, P., additional, Hivonnait, A., additional, Charpentier, F., additional, Mercadier, J., additional, Cobo, M., additional, Llano, M., additional, Montalvo, C., additional, Exposito, V., additional, Meems, L., additional, Westenbrink, B., additional, Biesmans, L., additional, Bito, V., additional, Driessen, R., additional, Huysmans, C., additional, Mourouzis, I., additional, Pantos, C., additional, Galanopoulos, G., additional, Gavra, M., additional, Perimenis, P., additional, Spanou, D., additional, Cokkinos, D., additional, Panasenko, T., additional, Partsch, S., additional, Harjung, C., additional, Bogdanova, A., additional, Mihov, D., additional, Mocharla, P., additional, Yakushev, S., additional, Vogel, J., additional, Gassmann, M., additional, Tavakoli, R., additional, Johansen, D., additional, Sanden, E., additional, Xi, C., additional, Sundset, R., additional, Ytrehus, K., additional, Bliksoen, M., additional, Rutkovskiy, A., additional, Mariero, L., additional, Vaage, I., additional, Stenslokken, K., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Studneva, I., additional, Serebryakova, L., additional, Tskitishvili, O., additional, Pelogeykina, Y., additional, Timoshin, A., additional, Vanin, A., additional, Ziberna, L., additional, Lunder, M., additional, Drevensek, G., additional, Passamonti, S., additional, Gorza, L., additional, Ravara, B., additional, Scapin, C., additional, Vitadello, M., additional, Zigrino, F., additional, Gwathmey, J., additional, Del Monte, F., additional, Vilahur, G., additional, Juan-Babot, O., additional, Onate, B., additional, Casani, L., additional, Lemoine, S., additional, Calmettes, G., additional, Jaspard-Vinassa, B., additional, Duplaa, C., additional, Couffinhal, T., additional, Diolez, P., additional, Dos Santos, P., additional, Fusco, A., additional, Sorriento, D., additional, Cervero, P., additional, Feliciello, A., additional, Barnucz, E., additional, Kozichova, K., additional, Hlavackova, M., additional, Neckar, J., additional, Kolar, F., additional, Novakova, O., additional, Novak, F., additional, Barsanti, C., additional, Abraham, N., additional, Muntean, D., additional, Mirica, S., additional, Duicu, O., additional, Raducan, A., additional, Hancu, M., additional, Fira-Mladinescu, O., additional, Ordodi, V., additional, Voelkl, J., additional, Haubner, B., additional, Neely, G., additional, Moriell, C., additional, Seidl, S., additional, Pachinger, O., additional, Penninger, J., additional, and Metzler, B., additional
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- 2010
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13. Pannexin1 in the outer retina of the zebrafish, Danio rerio
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Prochnow, N., primary, Hoffmann, S., additional, Vroman, R., additional, Klooster, J., additional, Bunse, S., additional, Kamermans, M., additional, Dermietzel, R., additional, and Zoidl, G., additional
- Published
- 2009
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14. Receptor protein tyrosine phosphatases are expressed by cycling retinal progenitor cells and involved in neuronal development of mouse retina
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Horvat-Bröcker, A., primary, Reinhard, J., additional, Illes, S., additional, Paech, T., additional, Zoidl, G., additional, Harroch, S., additional, Distler, C., additional, Knyazev, P., additional, Ullrich, A., additional, and Faissner, A., additional
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- 2008
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15. Localization of the pannexin1 protein at postsynaptic sites in the cerebral cortex and hippocampus
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Zoidl, G., primary, Petrasch-Parwez, E., additional, Ray, A., additional, Meier, C., additional, Bunse, S., additional, Habbes, H.-W., additional, Dahl, G., additional, and Dermietzel, R., additional
- Published
- 2007
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16. Evidence for a role of the N‐terminal domain in subcellular localization of the neuronal connexin36 (Cx36)
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Zoidl, G., primary, Meier, C., additional, Petrasch‐Parwez, E., additional, Zoidl, C., additional, Habbes, H.‐W., additional, Kremer, M., additional, Srinivas, M., additional, Spray, D.C., additional, and Dermietzel, R., additional
- Published
- 2002
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17. Helix-loop-helix proteins in Schwann cells: A study of regulation and subcellular localization of Ids, REB, and E12/47 during embryonic and postnatal development
- Author
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Stewart, H.J.S, primary, Zoidl, G., additional, Rossner, M., additional, Brennan, A., additional, Zoidl, C., additional, Nave, K.-A., additional, Mirsky, R., additional, and Jessen, K.R., additional
- Published
- 1997
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18. Identification of transcriptionally regulated mRNAs from mouse Schwann cell precursors using modified RNA fingerprinting methods
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Zoidl, G., primary, Blanchard, A.D., additional, Zoidl, C., additional, Dong, Z., additional, Brennan, A., additional, Parmantier, E., additional, Mirsky, R., additional, and Jessen, K.R., additional
- Published
- 1997
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19. P0Is Constitutively Expressed in the Rat Neural Crest and Embryonic Nerves and Is Negatively and Positively Regulated by Axons to Generate Non-Myelin-Forming and Myelin-Forming Schwann Cells, Respectively
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Lee, M.-J., primary, Brennan, A., additional, Blanchard, A., additional, Zoidl, G., additional, Dong, Z., additional, Tabernero, A., additional, Zoidl, C., additional, Dent, M.A.R., additional, Jessen, K.R., additional, and Mirsky, R., additional
- Published
- 1997
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20. Full‐length Cloning, Expression and Cellular Localization of Rat Plasmolipin mRNA, a Proteolipid of PNS and CNS
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Gillen, C., primary, Gleichmann, M., additional, Greiner‐Petter, R., additional, Zoidl, G., additional, Kupfer, S., additional, Bosse, F., additional, Auer, J., additional, and Müller, H. W., additional
- Published
- 1996
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21. Retroviral-mediated gene transfer of the peripheral myelin protein PMP22 in Schwann cells: modulation of cell growth.
