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572 results on '"Borst J"'

2. Association of hyperglycemia and computed tomographic perfusion deficits in patients who underwent endovascular treatment for acute ischemic stroke caused by a proximal intracranial occlusion: A subgroup analysis of a randomized phase 3 trial (MR CLEAN)

Author

Kersten, C.J.B.A., Zandbergen, A.A.M., Berkhemer, O.A., Borst, J., Haalboom, M., Roos, Y.B.W.E.M., Dippel, D.W.J., van Oostenbrugge, R.J., van der Lugt, A., van Zwam, W.H., Majoie, C.B., and den Hertog, H.M.

Published
2022
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3. Developmental fine-tuning of medial superior olive neurons mitigates their predisposition to contralateral sound sources.

Author

Sierksma, Martijn C. and Borst, J. Gerard G.

Subjects
*EAR, *INTERAURAL time difference, *DIRECTIONAL hearing, *NEURONS, *ACOUSTIC localization, *SPEED of sound, *OLIVE leaves
Abstract

Having 2 ears enables us to localize sound sources by exploiting interaural time differences (ITDs) in sound arrival. Principal neurons of the medial superior olive (MSO) are sensitive to ITD, and each MSO neuron responds optimally to a best ITD (bITD). In many cells, especially those tuned to low sound frequencies, these bITDs correspond to ITDs for which the contralateral ear leads, and are often larger than the ecologically relevant range, defined by the ratio of the interaural distance and the speed of sound. Using in vivo recordings in gerbils, we found that shortly after hearing onset the bITDs were even more contralaterally leading than found in adult gerbils, and travel latencies for contralateral sound-evoked activity clearly exceeded those for ipsilateral sounds. During the following weeks, both these latencies and their interaural difference decreased. A computational model indicated that spike timing-dependent plasticity can underlie this fine-tuning. Our results suggest that MSO neurons start out with a strong predisposition toward contralateral sounds due to their longer neural travel distances, but that, especially in high-frequency neurons, this predisposition is subsequently mitigated by differential developmental fine-tuning of the travel latencies. Neurons in the medial superior olive are important for sound localization, as they are sensitive to the relative arrival time of sounds at both ears. This study reveals the developmental dynamics of this sensitivity, reporting that shortly after hearing onset these cells have a strong preference for contralateral leading sounds, which is fine-tuned towards sounds coming from the front in adulthood. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Somatic Integration of Incoherent Dendritic Inputs in the Gerbil Medial Superior Olive.

Author

Mackenbach, Yarmo and Borst, J. Gerard G.

Abstract

The medial superior olive (MSO) is a binaural nucleus that is specialized in detecting the relative arrival times of sounds at both ears. Excitatory inputs to its neurons originating from either ear are segregated to different dendrites. To study the integration of synaptic inputs both within and between dendrites, we made juxtacellular and whole-cell recordings from the MSO in anesthetized female gerbils, while presenting a "double zwuis" stimulus, in which each ear received its own set of tones, which were chosen in a way that all second-order distortion products (DP2s) could be uniquely identified. MSO neurons phase-locked to multiple tones within the multitone stimulus, and vector strength, a measure for spike phase-locking, generally depended linearly on the size of the average subthreshold response to a tone. Subthreshold responses to tones in one ear depended little on the presence of sound in the other ear, suggesting that inputs from different ears sum linearly without a substantial role for somatic inhibition. The "double zwuis" stimulus also evoked response components in the MSO neuron that were phase-locked to DP2s. Bidendritic subthreshold DP2s were quite rare compared with bidendritic suprathreshold DP2s. We observed that in a small subset of cells, the ability to trigger spikes differed substantially between both ears, which might be explained by a dendritic axonal origin. Some neurons that were driven monaurally by only one of the two ears nevertheless showed decent binaural tuning. We conclude that MSO neurons are remarkably good in finding binaural coincidences even among uncorrelated inputs. [ABSTRACT FROM AUTHOR]

Published
2023
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13. Doc2b is a high-affinity [Ca.sup.2+] sensor for spontaneous neurotransmitter release

Author

Groffen, Alexander J., Martens, Sascha, Arazola, Rocio Diez, Cornelisse, L. Niels, Lozovaya, Natalia, de Jong, Arthur P.H., Goriounova, Natalia A., Habets, Ron L.P., Takai, Yoshimi, Borst, J. Gerard, Brose, Nils, McMahon, Harvey T., and Verhage, Matthijs

Subjects
Protein binding -- Research, Neurotransmitters -- Research, Action potentials (Electrophysiology) -- Research, Synaptic vesicles -- Chemical properties, Neurons -- Chemical properties, Cellular proteins -- Properties, Science and technology
Abstract

Synaptic vesicle fusion in brain synapses occurs in phases that are either tightly coupled to action potentials (synchronous), immediately following action potentials (asynchronous), or as stochastic events in the absence of action potentials (spontaneous). Synaptotagmin-1, -2, and -9 are vesicle-associated [Ca.sup.2+] sensors for synchronous release. Here we found that double C2 domain (Doe2) proteins act as [Ca.sup.2+] sensors to trigger spontaneous release. Although Doc2 proteins are cytosolic, they function analogously to synaptotagmin-1 but with a higher [Ca.sup.2+] sensitivity. Doe2 proteins bound to N-ethylmaleimide--sensitive factor attachment receptor (SNARE) complexes in competition with synaptotagmin-1. Thus, different classes of multiple C2 domain--containing molecules trigger synchronous versus spontaneous fusion, which suggests a general mechanism for synaptic vesicle fusion triggered by the combined actions of SNAREs and multiple C2 domain--containing proteins. 10.1126/science.1183765

Published
2010
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22. R-type Ca2+ currents evoke transmitter release at a rat central synapse

Author

Wu, Ling-Gang, Borst, J. Gerard G., and Sakmann, Bert

Subjects
Synapses -- Research, Rats -- Research, Calcium channels -- Research, Science and technology
Abstract

Voltage-dependent [Ca.sup.2+] currents evoke synaptic transmitter release. Of six types of [Ca.sup.2+] channels, L-, N-, P-, Q-, R-, and T-type, only N- and P/Q-type channels have been pharmacologically identified to mediate action-potential-evoked transmitter release in the mammalian central nervous system. We tested whether [Ca.sup.2+] channels other than N- and P/Q-type control transmitter release in a calyx-type synapse of the rat medial nucleus of the trapezoid body. Simultaneous recordings of presynaptic [Ca.sup.2+] influx and the excitatory postsynaptic current evoked by a single action potential were made at single synapses. The R-type channel, a high-voltage-activated [Ca.sup.2+] channel resistant to L-, N-, and P/Q-type channel blockers, contributed 26% of the total [Ca.sup.2+] influx during a presynaptic action potential. This [Ca.sup.2+] current evoked transmitter release sufficiently large to initiate an action potential in the postsynaptic neuron. The R-type current controlled release with a lower efficacy than other types of [Ca.sup.2+] currents. Activation of metabotropic glutamate receptors and [Gamma]-aminobutyric acid type B receptors inhibited the R-type current. Because a significant fraction of presynaptic [Ca.sup.2+] channels remains unidentified in many other central synapses, the R-type current also could contribute to evoked transmitter release in these synapses.

Published
1998

26. Using ephaptic coupling to estimate the synaptic cleft resistivity of the calyx of Held synapse.

Author

Sierksma, Martijn C. and Borst, J. Gerard G.

Subjects
*SYNAPSES, *CENTRAL nervous system, *CALCIUM channels, *NEURAL transmission, *CONFORMAL geometry, *ADULTS
Abstract

At synapses, the pre- and postsynaptic cells get so close that currents entering the cleft do not flow exclusively along its conductance, gcl. A prominent example is found in the calyx of Held synapse in the medial nucleus of the trapezoid body (MNTB), where the presynaptic action potential can be recorded in the postsynaptic cell in the form of a prespike. Here, we developed a theoretical framework for ephaptic coupling via the synaptic cleft, and we tested its predictions using the MNTB prespike recorded in voltage-clamp. The shape of the prespike is predicted to resemble either the first or the second derivative of the inverted presynaptic action potential if cleft currents dissipate either mostly capacitively or resistively, respectively. We found that the resistive dissipation scenario provided a better description of the prespike shape. Its size is predicted to scale with the fourth power of the radius of the synapse, explaining why intracellularly recorded prespikes are uncommon in the central nervous system. We show that presynaptic calcium currents also contribute to the prespike shape. This calcium prespike resembled the first derivative of the inverted calcium current, again as predicted by the resistive dissipation scenario. Using this calcium prespike, we obtained an estimate for gcl of ~1 μS. We demonstrate that, for a circular synapse geometry, such as in conventional boutons or the immature calyx of Held, gcl is scale-invariant and only defined by extracellular resistivity, which was ~75 Ωcm, and by cleft height. During development the calyx of Held develops fenestrations. We show that these fenestrations effectively minimize the cleft potentials generated by the adult action potential, which might otherwise interfere with calcium channel opening. We thus provide a quantitative account of the dissipation of currents by the synaptic cleft, which can be readily extrapolated to conventional, bouton-like synapses. Author summary: At chemical synapses two neurons are separated by a cleft, which is very narrow. As a result, the concentration of released neurotransmitter can rapidly peak, which is essential for fast synaptic transmission. At the same time, the currents that flow across the membranes that face the synaptic cleft are also substantial, and a fraction of these currents will enter the other cell. We made an electronic model of the synaptic cleft, which indicated that if the shape and fraction of these currents are known, the electrical resistance of the synaptic cleft can be inferred. We tested several of the predictions of our model by comparing the membrane currents during a presynaptic action potential in a giant terminal, the calyx of Held, with the much smaller prespike evoked by these currents in the postsynaptic cell. We estimate the cleft resistance to be about 1 MΩ, which means that the changes in the cleft potential due to the membrane currents can become large enough to have an impact on voltage-dependent calcium channels controlling neurotransmitter release. [ABSTRACT FROM AUTHOR]

Published
2021
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28. Contributory presentations/posters