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Zoidl, G., primary, Blass-Kampmann, S., additional, D'Urso, D., additional, Schmalenbach, C., additional, and Müller, H.W., additional
- Published
- 1995
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22. Differential expression of two mRNA species indicates a dual function of peripheral myelin proteinPMP22in cell growth and myelination
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Bosse, F., primary, Zoidl, G., additional, Wilms, S., additional, Gillen, C. P., additional, Kuhn, H. G., additional, and Müller, H. W., additional
- Published
- 1994
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23. Differential expression of two mRNA species indicates a dual function of peripheral myelin protein PMP22 in cell growth and myelination.
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Bosse, F., Zoidl, G., Wilms, S., Gillen, C. P., Kuhn, H. G., and Müller, H. W.
- Published
- 1994
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24. Influence of elevated expression of rat wild-type PMP22 and its mutant PMP22 Trembler on cell growth of NIH3T3 fibroblasts.
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Zoidl, G., D’Urso, D., Blass-Kampmann, S., Schmalenbach, C., Kuhn, R., and Müller, H. W.
- Abstract
The peripheral myelin gene PMP22 is the rat and human homologue of the murine growth-arrest-specific gene gas3. The biological function of PMP22 is unknown, but recent progress in the analysis of rat Schwann cells expressing altered levels of PMP22 revealed that one role of PMP22 is as a negative growth modulator. We have investigated the influence of rat PMP22 (rPMP22) and a mutant of PMP22 (rPMP22
Tr ) resembling the murine trembler mutation on cell growth of retrovirus-vector-infected mouse NIH3T3 cells. Transduced cells carrying the two different sense constructs expressed rPMP22 and rPMP22Tr mRNAs and proteins. Elevated levels of rPMP22 and rPMP22Tr significantly reduced fibroblast growth as judged by proliferation assays. Despite a negative modulatory influence of rPMP22 and rPMP22Tr on cell proliferation, cell cycle analyses by flow cytometry did not reveal an influence of rPMP22 or rPMP22Tr on the synchronous progression of resting NIH3T3 cells from G0 into S phase. However, cell cycle analyses by flow cytometry of asynchronously dividing cultures demonstrated that the expression of rPMP22 and rPMP22Tr increased the fraction of cells in the G1 phase of the cell cycle. Furthermore, cell death analyses revealed that, in contrast to control cells and cells carrying the rPMP22Tr construct, a significantly increased fraction of NIH3T3 cells expressing rPMP22 exit the proliferation compartment showing hallmarks of programmed cell death. These results indicate that (i) rPMP22 and rPMP22Tr act as negative modulators of proliferation in murine fibroblasts probably through extension of the G1 phase of the cell cycle and (ii) rPMP22 but not rPMP22Tr promotes programmed death of these cells. [ABSTRACT FROM AUTHOR]- Published
- 1997
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- View/download PDF
25. Influence of elevated expression of rat wild-type PMP22 and its mutant PMP22<SUP>Trembler</SUP> on cell growth of NIH3T3 fibroblasts
- Author
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Zoidl, G., D'Urso, D., Blass-Kampmann, S., Schmalenbach, C., Kuhn, R., and Müller, H. W.
- Abstract
Abstract. The peripheral myelin gene PMP22 is the rat and human homologue of the murine growth-arrest-specific gene gas3. The biological function of PMP22 is unknown, but recent progress in the analysis of rat Schwann cells expressing altered levels of PMP22 revealed that one role of PMP22 is as a negative growth modulator. We have investigated the influence of rat PMP22 (rPMP22) and a mutant of PMP22 (rPMP22Tr) resembling the murine trembler mutation on cell growth of retrovirus-vector-infected mouse NIH3T3 cells. Transduced cells carrying the two different sense constructs expressed rPMP22 and rPMP22Tr mRNAs and proteins. Elevated levels of rPMP22 and rPMP22Tr significantly reduced fibroblast growth as judged by proliferation assays. Despite a negative modulatory influence of rPMP22 and rPMP22Tr on cell proliferation, cell cycle analyses by flow cytometry did not reveal an influence of rPMP22 or rPMP22Tr on the synchronous progression of resting NIH3T3 cells from G0 into S phase. However, cell cycle analyses by flow cytometry of asynchronously dividing cultures demonstrated that the expression of rPMP22 and rPMP22Tr increased the fraction of cells in the G1 phase of the cell cycle. Furthermore, cell death analyses revealed that, in contrast to control cells and cells carrying the rPMP22Tr construct, a significantly increased fraction of NIH3T3 cells expressing rPMP22 exit the proliferation compartment showing hallmarks of programmed cell death. These results indicate that (i) rPMP22 and rPMP22Tr act as negative modulators of proliferation in murine fibroblasts probably through extension of the G1 phase of the cell cycle and (ii) rPMP22 but not rPMP22Tr promotes programmed death of these cells.
- Published
- 1997
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26. A microfluidic device for head immobilization, chemical exposure, and behavioral screening of Zebrafish larvae
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Nady, A., Peimani, A. R., Zoidl, G., and Pouya Rezai
27. Neurotoxin-induced impairment and neuroprotective-based recovery of electrotactic locomotion in zebrafish larvae as a model for neurobehavioral studies in Parkinson’s disease
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Khalili, A., Khaled Youssef, Zoidl, G., and Rezai, P.