Author

Gries, A., Singh, Balwinder, Nakazawal, Chicko, Genest, D., Getzoff, E. D., Matsuo, H., Kaur, Harpreet, Borst, J. W., Chadha, K. C., Tingyun, Kuang, Jagannadham, M. V., Leijon, Mikael, Sato, S., Bhakuni, Vlnod, Vijayan, M., Surolia, A., Suguna, K., Manoj, N., Srinivas, V. R., Ravishankar, R., Laggner, P., Prassl, R., Schwarzenbacher, R., Zeth, K., Kostner, G. M., Taylor, Susan S., Xuong, Nguyen-huu, Akamine, Pearl, Sagar, Bidva M., Saikrishnan, K., Purnapatre, K., Handa, P., Roy, S., Varshney, U., Biswal, B. K., Sukumar, N., Rao, J. K. Mohana, Johnson, A., Pattabhi, Vasantha, Murthy, M. R. N., Krishna, Sri S., Savithri, H. S., Sastri, Mira, Hosur, M. V., Pillai, Bindu, Kannan, K. K., Kumar, Mukesh, Patwardhan, Swati, Padmanabhaa, B., Sasaki-Sugio, S., Matsuzaki, T., Nukaga, M., Singh, T. P., Sharma, A. K., Srinivasan, A., Khan, J. A., Paramasivam, M., Kumar, P., Karthikevan, S., Sharma, S., Yadav, S., Srintvasan, A., Alam, Neelima, Gourinath, S., Kaur, Punit, Chandra, Vikas, Betzel, Ch., Ghosh, S., Bera, A. K., Pal, A. K., Baneriee, Asok, Mukhopadhyay, B. P., Bhattacharya, S., Chakraborty, S., Haldar, U., Dey, I., Solovicova, Adriana, Sevcik, Jozef, Sekar, K., Sundaralingam, M., Genov, N., Liang, Dong-cai, Zhang, Ji-ping, Jiang, Tao, Chang, Wen-rui, Blommers, Marcel, Jahnke, Wolfgang, Hosur, R. V., Panchal, S. C., Pillay, Bindu, Jaganathan, N. R., Mathur, Puniti, Srivatsun, S., Joshi, Ratan Mani, Chauhan, V. S., Govil, Girjesh, Atreya, H. S., Sahu, S. C., Quinjou, Éric, Adjadj, Elisabeth, Mispelter, Joël, Izadi-Pruneyre, Nadia, Blouquit, Yves, Heyd, Bernadette, Lerat, Guilhem, Desmadreil, Michel, Milnard, Philippe, Lin, Y., Rao, B. D. Nageswara, Raghunathan, Vidva, Chau, Mei H., Coutinho, Evans, Pesais, Prashant, Srivastava, Sudha, Saran, Anil, Srikrishnan, Thamarapu, Lijima, Herbert, Gesme, Jayson, Sapico, Leizl F., Paxton, Raymond, Grace, C. R., Nagenagowda, G., Lynn, A. M., Cowsik, Sudha M., Govil, G., Sahu, Sarata C., Bhattacharya, A., Chauhan, S., Kumar, Anil, Zuiderweg, Erik R. P., Pellecchia, Maurizio, Nitta, Katsutoshi, Ohnishi, Atsushi, Kawano, Keiichi, Hikichi, Kunio, Fujitani, Naoki, Ohkubo, Tadayasu, Aizawa, Tomoyasu, Kumaki, Yasuhiro, Hayakawa, Yoichi, Parvathy, Rani V., Kini, R. M., Nakagawa, Astushi, Tanaka, Isao, Demura, Makoto, Yao, Min, Koshiba, Takumi, Kobashigawa, Yoshihiro, Kuwajima, Kunihiro, Linge, Jens, Nilges, Michael, Donoghue, Seán O., Chakshusmathi, G., Ratnaparkhi, Girish S., Madhu, P. K., Varadarajan, R., Tetreau, C., Tourbez, M., Lavalette, D., Bulone, D., Manno, M., Emanuele, A., Palma-Vittorelli, M. B., Palma, M. U., Vaiana, S. M., Martorana, V., Biagio, P. L. San, Chang, D. K., Cheng, S. F., Yang, S. H., Francis, S., Trivedi, V. D., Chien, W. J., Manstein, Dietmar J., Batra, Renn, Geeves, Michael A., Geller, Maciej, Trvlska, Joanna, Grochowski, Pawel, Lesyng, B., Ginalski, K., Grochowski, P., Lavalette, P., Blouquit, Y., Roccatano, D., Berendsen, H. J. C., Amadei, A., Nola, Di A., Ho, Bosco, Curmi, P. M. G., Berry, H., Pelta, J., Pauthe, E., Lairez, D., Srinivasan, M., Sahi, Shakti, Kothekar, V., Madhusudnan, Kartha S., Nandel, Fateh S., Jain, D. V. S., Berendsen, Herman J. C., Feenstra, Anton K., Tama, F., Sanejouand, Y.-H., Go, N., Sharma, Deepak, Pasha, Santosh, Sharma, Sunita, Brahmachari, Samir K., Makker, Jyoti, Viiavaraghavan, R., Kumar, S., Dey, Sharmisllia, Krishnamoorthy, G., Lakshmikanth, G. S., Zaitseva, E. M., Mazhul, V. M., Kierdaszuk, Borys, Widengren, J., Rigler, R., Terry, B., Mets, Ü., Swaminathan, R., Yathindra, N., Thamotharan, S., Chosrowjan, H., Mataga, N., Shibata, Y., Morisima, I., Xiao, Ming, Selvin, Paul, Chakraharty, Tania, Cooke, Roger, Faraone, A., Branca, C., Maisano, G., Migliardo, P., Magazù, S., Villari, V., Behere, Digambar V., Deva, Sharique Zahida Waheed M., Vallone, B., Savino, C., Travaglini-Allocatelli, C., Cutruzzolà, F., Brunori, M., Gibson, Q. H., Mazumdar, Shyamalava, Mitra, Samaresh, Prasad, Swati, Soto, P., Fayad, R., Tyulkova, N. A., Sukovataya, I. E., Mamedov, Sh. V., Aksakal, B., Canturk, M., Aktas, B., Yilgin, R., Bogutska, K. I., Miroshnichenko, N. S., Wein, A. J., Hypolite, J. A., DiSanto, M., Chacko, S., Zheng, Y-M., Antosiewicz, J., Wojciechowski, M., Grycuk, T., Di Nola, Alfredo, Ceruso, Marc A., Chatterjee, Bishnu P., Bandvopadhvay, Subhasis, Choudhury, Devapriva, Khight, Stefan, Thompson, Andrew, Stojanoff, Vivian, Pinkner, Jerome, Hultgren, Scott, Flatters, Delphine, Goodfellow, Julia, Takazawatt, Fumi, Kanehisa, Minoru, Sasai, Masaki, Nakamura, Hironori, Wang, Bao Han, Pan, xin Min, Zheng, Yuan, Wang, Zhi Xin, Ahmad, Atta, Kulkarni, Sangeeta, Prakash, Koodathingal, Prajapati, Shashi, Surin, Alexey, Kihara, Hiroshi, Yang, Li, Matsumoto, Tomoharu, Nakagawa, Yuki, Semisotnov, Gennady V., Kimura, Kazumoto, Amemiya, Yoshiyuki, Tayyab, Saad, Muzammil, Salman, Kumar, Yogesh, Bhakuni, Vinod, Sundd, Monica, Kundu, Suman, Jagannadham, Medicherla V., Chandani, Bina, Warrier, Deepti, Sinha, Lalankumar, Dhar, Ruby, Mehrotra, Sonam, Khandelwal, Purnima, Seth, Subhendu, Gidwani, Arun, Prabha, Ratna C., Sasidhar, Y. U., Madhusudan, K. P., Nishikawa, Ken, Kinjo, Akira