28. Zebrafish larva's cyclic electrotaxis behavior and its dependency on dopamine level enabled by a novel microfluidic assay
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Peimani, A. R., Zoidl, G., and Pouya Rezai
29. Pannexin1 is a novel protein component of postsynaptic sites
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Dahl Gerhard, Habbes Hans-Werner, Bunse Stephanie, Meier Carola, Ray Arundhati, Petrasch-Parwez Elisabeth, Zoidl Georg, and Dermietzel Rolf
- Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 ,Neurophysiology and neuropsychology ,QP351-495 - Published
- 2007
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30. Non-viral siRNA delivery into the mouse retina in vivo
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Zoidl Georg, Turchinovich Andrey, and Dermietzel Rolf
- Subjects
Ophthalmology ,RE1-994 - Abstract
Abstract Background Gene silencing in the retina using RNA interference could open broad possibilities for functional studies of genes in vivo and for therapeutic interventions in eye disorders. Therefore, there is a considerable demand for protocols to deliver siRNA into the vertebrate retina. In this work we explored a possibility to deliver synthetic 21 bp siRNA into the mouse retina after intravitreal application using a non-viral carrier. Methods Fluorescently labelled synthetic 21 bp siRNA duplex was combined with Transit-TKO transfection reagent and injected intravitreally into adult mice eyes. Eyes cryostat sections and whole mount retinas were prepared 24-48 h post-injection, stained with either Hoechst 33342 (cell nuclei) or immunostained with anti-GFAP antibody (astroglia cells marker). Distribution of fluorescent siRNA signal in the retina was investigated. Results Single intravitreal injection of as little as 5 ng of siRNA combined with Transit-TKO transfection reagent by a modified protocol provided robust and non-toxic delivery of the siRNA into the retina. However, siRNA accumulation was predominantly confined to ganglion cells layer as analysed 24 h post-injection. Furthermore, siRNA containing particles were localized along GFAP cytoskeleton of retinal astroglial cells hinting on intracellular localization of the siRNA Conclusions In this work we demonstrated that siRNA can be efficiently delivered into the vertebrate retina in vivo with low-toxicity using a non-viral carrier, specifically Transit-TKO transfection reagent. However, the capacity of siRNA delivered by our protocol to induce gene silencing in the retina has to be further evaluated. Our report could raise a closer look on Transit-TKO transfection reagent as a promising siRNA carrier in vivo and be of interest for the researchers and companies who work on development of ocular RNAi techniques.
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- 2010
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31. Elevated intracellular chloride level in albino visual cortex neurons is mediated by Na-K-Cl co-transporter
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Turchinovich Andrey, Diykov Dmitry, Zoidl Georg, and Hoffmann Klaus-Peter
- Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 ,Neurophysiology and neuropsychology ,QP351-495 - Abstract
Abstract Background During development the switch from a depolarizing to a hyperpolarizing action of GABA is a consequence of a decrease of the Na+-K+-2Cl- co-transporter (NKCC1, Cl--uptake) and increase of the K+-Cl- co-transporter (KCC2, Cl--extrusion) expression. However albino visual cortex neurons don't show a corresponding decrease in intracellular chloride concentration during development of the visual system as compared to pigmented animals. Results Our study revealed that more cells express NKCC1 in albinos compared to pigmented rat visual cortex neurons whereas KCC2 is expressed in all cells in both strains. We determined a positive relationship between the presence of NKCC1 and an inhibitory deficit in single neurons of the albino visual cortex. After pharmacological blockade of NKCC1 function with its specific inhibitor, bumetanide, the reversal potential of electrically evoked GABAA receptor-mediated postsynaptic currents and, as a consequence, [Cl-]i in albino visual cortex neurons shifted to the pigmented rat brain value. In conclusion, our pharmacological experiments and subsequent single cell real time PCR analysis of the co-transporter mRNA demonstrated that the inhibitory deficit present in the albino visual cortical network is almost exclusively mediated by NKCC1. Conclusion Our findings suggest that blocking of NKCC1 in albino visual cortex neurons could improve processing in visual cortex and therefore might be beneficial for vision in albinos.
- Published
- 2008
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32. Elevated intracellular chloride level in albino visual cortex neurons is mediated by Na-K-Cl co-transporter.
- Author
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Diykov D, Turchinovich A, Zoidl G, Hoffmann KP, Diykov, Dmitry, Turchinovich, Andrey, Zoidl, Georg, and Hoffmann, Klaus-Peter
- Abstract
Background: During development the switch from a depolarizing to a hyperpolarizing action of GABA is a consequence of a decrease of the Na+-K+-2Cl- co-transporter (NKCC1, Cl--uptake) and increase of the K+-Cl- co-transporter (KCC2, Cl--extrusion) expression. However albino visual cortex neurons don't show a corresponding decrease in intracellular chloride concentration during development of the visual system as compared to pigmented animals.Results: Our study revealed that more cells express NKCC1 in albinos compared to pigmented rat visual cortex neurons whereas KCC2 is expressed in all cells in both strains. We determined a positive relationship between the presence of NKCC1 and an inhibitory deficit in single neurons of the albino visual cortex. After pharmacological blockade of NKCC1 function with its specific inhibitor, bumetanide, the reversal potential of electrically evoked GABAA receptor-mediated postsynaptic currents and, as a consequence, [Cl-]i in albino visual cortex neurons shifted to the pigmented rat brain value. In conclusion, our pharmacological experiments and subsequent single cell real time PCR analysis of the co-transporter mRNA demonstrated that the inhibitory deficit present in the albino visual cortical network is almost exclusively mediated by NKCC1.Conclusion: Our findings suggest that blocking of NKCC1 in albino visual cortex neurons could improve processing in visual cortex and therefore might be beneficial for vision in albinos. [ABSTRACT FROM AUTHOR]- Published
- 2008
- Full Text
- View/download PDF
33. Deletion of the -turn/a-helix motif at the exon 2/3 boundary of human c-Myc leads to the loss of its immortalizing function
- Author
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Zoidl, G., Brockmann, D., and Esche, H.
- Published
- 1993
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34. Intralumenal docking of connexin 36 channels in the ER isolates mistrafficked protein.