R., Varadarajan, Raghavan, Chakravarty, Suvobrata, Van Dael, H., Noyelle, K., Joniau, M., Haezebrouck, P., Jha, Indra Brata, Bhat, Rajiv, Dash, Sheffali, Mohanty, Prasanna, Bandyopadhyay, A. K., Sonawat, H. M., Rao, Ch. Mohan, Datta, Siddhartha, Raman, B., Rajaraman, K., Ramakrishna, T., Pande, A., Benedek, G., King, J., Betts, S., Pande, J., Asherie, N., Ogun, O., Kalacheva, G. S., Sokolova, I. V., Mitaku, Shigeki, Sonoyama, Masashi, Taira, Kunihiro, Yokoyama, Yasunori, Sasakil, Takanori, Kamo, Naoki, Mukai, Yuri, Dalal, Seema, Regan, Lynne, Mituku, Shigeki, Kumar, Devesh, Roychoudhury, Mihir, Lőrinczv, Dénes, Könczöl, Franciska, Farkas, László, Belagyi, Joseph, Schick, Christoph, Thomson, Christy A., Ananthanarayanan, Vettai S., Alirzayeva, E. G., Baba-Zade, S. N., Sarai, A., Kono, H., Uedaira, H., An, J., Gromiha, Michael M., Oobatake, M., Yutani, Katsuhide, Takano, Kazufumi, Yamagata, Yuriko, Jas, Gouri S., Hofrichter, James, Muñoz, Victor, Eaton, William A., Penoyar, Jonathan, Lo Verde, Philip T., Bódi, Á., Venekei, I., Kardos, J., Gráf, L., Závodszky, P., Szilágyi, András, Závodszky, Péter, Woolfson, D. N., Walshaw, J., Allan, R. D., Funahashi, Jun, Gupta, Savan, Di Nola, A., Mangoni, M., Roccatano, P., Ramachandraiah, Gosu, Chandra, Nagasuma R., Ciani, Barbara, Woolfson, Derek N., Nair, Usha B., Salunke, Dinakar M., Kaur, Kanwal J., Swaminathan, Chittoor P., Surolia, Avadhesha, Pramanik, A., Jörnvall, H., Nygren, P.-Å., Jonasson, P., Ståhl, S., Johansson, B.-L., Kratz, G., Wahren, J., Ekberg, K., Uhlén, M., Jansson, O. T., Uhlén, S., Misselwitz, Rolf, Welfle, Heinz, Welfle, Karin, Höhne, Wolfgang, Kurganov, B. I., Mitskevich, L. G., Fedurkina, N. V., Jarori, Gotam K., Maity, Haripada, Guharay, J., Sengupta, P. K., Sengupta, B., Sridevi, K., Kasturi, S. R., Gupta, S. P., Agarwal, Gunjan, Briehl, Robin W., Kwong, Suzanne, Tyulkova, N A., Ismailova, O. I., Parola, A. H., Yayon, A., Hariharan, C., Pines, D., Pines, E., Zamai, M., Cohen-Luria, R., Woolfeon, D. N., Spooner, G. A., Padya, M. J., Bharadwaj, D. K., Bakshi, Panchan, Jagannathan, N. R., Sharma, U., Srivastava, N., Barthwal, R., Matsuda, Keiko, Nishioka, Takaaki, Go, Nobuhiro, Urata, S., Aita, T., Husimi, Y., Majumder, Mainak, Subirana, Juan A., Malinina, Lucy, Abrescia, Nicola G. A., Aymami, Juan, Coll, Miquel, Eritxa, Ramón, Premraj, B. J., Thenmalarchelvi, R., Gautham, N., Kumar, Satheesh P., Kan, Lou-Sing, Hou, Ming, Lin, Shwu-Bin, Roy, Kanal B., Sana, Tapas, Bruant, N., Flatters, D., Lavery, R., Sklenar, Heinz, Rons, Remo, Lavery, Richard, Thakur, Ashoke Ranjan, Kundu, Sudip, Bandyopadhyay, Debashree, Bhattacharyya, Dhananjay, Majumdar, Rabi, Barceló, F., Portugal, J., Rao, B. J., Ramanathan, Sunita, Gliosli, Mahua, Varshney, Umesh, Kumar, Vinay N., Pataskar, Shashank S., Sarojini, R., Selvasekarapandian, S., Kolandaivel, P., Sukumar, S., Kolmdaivel, P., Maiti, Motilal, Das, Suman, Sen, Anjana, Xodo, Luigi, Suraci, Chiara, Del Terra, Elisa, Quadrifoglio, Franco, Diviacco, Silvia, Ray, Arghya, Rao, Basuthkar J., Karthikeyan, G., Chary, Kandala V. R., Mujeeb, Anwer, James, Thomas L., Bogdanov, A., Zanina, A., Haya, E. E. F., Kasyanenko, N., Cornélio, M. L., Bugs, M. R., Tolstorukov, Ye. M., Sanval, Nitish K., Tiwari, S. N., Sanyal, Nitish K., Choudhury, Mihir Roy, Patel, P. K., Bhavesh, Neel S., Gabrielian, Anna, Rigler, Rudolf, Edman, Lars, Wennmalm, Stefan, Constantinescu, B., Gazdaru, D., Radulcscu, I., Radu, L., Wärmländer, Sebastian, Aoki, Setsuyuki, Ishiura, Masahiro, Kondo, Takao, Pashinskaya, V. A., Kosevich, M. V., Shelkovsky, V. S., Blagoy, Yu. P., Wang, Ji-hua, Malathi, R., Chandrasekhar, K., Kandimalla, E. R., Agrawal, S., Rastogi, V. K., Palafox, Alcolea M., Singh, Chatar, Beniaminov, A. D., Minyat, E. E., Zdobnov, E. M., Ulyanov, N. B., Bondarenko, S. A., Ivanov, V. I., Singh, J. S., Tewari, Ravindra, Sonawane, Kailas D., Grosjean, Henri, Sonavane, Uddhavesh B., Morin, Annie, Doherty, Elizabeth A., Doudna, Jennifer A., Tochio, H., Shirakawa, M., Kyogoku, Y., Das, Achintya, Javaram, B., Kalra, Parul, Shukla, Piyush, Dixit, Surjit B., Beveridge, David L., McConnell, Kevin, Davidson, B. E., Chan, R. Y. S., Sawyer, W. H., Eccelston, J. F., Yan, Yuling, Norden, Bengt, Tuite, Eimer, Nielsen, Peter, Takahashi, Masayuki, Ghosh, Anirban, Bansal, Manju, Pingoud, Alfred, Christ, Frauke, Thole, Hubert, Pingoud, Vera, Wende, Wolfgang, Luthra, Pratibha Mehta, Chandra, Ramesh, Sen, Ranjan, Weisberg, Robert, King, Rodney, Gobets, Bas, van Amerongen, Herbert, van Stokkum, Ivo H. M., Larsen, Olaf F. A., van Grondelle, Rienk, Hilbers, Cornelis W., Heus, Hans A., Berends, Jos, Sngrvan, H E., Khudaverdian, N. V., Babayan, Yu. S., Pichierri, F., Gromiha, M., Prabakaran, P., Aida, M., Sayano, K., Merkienė, Eglė, Vilkaitis, Giedrius, Klimašauskas, Saulius, Serva, Saulius, Weinhold, Elmar, Bandiera, Antonella, Marsich, Eleonora, Manzini, Giorgio, Potikyan, G., Arakelyan, V., Babayan, Yu., Ninaber, Alex, Goodfellow, Julia M., Ohta, Shigeru, Ito, Yoichiro, Husimi, Yuzuru, Usukura, J., Aiba, H., Tagami, H., Nunes, Elia, Suarez, Mougli, Candreva, Carmen E., Keszenman, Deborah, Thyberg, Per, Földes-Papp, Zeno, Joshi, Amita, Singh, Dinesh, Rajeswari, M. R., Amenitsch, H., Pregetter, M., Chapman, J., Mishra, K. P., Pandev, B. N., Tonevitsky, A. G., Pohl, E. E., Agapov, I. I., Sun, J., Pohl, P., Dennison, S. M., Gorbeako, G. P., Dynbko, T. S., Mishra, A. K., Pappavee, N., Luis, Loura, Rodrigo, Almeida, Manuel, Prieto, Gendel, Ya. L., Kleszczyńska, H., Kuczera, J., Przestalski, S., Kral, T., Chernitsky, E. A., Senkovich, O. A., Rosin, V. V., Gasanov, R. A., Allakhverdieva, Y. M., Papageorgiou, G. C., Savopol, Tudor, Apetrei, Calin, Balea, Marius, Cucu, D., Mihailescu, D., Ramanathan, K. V., Bačić, Goran, Genest, Monique, Sajot, Nicolas, Garnier, Norbert, Crouzy, Serge, Zsiros, O., Várkonyi, Z. S., Combos, Z., Farkas, T., Cribier, Sophie, de Paula, F., Fraceto, I. F., Schreier, S., Spisni, A., Sevšek, F., Žekš, B., Gomišček, G., Svetina, S., Arrigler, V., Hotani, Hirokazu, Nomura, Fumimasa, Takiguchi, Kingo, Nagata, Miki, Panicker, Lata, Parvathanathan, P. S., Hotani, H., Takiguchi, K., Ishino, A., Saitoh, A., Afonin, S., Takahashi, A., Takizawa, T., Nakato, Y., Marathe, Dipti, Jørgensen, Kent, Chattopadhyay, Amitabha, Rukmini, R., Rawat, Satinder S., Pečar, S., Štrancar, J., Šentiurc, M., Stolič, Z., Filipin, K., Biswas, S. C., Samanta, Anunay, Sana, Satyen, Kinoshita, Koji, Yamazaki, Masahito, Ohki, Kazuo, Goto, Akira, Kiuchi, Tai, Kumeta, Takaaki, Ohba, Tetsuhiko, Sugar, I. P., Thompson, K. K., Biltonen, R. L., Thompson, T. 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M., Goel, Manisha, Kovalenko, E. I., Semenkova, G. N., Cherenkevich, S. N., Loganathan, D., Lakshmanan, T., Sriram, D., Srinivasan, S., Lebrón, J. A., Bjorkman, P. J., Ramalingam, T. S., Singh, A. K., Gayatri, T. N., Bisch, Paulo M., Caffarena, Ernesto R., Grigera, Raul J., Fromherz, P., Kiessling, V., Suresh, C. G., Rao, K. N., Khan, M. I., Gaikwad, S. M., Elanthiraiyan, M., Kaliannan, P., Payne, J., Chadha, K., Ambrus, J. L., Nair, M. P. N., Nair, Madhavan P. N., Hewitt, R., Schwartz, S. A., Mahajan, S., Macherel, D., Bourguignon, J., Neuburger, M., Douce, R., Cohen-Addad, C., Faure, M., Ober, R., Sieker, L., Gurumurthy, D. S., Velmurugan, S., Lobo, Z., Phadke, Ratna S., Desai, Prashant, Alieva, D. R., Guseinova, I. M., Zulfugarov, I. S., Aliev, J. A., Ismayilov, M. A., Novruzova, S. N., Savchenko, T. V., Suleimanov, Yu. S., Bartošková, Hana, Nauš, Jan, Ilík, Petr, Kouřil, Roman, Vidyasagar, P. 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C., Neagu, Monica, Neagu, Adrian, Janežič, Dušanka, Praprotnik, Matej, Nilsson, Lennart, Mark, Pekka, Fata, La L., Dardenne, Laurent E., Werneck, Araken S., Neto, Marçal de O., Kannan, N., Vishveshwara, S., Veluraja, K., Opitz, David, Balasubramanian, Krishnan, Gute, Brian D., Mills, Denise, Lungeanu, Diana, Mihalas, G. I., Macovievici, G., Gruia, Raluca, Dalcin, B., Cortez-Maghelly, C., Passos, E. P., Ljubisavljevic, M., Blesic, S., Milosevic, S., Stratimirovic, D. J., Bachhawat, Nandita, Mande, Shekhar C., Nandy, A., Nishigaki, Koichi, Saito, Ayumu, Naimuddin, Mohammed, Takaesu, Hirotomo, Ono, Mitsuo, Hirokawa, Takatsugu, Eissa, A. M., Ahmed, Abdalla S., El Gohary, M. I., Nakashima, Hiroshi, Raghava, G. P. S., Kurgalvuk, N., Goryn, O., Gerstman, Bernard S., Kratasyuk, V. A., Esimbekova, E. N., Gritsenko, E. V., Remmel, N. N., Maznyak, O. 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G., Antonyuk, S. V., Khachatryan, A., Kumar, A., Arakelian, H., Khachatryan, R., Agadjanyan, S., Ayrapetyan, S., Mkheyan, V., Rajan, S. S., Kabaleeswaran, V., Gopalakrishnan, Geetha, Govindachari, T. R., Ramrakhiani, Meera, Cullen, David C., Lowe, Phillip, Badley, Andrew, Hermel, H., Möhwald, H., Schmahl, W., Singh, Anil K., Das, Joydip, Majumdar, Nirmalya, Dér, András, Oroszi, László, Kelemen, Loránd, Ormos, Pál, Hámori, András, Ramsden, Jeremy J., Mitra, Chanchal K., Savitri, D., Yanagida, Toshio, Esaki, Seiji, Sowa, Yosiyuki, Nishida, Tomoyuki, Kimura, Yuji, Radu, M., Laukhina, E. E., Kasumova, L. A., Koltover, V. K., Bubnov, V. P., Estrin, Ya. I., Dotta, Rajiv, Zahradník, Ivan, Marko, Milan, Novák, Pavel, Miyata, Hidetake, Hirata, Hiroaki, Sengupta, P., Maiti, S., Balaji, J., Banerjee, S., Barker, A. L., Winlove, C. P., OʼHare, D., Macpherson, J. V., Gonsalves, M., Unwin, P. R., Phillip, R., Kumar, Ravindra G., Murata, K., Nagayaka, K., Danev, R., Sugitani, S., Gősch, Michael, Thyberg, P., Földes-Papp, Z., Björk, G., Blom, H., Holm, J., Heino, T., Inagaki, Fuyuhiko, Yokochi, Masashi, Kusunoki, Masami, Matthews, E. K., Pines, J., Chukova, Yu. P., Koltover, Vitaly K., Kang, B. P. S., Bansal, Geetanjali, Bansal, M. P., Singh, U., Singh, Uma, Nakata, Kotoko, Nakano, Tastuya, Kaminuma, Tsuguchika, Kirn, Bonn, Potocnik, Neja, Stare, Vito, Shukla, Latal, Sastry, M. D., Natarajan, V., Devasagayam, T. P. A., Kesavan, P. C., Sayfutdinov, R., Degermendzhy, A. G., Adamovich, V. V., Rogozin, Yu. D., Khetrapal, C. L., Gowda, G. A. Nagana, Ghimire, Kedar Nath, Masaru, Ishida, Fujita, H., Ishiwata, S., Suzuki, M., Kawahara, S., Kirino, Y., Kishimoto, Y., Mori, H., Mishina, M., Ohshima, H., Dukhin, A. S., Goetz, P. J., Shilov, V. N., and Mishra, R. K.