- Author
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Tetenborg S, Liss V, Breitsprecher L, Timonina K, Kotova A, Acevedo Harnecker AJ, Yuan C, Shihabeddin E, Ariakia F, Qin G, Chengzhi C, Dedek K, Zoidl G, Hensel M, and O'Brien J
- Subjects
- Humans, HEK293 Cells, Protein Domains, Amino Acid Motifs, Electrical Synapses physiology, Mutation, Protein Transport genetics, Synaptic Vesicles pathology, Synaptic Vesicles ultrastructure, Microscopy, Electron, Scanning, Gap Junction delta-2 Protein, Connexins genetics, Connexins metabolism, Endoplasmic Reticulum metabolism, Gap Junctions metabolism
- Abstract
The intracellular domains of connexins are essential for the assembly of gap junctions. For connexin 36 (Cx36), the major neuronal connexin, it has been shown that a dysfunctional PDZ-binding motif interferes with electrical synapse formation. However, it is still unknown how this motif coordinates the transport of Cx36. In the present study, we characterize a phenotype of Cx36 mutants that lack a functional PDZ-binding motif using HEK293T cells as an expression system. We provide evidence that an intact PDZ-binding motif is critical for proper endoplasmic reticulum (ER) export of Cx36. Removing the PDZ-binding motif of Cx36 results in ER retention and the formation of multimembrane vesicles containing gap junction-like connexin aggregates. Using a combination of site-directed mutagenesis and electron micrographs, we reveal that these vesicles consist of Cx36 channels that docked prematurely in the ER. Our data suggest a model in which ER-retained Cx36 channels reshape the ER membrane into concentric whorls that are released into the cytoplasm., Competing Interests: Conflicts of interests The authors declare that they have no conflicts of interests with the contents of this article., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2023
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35. An Implantable Optogenetic Neuro-Stimulator SoC With Extended Optical Pulse-Width Enabled by Supply-Variation-Immune Cycled Light-Toggling Stimulation.
- Author
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Yousefi T, Timonina K, Zoidl G, and Kassiri H
- Subjects
- Calcium, Equipment Design, Prostheses and Implants, Signal Processing, Computer-Assisted, Wireless Technology, Optogenetics, Silicon
- Abstract
The design, development, and experimental validation of an inductively-powered four-channel optical neuro-stimulator system on a chip (SoC) with on-chip neural recording, temperature monitoring, signal processing, and bidirectional wireless data communication are presented. A biologically-inspired optical stimulation approach is employed that extends the limitations on the stimulation pulse-width and frequency (i.e., enabling wirelessly-powered optical stimulation at very low frequencies (e.g., 10 Hz)) while significantly reducing the required on-device storage capacitor size. The biological efficacy of the proposed approach is validated and compared with conventional stimulation through in vitro experiments. The stimulator's energy efficiency is enhanced by employing a high-gain (850 A/A) current amplifier/driver in each channel that steers up to 10 mA into the optical source with an excellent linearity ( 0.5LSB), while 1) yielding the lowest-in-literature required voltage headroom, and 2) being insensitive to large (up to 12%) supply voltage drops, which is ideal for battery-less implantable devices. Additionally, to maximize the percentage of the generated optical power that reaches the targeted cells (thus, further energy efficiency enhancement), inkjet printing is utilized to fabricate custom-designed optical μlenses that are placed directly on top of the silicon SoC to enhance the generated light's directivity by > 30×. An electrophysiological recording channel for real-time monitoring of the stimulation efficacy and a high-precision (0.1
° C resolution) temperature readout circuit for shutting off stimulation upon detection of an unsafe temperature increase are also integrated on the chip. Additionally, the SoC hosts an ASK receiver and an LSK transmitter for downlink and uplink wireless data communication, respectively. The SoC is fabricated in a standard 130 nm CMOS process and occupies 6 mm2 . Measurement results for different sensory and communication blocks are presented, as well as in vitro experimental validation results showing simultaneous optical stimulation, electrical recording, and calcium imaging.- Published
- 2022
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36. An Energy-Efficient Optically-Enhanced Highly-Linear Implantable Wirelessly-Powered Bidirectional Optogenetic Neuro-Stimulator.
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Yousefi T, Taghadosi M, Dabbaghian A, Siu R, Grau G, Zoidl G, and Kassiri H
- Subjects
- Humans, Models, Biological, Implantable Neurostimulators, Optogenetics instrumentation, Wireless Technology instrumentation
- Abstract
This paper presents an energy-efficient mm-scale self-contained bidirectional optogenetic neuro-stimulator, which employs a novel highly-linear μLED driving circuit architecture as well as inkjet-printed custom-designed optical μlenses for light directivity enhancement. The proposed current-mode μLED driver performs linear control of optical stimulation for the entire target range ( 10 mA) while requiring the smallest reported headroom, yielding a significant boost in the energy conversion efficiency. A 30.46× improvement in the power delivery efficiency to the target tissue is achieved by employing a pair of printed optical μlenses. The fabricated SoC also integrates two recording channels for LFP recording and digitization, as well as power management blocks. A micro-coil is also embedded on the chip to receive inductive power and our experimental results show a PTE of 2.24 % for the wireless link. The self-contained system including the μLEDs, μlenses and the capacitors required by the power management blocks is sized 6 mm
3 and weighs 12.5 mg. Full experimental measurement results for electrical and optical circuitry as well as in vitro measurement results are reported.- Published
- 2020
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37. Visuomotor deficiency in panx1a knockout zebrafish is linked to dopaminergic signaling.