Published
1999
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32. Structure–function relation of the developing calyx of Held synapse in vivo.

Author

Sierksma, Martijn C., Slotman, Johan A., Houtsmuller, Adriaan B., and Borst, J. Gerard G.

Subjects
GLYCOCALYX, GLUTAMATE transporters, SYNAPSES, INNERVATION, NEURON development, NEURONS
Abstract

Key points: During development the giant, auditory calyx of Held forms a one‐to‐one connection with a principal neuron of the medial nucleus of the trapezoid body.While anatomical studies described that most of the target cells are temporarily contacted by multiple calyces, multi‐calyceal innervation was only sporadically observed in in vivo recordings, suggesting a structure–function discrepancy.We correlated synaptic strength of inputs, identified in in vivo recordings, with post hoc labelling of the recorded neuron and synaptic terminals containing vesicular glutamate transporters (VGluT).During development only one input increased to the level of the calyx of Held synapse, and its strength correlated with the large VGluT cluster contacting the postsynaptic soma.As neither competing strong inputs nor multiple large VGluT clusters on a single cell were observed, our findings did not indicate a structure–function discrepancy. In adult rodents, a principal neuron in the medial nucleus of the trapezoid (MNTB) is generally contacted by a single, giant axosomatic terminal called the calyx of Held. How this one‐on‐one relation is established is still unknown, but anatomical evidence suggests that during development principal neurons are innervated by multiple calyces, which may indicate calyceal competition. However, in vivo electrophysiological recordings from principal neurons indicated that only a single strong synaptic connection forms per cell. To test whether a mismatch exists between synaptic strength and terminal size, we compared the strength of synaptic inputs with the morphology of the synaptic terminals. In vivo whole‐cell recordings of the MNTB neurons from newborn Wistar rats of either sex were made while stimulating their afferent axons, allowing us to identify multiple inputs. The strength of the strongest input increased to calyceal levels in a few days across cells, while the strength of the second strongest input was stable. The recorded cells were subsequently immunolabelled for vesicular glutamate transporters (VGluT) to reveal axosomatic terminals with structured‐illumination microscopy. Synaptic strength of the strongest input was correlated with the contact area of the largest VGluT cluster at the soma (r = 0.8), and no indication of a mismatch between structure and strength was observed. Together, our data agree with a developmental scheme in which one input strengthens and becomes the calyx of Held, but not with multi‐calyceal competition. Key points: During development the giant, auditory calyx of Held forms a one‐to‐one connection with a principal neuron of the medial nucleus of the trapezoid body.While anatomical studies described that most of the target cells are temporarily contacted by multiple calyces, multi‐calyceal innervation was only sporadically observed in in vivo recordings, suggesting a structure–function discrepancy.We correlated synaptic strength of inputs, identified in in vivo recordings, with post hoc labelling of the recorded neuron and synaptic terminals containing vesicular glutamate transporters (VGluT).During development only one input increased to the level of the calyx of Held synapse, and its strength correlated with the large VGluT cluster contacting the postsynaptic soma.As neither competing strong inputs nor multiple large VGluT clusters on a single cell were observed, our findings did not indicate a structure–function discrepancy. [ABSTRACT FROM AUTHOR]

Published
2020
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38. Single-Cell Stimulation in Barrel Cortex Influences Psychophysical Detection Performance.