- Author
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Safarian N, Whyte-Fagundes P, Zoidl C, Grigull J, and Zoidl G
- Subjects
- Animals, Dopamine D2 Receptor Antagonists pharmacology, Haloperidol pharmacology, Larva drug effects, Larva metabolism, Neurons drug effects, Receptors, Dopamine D2 metabolism, Retina drug effects, Retina metabolism, Signal Transduction drug effects, Superior Colliculi drug effects, Superior Colliculi metabolism, Swimming physiology, Vision, Ocular drug effects, Connexins metabolism, Dopamine metabolism, Neurons metabolism, Signal Transduction physiology, Vision, Ocular physiology, Zebrafish metabolism, Zebrafish Proteins metabolism
- Abstract
Pannexin 1 (Panx1) forms ATP-permeable membrane channels that play roles in the nervous system. The analysis of roles in both standard and pathological conditions benefits from a model organism with rapid development and early onset of behaviors. Such a model was developed by ablating the zebrafish panx1a gene using TALEN technology. Here, RNA-seq analysis of 6 days post fertilization larvae were confirmed by Real-Time PCR and paired with testing visual-motor behavior and in vivo electrophysiology. Results demonstrated that loss of panx1a specifically affected the expression of gene classes representing the development of the visual system and visual processing. Abnormal swimming behavior in the dark and the expression regulation of pre-and postsynaptic biomarkers suggested changes in dopaminergic signaling. Indeed, altered visuomotor behavior in the absence of functional Panx1a was evoked through D1/D2-like receptor agonist treatment and rescued with the D2-like receptor antagonist Haloperidol. Local field potentials recorded from superficial areas of the optic tectum receiving input from the retina confirmed abnormal responses to visual stimuli, which resembled treatments with a dopamine receptor agonist or pharmacological blocking of Panx1a. We conclude that Panx1a functions are relevant at a time point when neuronal networks supporting visual-motor functions undergo modifications preparing for complex behaviors of freely swimming fish.
- Published
- 2020
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38. Role of an Aromatic-Aromatic Interaction in the Assembly and Trafficking of the Zebrafish Panx1a Membrane Channel.
- Author
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Timonina K, Kotova A, and Zoidl G
- Subjects
- Amino Acids, Aromatic genetics, Animals, Cell Line, Tumor, Cell Membrane metabolism, Connexins genetics, Endoplasmic Reticulum metabolism, Glycosylation, Golgi Apparatus metabolism, Mice, Mutagenesis, Site-Directed, Mutant Proteins chemistry, Mutant Proteins metabolism, Mutant Proteins physiology, Protein Folding, Protein Multimerization, Protein Processing, Post-Translational, Protein Stability, Protein Transport, Zebrafish genetics, Zebrafish Proteins genetics, Amino Acids, Aromatic metabolism, Connexins chemistry, Connexins metabolism, Zebrafish metabolism, Zebrafish Proteins chemistry, Zebrafish Proteins metabolism
- Abstract
Pannexin 1 (Panx1) is a ubiquitously expressed hexameric integral membrane protein known to function as an adenosine triphosphate (ATP) release channel. Panx1 proteins exist in unglycosylated core form (Gly0). They undergo critical post-translational modifications forming the high mannose glycosylation state (Gly1) in the endoplasmic reticulum (ER) and the complex glycosylation state (Gly2) in the Golgi apparatus. The regulation of transition from the ER to the cell membrane is not fully understood. Using site-specific mutagenesis, dye uptake assays, and interaction testing, we identified two conserved aromatic residues, Trp123 and Tyr205, in the transmembrane domains 2 and 3 of the zebrafish panx1a protein . Results suggest that both residues primarily govern the assembly of panx1a subunits into channels, with mutant proteins failing to interact. The results provide insight into a mechanism enabling regulation of Panx1 oligomerization, glycosylation, and trafficking., Competing Interests: The authors declare no conflict of interest.
- Published
- 2020
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39. Phenotypic chemical and mutant screening of zebrafish larvae using an on-demand response to electric stimulation.
- Author
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Khalili A, Peimani AR, Safarian N, Youssef K, Zoidl G, and Rezai P
- Subjects
- Animals, Animals, Genetically Modified, Behavior, Animal, Connexins genetics, Lab-On-A-Chip Devices, Levodopa pharmacology, Oxidopamine toxicity, Phenotype, Risk Factors, Zebrafish Proteins genetics, DNA Mutational Analysis, Electric Stimulation, Mutation, Zebrafish embryology
- Abstract
Behavioral responses of zebrafish larvae to environmental cues are important functional readouts that should be evoked on-demand and studied phenotypically in behavioral, genetical and developmental investigations. Very recently, it was shown that zebrafish larvae execute a voluntary and oriented movement toward the positive electrode of an electric field along a microchannel. Phenotypic characterization of this response was not feasible due to larva's rapid movement along the channel. To overcome this challenge, a microfluidic device was introduced to partially immobilize the larva's head while leaving its mid-body and tail unrestrained in a chamber to image motor behaviors in response to electric stimulation, hence achieving quantitative phenotyping of the electrically evoked movement in zebrafish larvae. The effect of electric current on the tail-beat frequency and response duration of 5-7 days postfertilization zebrafish larvae was studied. Investigations were also performed on zebrafish exposed to neurotoxin 6-hydroxydopamine and larvae carrying a pannexin1a (panx1a) gene knockout, as a proof of principle applications to demonstrate on-demand movement behavior screening in chemical and mutant assays. We demonstrated for the first time that 6-hydroxydopamine leads to electric response impairment, levodopa treatment rescues the response and panx1a is involved in the electrically evoked movement of zebrafish larvae. We envision that our technique is broadly applicable as a screening tool to quantitatively examine zebrafish larvae's movements in response to physical and chemical stimulations in investigations of Parkinson's and other neurodegenerative diseases, and as a tool to combine recent advances in genome engineering of model organisms to uncover the biology of electric response., (© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permission@oup.com.)
- Published
- 2019
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40. Tubulin-Dependent Transport of Connexin-36 Potentiates the Size and Strength of Electrical Synapses.