Author

Tanke, Nouk, Borst, J. Gerard G., and Houweling, Arthur R.

Subjects
*SOMATOSENSORY cortex, *PSYCHOPHYSIOLOGY, *SENSES, *INTERNEURONS, *WHISKERS
Abstract

Asingle whisker stimulus elicits action potentials in a sparse subset of neurons in somatosensory cortex. The precise contribution of these neurons to the animal's perception of a whisker stimulus is unknown. Hereweshow that single-cell stimulation in rat barrel cortex of both sexes influences the psychophysical detection of a near-threshold whisker stimulus in a cell type- dependent manner, without affecting false alarm rate. Counterintuitively, stimulation of single fast-spiking putative inhibitory neurons increased detection performance. Single-cell stimulation of putative excitatory neurons failed to change detection performance, except for a small subset of deep-layer neurons that were highly sensitive to whisker stimulation and that had an unexpectedly strong impact on detection performance. These findings indicate that the perceptual impact of excitatory barrel cortical neurons relates to their firing response to whisker stimulation and that strong activity in a single highly sensitive neuron in barrel cortex can already enhance sensory detection. Our data suggest that sensory detection is based on a decoding mechanism that lends a disproportionally large weight to interneurons and to deep-layer neurons showing a strong response to sensory stimulation. [ABSTRACT FROM AUTHOR]

Published
2018
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39. Enhanced Transmission at the Calyx of Held Synapse in a Mouse Model for Angelman Syndrome.

Author

Wang, Tiantian, van Woerden, Geeske M., Elgersma, Ype, and Borst, J. Gerard G.

Subjects
ANGELMAN syndrome, NEURODEVELOPMENTAL treatment, AXONS, CELL nuclei, ACTION potentials
Abstract

The neurodevelopmental disorder Angelman syndrome (AS) is characterized by intellectual disability, motor dysfunction, distinct behavioral aspects, and epilepsy. AS is caused by a loss of the maternally expressed UBE3A gene, and many of the symptoms are recapitulated in a Ube3a mouse model of this syndrome. At the cellular level, changes in the axon initial segment (AIS) have been reported, and changes in vesicle cycling have indicated the presence of presynaptic deficits. Here we studied the role of UBE3A in the auditory system by recording synaptic transmission at the calyx of Held synapse in the medial nucleus of the trapezoid body (MNTB) through in vivo whole cell and juxtacellular recordings. We show that MNTB principal neurons in Ube3a mice exhibit a hyperpolarized resting membrane potential, an increased action potential (AP) amplitude and a decreased AP half width. Moreover, both the pre- and postsynaptic AP in the calyx of Held synapse of Ube3a mice showed significantly faster recovery from spike depression. An increase in AIS length was observed in the principal MNTB neurons of Ube3a mice, providing a possible substrate for these gain-of-function changes. Apart from the effect on APs, we also observed that EPSPs showed decreased shortterm synaptic depression (STD) during long sound stimulations in AS mice, and faster recovery from STD following these tones, which is suggestive of a presynaptic gain-of-function. Our findings thus provide in vivo evidence that UBE3A plays a critical role in controlling synaptic transmission and excitability at excitatory synapses. [ABSTRACT FROM AUTHOR]

Published
2018
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40. Netherlands Society for Microbiology Meeting at Utrecht on 23 May 1969

Author

Storm, P. K., Hoekstra, W. P. M., Verhoef, C., de Haan, P. G., Wels-Douw, M. H., Broekman, J. H. F. F., Hoekstra, W. P. M., Kothari, Gunvanti, Stouthamer, A. H., Scholtens, R. Th., Cornelisse, J. L., Atteveld, J. C., Mouton, R. P., van der Schaaf, A., van Eyk, J., Thijsse, G. J. E., Wanders, Thea H., Kuenen, J. G., Veldkamp, H., Kortstee, G. J. J., De Vleesschauwer, L., Pattyn, S. R., Kokke, R., Borst, J., and de Jong, Jeanne H. L.

Published
1970
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42. A Test of the Stereausis Hypothesis for Sound Localization in Mammals.

Author

Plauška, Andrius, van der Heijden, Marcel, and Borst, J. Gerard G.

Subjects
DIRECTIONAL hearing, INTERAURAL time difference, ACOUSTIC nerve, MAMMAL physiology, AUDITORY perception, AXONS, COCHLEA, PHYSIOLOGY
Abstract

The relative arrival times of sounds at both ears constitute an important cue for localization of low-frequency sounds in the horizontal plane. The binaural neurons of the medial superior olive (MSO) act as coincidence detectors that fire when inputs from both ears arrive near simultaneously. Each principal neuron in the MSO is tuned to its own best interaural time difference (ITD), indicating the presence of an internal delay, a difference in the travel times from either ear to the MSO. According to the stereausis hypothesis, differences in wave propagation along the cochlea could provide the delays necessary for coincidence detection if the ipsilateral and contralateral inputs originated from different cochlear positions, with different frequency tuning. We therefore investigated the relation between interaural mismatches in frequency tuning and ITD tuning during in vivo loose-patch (juxtacellular) recordings from principal neurons of the MSO of anesthetized female gerbils. Cochlear delays can be bypassed by directly stimulating the auditory nerve; in agreement with the stereausis hypothesis, tuning for timing differences during bilateral electrical stimulation of the round windows differed markedly from ITD tuning in the same cells. Moreover, some neurons showed a frequency tuning mismatch that was sufficiently large to have a potential impact on ITD tuning. However, we did not find a correlation between frequency tuning mismatches and best ITDs. Our data thus suggest that axonal delays dominate ITD tuning. [ABSTRACT FROM AUTHOR]

Published
2017
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43. Encapsulation into complex coacervate core micelles promotes EGFP dimerization.