- Author
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Brown CA, Del Corsso C, Zoidl C, Donaldson LW, Spray DC, and Zoidl G
- Subjects
- Animals, Biomechanical Phenomena, Connexins genetics, Electrical Synapses genetics, Gap Junctions genetics, Mice, Neuronal Plasticity physiology, Protein Binding, Protein Transport, Rats, Tumor Cells, Cultured, Gap Junction delta-2 Protein, Connexins metabolism, Electrical Synapses physiology, Gap Junctions metabolism, Neurons physiology, Tubulin physiology
- Abstract
Connexin-36 (Cx36) electrical synapses strengthen transmission in a calcium/calmodulin (CaM)/calmodulin-dependent kinase II (CaMKII)-dependent manner similar to a mechanism whereby the N-methyl-D-aspartate (NMDA) receptor subunit NR2B facilitates chemical transmission. Since NR2B-microtubule interactions recruit receptors to the cell membrane during plasticity, we hypothesized an analogous modality for Cx36. We determined that Cx36 binding to tubulin at the carboxy-terminal domain was distinct from Cx43 and NR2B by binding a motif overlapping with the CaM and CaMKII binding motifs. Dual patch-clamp recordings demonstrated that pharmacological interference of the cytoskeleton and deleting the binding motif at the Cx36 carboxyl-terminal (CT) reversibly abolished Cx36 plasticity. Mechanistic details of trafficking to the gap-junction plaque (GJP) were probed pharmacologically and through mutational analysis, all of which affected GJP size and formation between cell pairs. Lys279, Ile280, and Lys281 positions were particularly critical. This study demonstrates that tubulin-dependent transport of Cx36 potentiates synaptic strength by delivering channels to GJPs, reinforcing the role of protein transport at chemical and electrical synapses to fine-tune communication between neurons., Competing Interests: The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
- Published
- 2019
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41. A Multidisciplinary Approach Toward High Throughput Label-Free Cytotoxicity Monitoring of Superparamagnetic Iron Oxide Nanoparticles.
- Author
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Abad Tan S, Zoidl G, and Ghafar-Zadeh E
- Abstract
A bstract: This paper focuses on cytotoxicity examination of superparamagnetic iron oxide nanoparticles (SPIONs) using different methods, including impedance spectroscopy. Recent advances of SPIONs for clinical and research applications have triggered the need to understand their effects in cells. Despite the great advances in adapting various biological and chemical methods to assess in-vitro toxicity of SPIONs, less attention has been paid on the development of a high throughput label-free screening platform to study the interaction between the cells and nanoparticles including SPIONs. In this paper, we have taken the first step toward this goal by proposing a label-free impedimetric method for monitoring living cells treated with SPIONs. We demonstrate the effect of SPIONs on the adhesion, growth, proliferation, and viability of neuroblastoma 2A (N2a) cells using impedance spectroscopy as a label-free method, along with other standard microscopic and cell viability testing methods as control methods. Our results have shown a decreased viability of the cells as the concentration of SPIONs increases with percentages of 59%, 47%, and 40% for 100 µg/mL (C4), 200 µg/mL (C5), 300 µg/mL (C6), respectively. Although all SPIONs concentrations have allowed the growth of cells within 72 hours, C4, C5, and C6 showed slower growth compared to the control (C1). The growth and proliferation of N2a cells are faster in the absence or low concentration of SPIONS. The percent coefficient of variation (% CV) was used to compare cell concentrations obtained by TBDE assay and a Scepter cell counter. Results also showed that the lower the SPIONs concentration, the lower the impedance is expected to be in the sensing electrodes without the cells. Meanwhile, the variation of surface area (∆S) was affected by the concentration of SPIONs. It was observed that the double layer capacitance was almost constant because of the higher attachment of cells, the lower surface area coated by SPIONs. In conclusion, impedance changes of electrodes exposed to the mixture of cells and SPIONs offer a wide dynamic range (>1 MΩ using Electric Cell-substrate Impedance electrodes) suitable for cytotoxicity studies. Based on impedance based, viability testing and microscopic methods' results, SPIONs concentrations higher than 100 ug/mL and 300 ug/mL cause minor and major effects, respectively. We propose that a high throughput impedance-based label-free platform provides great advantages for studying SPIONs in a cell-based context, opening a window of opportunity to design and test the next generation of SPIONs with reduced toxicity for biomedical or medical applications., Competing Interests: The authors declare no conflict of interest.
- Published
- 2019
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42. Pannexins in vision, hearing, olfaction and taste.
- Author
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Whyte-Fagundes P, Siu R, Brown C, and Zoidl G
- Subjects
- Animals, Connexins metabolism, Mice, Nerve Tissue Proteins metabolism, Connexins physiology, Hearing physiology, Nerve Tissue Proteins physiology, Smell physiology, Taste physiology, Vision, Ocular physiology
- Abstract
In mammals, the pannexin gene family consists of three members (Panx1, 2, 3), which represent a class of integral membrane channel proteins sharing some structural features with chordate gap junction proteins, the connexins. Since their discovery in the early 21st century, pannexin expression has been detected throughout the vertebrate body including eye, ear, nose and tongue, making the investigation of the roles of this new class of channel protein in health and disease very appealing. The localization in sensory organs, coupled with unique channel properties and associations with major signaling pathways make Panx1, and its relative's, significant contributors for fundamental functions in sensory perception. Until recently, cell-based studies were at the forefront of pannexin research. Lately, the availability of mice with genetic ablation of pannexins opened new avenues for testing pannexin functions and behavioural phenotyping. Although we are only at the beginning of understanding the roles of pannexins in health and disease, this review summarizes recent advances in elucidating the various emerging roles pannexins play in sensory systems, with an emphasis on unresolved conflicts., (Copyright © 2017 Elsevier B.V. All rights reserved.)
- Published
- 2019
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43. Pannexin-1 channels in epilepsy.