Author

Nolles, A., van Dongen, N. J. E., Westphal, A. H., Visser, A. J. W. G., Kleijn, J. M., van Berkel, W. J. H., and Borst, J. W.

Abstract

Complex coacervate core micelles (C3Ms) are colloidal structures useful for encapsulation of biomacromolecules. We previously demonstrated that enhanced green fluorescent protein (EGFP) can be encapsulated into C3Ms using the diblock copolymer poly(2-methyl-vinyl-pyridinium)41-b-poly(ethylene-oxide)205. This packaging resulted in deviating spectroscopic features of the encapsulated EGFP molecules. Here we show that for monomeric EGFP variant (mEGFP) micellar encapsulation affects the absorption and fluorescence properties to a much lesser extent, and that changes in circular dichroism characteristics are specific for encapsulated EGFP. Time-resolved fluorescence anisotropy of encapsulated (m)EGFP established the occurrence of homo-FRET (Förster resonance energy transfer) with larger transfer correlation times in the case of EGFP. Together, these findings support that EGFP dimerizes whereas the mEGFP mainly remains as a monomer in the densely packed C3Ms. We propose that dimerization of encapsulated EGFP causes a reorientation of Glu222, resulting in a pKa shift of the chromophore, which is fully reversible after release of EGFP from the C3Ms at a high ionic strength. [ABSTRACT FROM AUTHOR]

Published
2017
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44. Resistance to action potential depression of a rat axon terminal in vivo.

Author

Sierksmaa, Martijn C. and Borst, J. Gerard G.

Subjects
*ACTION potentials, *MENTAL depression, *AXONS, *NEUROTRANSMITTERS, *AUDITORY evoked response
Abstract

The shape of the presynaptic action potential (AP) has a strong impact on neurotransmitter release. Because of the small size of most terminals in the central nervous system, little is known about the regulation of their AP shape during natural firing patterns in vivo. The calyx of Held is a giant axosomatic terminal in the auditory brainstem, whose biophysical properties have been well studied in slices. Here, we made whole-cell recordings from calyceal terminals in newborn rat pups. The calyx showed a characteristic burst firing pattern, which has previously been shown to originate from the cochlea. Surprisingly, even for frequencies over 200 Hz, the AP showed little or no depression. Current injections showed that the rate of rise of the AP depended strongly on its onset potential, and that the membrane potential after the AP (Vafter) was close to the value at which no depression would occur during high-frequency activity. Immunolabeling revealed that Nav1.6 is already present at the calyx shortly after its formation, which was in line with the fast recovery from AP depression that we observed in slice recordings. Our findings thus indicate that fast recovery from depression and an inter-AP membrane potential that minimizes changes on the next AP in vivo, together enable high timing precision of the calyx of Held already shortly after its formation. [ABSTRACT FROM AUTHOR]

Published
2017
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48. The role of plasmodesma-located proteins in tubule-guided virus transport is limited to the plasmodesmata.

Author

Hollander, P., Kieper, S., Borst, J., and Lent, J.

Subjects
PLASMODESMATA, PLANT viruses, VIRAL genomes, VIRION, VIRAL proteins, PROTOPLASTS
Abstract

Intercellular spread of plant viruses involves passage of the viral genome or virion through a plasmodesma (PD). Some viruses severely modify the PD structure, as they assemble a virion carrying tubule composed of the viral movement protein (MP) inside the PD channel. Successful modulation of the host plant to allow infection requires an intimate interaction between viral proteins and both structural and regulatory host proteins. To date, however, very few host proteins are known to promote virus spread. Plasmodesmata-located proteins (PDLPs) localised in the PD have been shown to contribute to tubule formation in cauliflower mosaic virus and grapevine fanleaf virus infections. In this study, we have investigated the role of PDLPs in intercellular transport of another tubule-forming virus, cowpea mosaic virus. The MP of this virus was found to interact with PDLPs in the PD, as was shown for other tubule-forming viruses. Expression of PDLPs and MPs in protoplasts in the absence of a PD revealed that these proteins do not co-localise at the site of tubule initiation. Furthermore, we show that tubule assembly in protoplasts does not require an interaction with PDLPs at the base of the tubule, as has been observed in planta. These results suggest that a physical interaction between MPs and PDLPs is not required for assembly of the movement tubule and that the beneficial role of PDLPs in virus movement is confined to the structural context of the PD. [ABSTRACT FROM AUTHOR]

Published
2016
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49. Predicting binaural responses from monaural responses in the gerbil medial superior olive.

Author

Plauška, Andrius, Borst, J. Gerard, and van der Heijden, Marcel

Subjects
*BINAURAL audio, *PSYCHOLOGICAL feedback, *GERBILS, *EAR physiology, *COINCIDENCE circuits, *CROSS correlation, *INTERAURAL time difference
Abstract

Accurate sound source localization of low-frequency sounds in the horizontal plane depends critically on the comparison of arrival times at both ears. A specialized brainstem circuit containing the principal neurons of the medial superior olive (MSO) is dedicated to this comparison. MSO neurons are innervated by segregated inputs from both ears. The coincident arrival of excitatory inputs from both ears is thought to trigger action potentials, with differences in internal delays creating a unique sensitivity to interaural time differences (ITDs) for each cell. How the inputs from both ears are integrated by the MSO neurons is still debated. Using juxtacellular recordings, we tested to what extent MSO neurons from anesthetized Mongolian gerbils function as simple cross-correlators of their bilateral inputs. From the measured subthreshold responses to monaural wideband stimuli we predicted the rate-ITD functions obtained from the same MSO neuron, which have a damped oscillatory shape. The rate of the oscillations and the position of the peaks and troughs were accurately predicted. The amplitude ratio between dominant and secondary peaks of the rate-ITD function, captured in the width of its envelope, was not always exactly reproduced. This minor imperfection pointed to the methodological limitation of using a linear representation of the monaural inputs, which disregards any temporal sharpening occurring in the cochlear nucleus. The successful prediction of the major aspects of rate-ITD curves supports a simple scheme in which the ITD sensitivity of MSO neurons is realized by the coincidence detection of excitatory monaural inputs. [ABSTRACT FROM AUTHOR]

Published
2016
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