- Author
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Aquilino MS, Whyte-Fagundes P, Zoidl G, and Carlen PL
- Subjects
- Animals, Humans, Neurons metabolism, Receptors, Purinergic P2X7 metabolism, Connexins metabolism, Epilepsy metabolism, Nerve Tissue Proteins metabolism
- Abstract
Pannexin-1 (Panx1) expression is raised in several animal seizure models and in resected human epileptic brain tissue, suggesting relevance to epilepsy. Multiple factors that are characteristic of seizures are thought to regulate Panx1 channel opening, including elevated levels of extracellular K
+ . Panx1, when open, 1) releases ATP, glutamate, and other metabolites into the extracellular medium, and 2) may depolarize the membrane due to a channel reversal potential around 0mV. Resultant ATP release from stimulated Panx1 can activate purinergic receptors, including P2X7 receptors. Glutamate and other signaling molecules released by Panx1 opening may have both excitatory and inhibitory actions on seizure generation. This review examines the critical and complex roles of Panx1 channels in epilepsy, which could provide a basis for future therapeutics., (Copyright © 2017 Elsevier B.V. All rights reserved.)- Published
- 2019
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44. A Potential Compensatory Role of Panx3 in the VNO of a Panx1 Knock Out Mouse Model.
- Author
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Whyte-Fagundes P, Kurtenbach S, Zoidl C, Shestopalov VI, Carlen PL, and Zoidl G
- Abstract
Pannexins (Panx) are integral membrane proteins, with Panx1 being the best-characterized member of the protein family. Panx1 is implicated in sensory processing, and knockout (KO) animal models have become the primary tool to investigate the role(s) of Panx1 in sensory systems. Extending previous work from our group on primary olfaction, the expression patterns of Panxs in the vomeronasal organ (VNO), an auxiliary olfactory sense organ with a role in reproduction and social behavior, were compared. Using qRT-PCR and Immunohistochemistry (IHC), we confirmed the loss of Panx1, found similar Panx2 expression levels in both models, and a significant upregulation of Panx3 in mice with a global ablation of Panx1. Specifically, Panx3 showed upregulated expression in nerve fibers of the non-sensory epithelial layer in juvenile and adult KO mice and in the sensory layer of adults, which overlaps with Panx1 expression areas in WT populations. Since both social behavior and evoked ATP release in the VNO was not compromised in KO animals, we hypothesized that Panx3 could compensate for the loss of Panx1. This led us to compare Panx1 and Panx3 channels in vitro , demonstrating similar dye uptake and ATP release properties. Outcomes of this study strongly suggest that Panx3 may functionally compensate for the loss of Panx1 in the VNO of the olfactory system, ensuring sustained chemosensory processing. This finding extends previous reports on the upregulation of Panx3 in arterial walls and the skin of Panx1 KO mice, suggesting that roles of Panx1 warrant uncharacterized safeguarding mechanisms involving Panx3.
- Published
- 2018
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45. A microfluidic device to study electrotaxis and dopaminergic system of zebrafish larvae.
- Author
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Peimani AR, Zoidl G, and Rezai P
- Abstract
The zebrafish is a lower vertebrate model organism offering multiple applications for both fundamental and biomedical research into the nervous system from genes to behaviour. Investigation of zebrafish larvae's movement in response to various stimuli, which involves the dopaminergic system, is of interest in the field of sensory-motor integration. Nevertheless, the conventional methods of movement screening in Petri dishes and multi-well plates are mostly qualitative, uncontrollable, and inaccurate in terms of stimulus delivery and response analysis. We recently presented a microfluidic device built as a versatile platform for fluid flow stimulation and high speed time-lapse imaging of rheotaxis behaviour of zebrafish larvae. Here, we describe for the first time that this microfluidic device can also be used to test zebrafish larvae's sense of the electric field and electrotaxis in a systemic manner. We further show that electrotaxis is correlated with the dopamine signalling pathway in a time of day dependent manner and by selectively involving the D2-like dopamine receptors. The primary outcomes of this research opens avenues to study the molecular and physiological basis of electrotaxis, the effects of known agonist and antagonist compounds on the dopaminergic system, and the screen of novel pharmacological tools in the context of neurodegenerative disorders. We propose that this microfluidic device has broad application potential, including the investigation of complex stimuli, biological pathways, behaviors, and brain disorders.
- Published
- 2018
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46. Mechanisms of pannexin1 channel gating and regulation.
- Author
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Whyte-Fagundes P and Zoidl G
- Subjects
- Animals, Cell Membrane genetics, Central Nervous System Diseases genetics, Central Nervous System Diseases physiopathology, Connexins genetics, Humans, Ion Channels genetics, Nerve Tissue Proteins genetics, Cell Membrane metabolism, Central Nervous System Diseases metabolism, Connexins metabolism, Ion Channel Gating, Ion Channels metabolism, Nerve Tissue Proteins metabolism
- Abstract
Pannexins are a family of integral membrane proteins with distinct post-translational modifications, sub-cellular localization and tissue distribution. Panx1 is the most studied and best-characterized isoform of this gene family. The ubiquitous expression, as well as its function as a major ATP release and nucleotide permeation channel, makes Panx1 a primary candidate for participating in the pathophysiology of CNS disorders. While many investigations revolve around Panx1 functions in health and disease, more recently, details started emerging about mechanisms that control Panx1 channel activity. These advancements in Panx1 biology have revealed that beyond its classical role as an unopposed plasma membrane channel, it participates in alternative pathways involving multiple intracellular compartments, protein complexes and a myriad of extracellular participants. Here, we review recent progress in our understanding of Panx1 at the center of these pathways, highlighting its modulation in a context specific manner. This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve., (Copyright © 2017 Elsevier B.V. All rights reserved.)
- Published
- 2018
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47. Pannexin 1 Is Critically Involved in Feedback from Horizontal Cells to Cones.
- Author
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Cenedese V, de Graaff W, Csikós T, Poovayya M, Zoidl G, and Kamermans M
- Abstract
Retinal horizontal cells (HCs) feed back negatively to cone photoreceptors and in that way generate the center/surround organization of bipolar cell receptive fields. The mechanism by which HCs inhibit photoreceptors is a matter of debate. General consensus exists that horizontal cell activity leads to the modulation of the cone Ca-current. This modulation has two components, one fast and the other slow. Several mechanisms for this modulation have been proposed: a fast ephaptic mechanism, and a slow pH mediated mechanism. Here we test the hypothesis that the slow negative feedback signal from HCs to cones is mediated by Panx1 channels expressed at the tips of the dendrites of horizontal cell. We generated zebrafish lacking Panx1 and found that the slow component of the feedback signal was strongly reduced in the mutants showing that Panx1 channels are a fundamental part of the negative feedback pathway from HCs to cones.
- Published
- 2017
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48. A microfluidic device for partial immobilization, chemical exposure and behavioural screening of zebrafish larvae.
- Author
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Nady A, Peimani AR, Zoidl G, and Rezai P
- Subjects
- Animals, Arginine toxicity, Equipment Design, Female, Male, Toxicity Tests instrumentation, Zebrafish physiology, Behavior, Animal drug effects, Behavior, Animal physiology, Lab-On-A-Chip Devices, Larva drug effects, Larva physiology
- Abstract
The zebrafish larva is an important vertebrate model for sensory-motor integration studies, genetic screening, and drug discovery because of its excellent characteristics such as optical transparency, genetic manipulability, and genetic similarity to humans. Operations such as precise manipulation of zebrafish larvae, controlled exposure to chemicals, and behavioural monitoring are of utmost importance to the abovementioned studies. In this work, a novel microfluidic device is presented to easily stabilize an individual larva's head using a microfluidic trap while leaving the majority of the body and the tail unhindered to move freely in a downstream chamber. The device is equipped with a microvalve to prevent the larva's escape from the trap and a microchannel beside the larva's head to expose it to chemicals at desired concentrations and times, while investigating multiple behaviours such as the tail, eye, and mouth movement frequencies. An in situ air bubble removal module was also incorporated to increase the yield of experiments. The functionality of our device in comparison to a conventional droplet-based technique was tested using l-arginine exposure and viability assays. We found that the larvae in the device and the droplet exhibit similar tail and eye response trends to nM-mM concentrations of l-arginine, and that the survival of the larvae is not affected by the device. However, the tail responses in the device were numerically higher than the droplet-tested larvae at nM-mM l-arginine concentrations. In the future, our device has the potential to be used for conducting simultaneous whole-brain functional imaging, upon optimized immobilization of the brain, and behavioural analysis to uncover differences between diseased and healthy states in zebrafish.
- Published
- 2017
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49. A microfluidic device for quantitative investigation of zebrafish larvae's rheotaxis.
- Author
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Peimani AR, Zoidl G, and Rezai P
- Subjects
- Animals, Behavior, Animal physiology, Equipment Design, Lab-On-A-Chip Devices, Larva physiology, Zebrafish physiology
- Abstract
Zebrafish is a model organism for various sensory-motor biological studies. Rheotaxis, or the ability of zebrafish to orient and swim against the water stream, is a common behavior that involves multiple sensory-motor processes such as their lateral line and visual systems. Due to the lack of a controllable and easy-to-use assay, zebrafish rheotaxis at larval stages is not well-understood. In this paper, we report a microfluidic device that can be used to apply the flow stimulus precisely and repeatedly along the longitudinal axis of individual zebrafish larvae to study their coaxial rheotaxis. We quantified rheotaxis in terms of the response rate and location along the channel at various flow velocities (9.5-38 mm.sec
-1 ). The larvae effectively exhibited a similarly high rheotactic response at low and medium velocities (9.5 and 19 mm.sec-1 ); however, at high velocity of 38 mm.sec-1 , despite sensing the flow, their rheotactic response decreased significantly. The flow velocity also affected the response location along the channel. At 9.5 mm.sec-1 , responses were distributed evenly along the channel length while, at 19 and 38 mm.sec-1 , the larvae demonstrated higher rheotaxis responses at the anterior and posterior ends of the channel, respectively. This result shows that although the response is similarly high at low and medium flow velocities, zebrafish larvae become more sensitive to the flow at medium velocity, demonstrating a modulated rheotactic behavior. Employing our device, further investigations can be conducted to study the sensory-motor systems involved in rheotaxis of zebrafish larvae and other fish species.- Published
- 2017
- Full Text
- View/download PDF
50. Structural and Functional Consequences of Connexin 36 (Cx36) Interaction with Calmodulin.
- Author
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Siu RC, Smirnova E, Brown CA, Zoidl C, Spray DC, Donaldson LW, and Zoidl G
- Abstract
Functional plasticity of neuronal gap junctions involves the interaction of the neuronal connexin36 with calcium/calmodulin-dependent kinase II (CaMKII). The important relationship between Cx36 and CaMKII must also be considered in the context of another protein partner, Ca
2+ loaded calmodulin, binding an overlapping site in the carboxy-terminus of Cx36. We demonstrate that CaM and CaMKII binding to Cx36 is calcium-dependent, with Cx36 able to engage with CaM outside of the gap junction plaque. Furthermore, Ca2+ loaded calmodulin activates Cx36 channels, which is different to other connexins. The NMR solution structure demonstrates that CaM binds Cx36 in its characteristic compact state with major hydrophobic contributions arising from W277 at anchor position 1 and V284 at position 8 of Cx36. Our results establish Cx36 as a hub binding Ca2+ loaded CaM and they identify this interaction as a critical step with implications for functions preceding the initiation of CaMKII mediated plasticity at electrical synapses.- Published
- 2016
- Full Text
- View/download PDF
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