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575 results on '"Dowling, John E."'

2. Biological aspects of axonal damage in glaucoma: A brief review

Author

Tamm, Ernst R, Ethier, C Ross, Participants, The Lasker IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration, Dowling, John E, Downs, Crawford, Ellisman, Mark H, Fisher, Steven, Fortune, Brad, Fruttiger, Marcus, Jakobs, Tatjana, Lewis, Geoffrey, Masland, Richard H, Mitchell, Claire H, Morrison, John, Sharma, Sansar C, Sigal, Ian, Sofroniew, Michael, Wang, Lin, Wiggs, Janey, and Wu, Samuel

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Neurodegenerative, Neurosciences, Eye Disease and Disorders of Vision, Aging, Aetiology, 2.1 Biological and endogenous factors, Eye, Neurological, Animals, Astrocytes, Axons, Glaucoma, Gliosis, Humans, Intracranial Pressure, Intraocular Pressure, Nerve Degeneration, Optic Disk, Optic Nerve Diseases, Lasker/IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration Participants, Medical Biochemistry and Metabolomics, Opthalmology and Optometry, Ophthalmology & Optometry, Ophthalmology and optometry
Abstract

Intraocular pressure (IOP) is a critical risk factor in glaucoma, and the available evidence derived from experimental studies in primates and rodents strongly indicates that the site of IOP-induced axonal damage in glaucoma is at the optic nerve head (ONH). However, the mechanisms that cause IOP-induced damage at the ONH are far from understood. A possible sequence of events could originate with IOP-induced stress in the ONH connective tissue elements (peripapillary sclera, scleral canal and lamina cribrosa) that leads to an increase in biomechanical strain. In consequence, molecular signaling cascades might be activated that result in extracellular matrix turnover of the peripapillary sclera, changing its biomechanical properties. Peripapillary sclera strain might induce reactive changes in ONH astrocytes and cause astrogliosis. The biological changes that are associated with ONH astrocyte reactivity could lead to withdrawal of trophic or metabolic support for optic nerve axons and cause their degeneration. Alternatively, the expression of neurotoxic molecules might be induced. Unfortunately, direct experimental in vivo evidence for these or other scenarios is currently lacking. The pathogenic processes that cause axonal degeneration at the ONH in glaucoma need to be identified before any regenerative therapy is likely to succeed. Several topics and emerging techniques should be pursued to enhance our understanding of the mechanisms that are behind axonal degeneration. Among them are: Advanced imaging techniques, the development of in vivo markers to identify axonal injury, the generation of molecular approaches for in vivo detection of mechanosensitivity and for molecular manipulation of the ONH, a more complete characterization of retinal ganglion cells, the use of organ cultures, 3D-bioprinting, and the engineering of microdevices that can measure pressure. Questions that need to be answered relate to the specific roles of astrogliosis, neuroinflammation, blood flow and intracranial pressure in axonal degeneration at the ONH.

Published
2017

11. Building Bridges through Science

Author

Lissek, Thomas, Adams, Michelle, Adelman, John, Ahissar, Ehud, Akaaboune, Mohammed, Akil, Huda, al’Absi, Mustafa, Arain, Fazal, Arango-Lasprilla, Juan Carlos, Atasoy, Deniz, Avila, Jesus, Badawi, Ashraf, Bading, Hilmar, Baig, Abdul Mannan, Baleriola, Jimena, Belmonte, Carlos, Bertocchi, Ilaria, Betz, Heinrich, Blakemore, Colin, Blanke, Olaf, Boehm-Sturm, Philipp, Bonhoeffer, Tobias, Bonifazi, Paolo, Brose, Nils, Campolongo, Patrizia, Celikel, Tansu, Chang, Cathy C., Chang, Ta-Yuan, Citri, Ami, Cline, Hollis T., Cortes, Jesus M., Cullen, Kathleen, Dean, Kellie, Delgado-Garcia, José M., Desroches, Mathieu, Disterhoft, John F., Dowling, John E., Draguhn, Andreas, El-Khamisy, Sherif F., El Manira, Abdeljabbar, Enam, S. Ather, Encinas, Juan M., Erramuzpe, Asier, Esteban, José A., Fariñas, Isabel, Fischer, Edmond, Fukunaga, Izumi, Gabilondo, Iñigo, Ganten, Detlev, Gidon, Albert, Gomez-Esteban, Juan Carlos, Greengard, Paul, Grinevich, Valery, Gruart, Agnés, Guillemin, Roger, Hariri, Ahmad R., Hassan, Bassem, Häusser, Michael, Hayashi, Yasunori, Hussain, Natasha K., Jabbar, Adnan Abdul, Jaber, Mohamed, Jahn, Reinhardt, Janahi, Essam Mohammed, Kabbaj, Mohamed, Kettenmann, Helmut, Kindt, Merel, Knafo, Shira, Köhr, Georg, Komai, Shoji, Krugers, Harm, Kuhn, Bernd, Ghazal, Nouria Lakhdar, Larkum, Matthew E., London, Mickey, Lutz, Beat, Matute, Carlos, Martinez-Millan, Luis, Maroun, Mouna, McGaugh, James, Moustafa, Ahmed A., Nasim, Anwar, Nave, Klaus-Armin, Neher, Erwin, Nikolich, Karoly, Outeiro, Tiago, Palmer, Lucy M., Penagarikano, Olga, Perez-Otano, Isabel, Pfaff, Donald W., Poucet, Bruno, Rahman, Atta-ur, Ramos-Cabrer, Pedro, Rashidy-Pour, Ali, Roberts, Richard J., Rodrigues, Serafim, Sanes, Joshua R., Schaefer, Andreas T., Segal, Menahem, Segev, Idan, Shafqat, Saad, Siddiqui, Nikhat Ahmed, Soreq, Hermona, Soriano-García, Eduardo, Spanagel, Rainer, Sprengel, Rolf, Stuart, Greg, Südhof, Thomas C., Tønnesen, Jan, Treviño, Mario, Uthman, Basim M., Venter, J. Craig, Verkhratsky, Alexei, Weiss, Craig, Wiesel, Torsten N., Yaksi, Emre, Yizhar, Ofer, Young, Larry J., Young, Paul, Zawia, Nasser H., Zugaza, José L., and Hasan, Mazahir T.

Published
2017
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14. Biomechanical aspects of axonal damage in glaucoma: A brief review

Author

Dowling, John E., Downs, Crawford, Ellisman, Mark H., Fisher, Steven, Fortune, Brad, Fruttiger, Marcus, Jakobs, Tatjana, Lewis, Geoffrey, Masland, Richard H., Mitchell, Claire H., Morrison, John, Sharma, Sansar C., Sigal, Ian, Sofroniew, Michael, Wang, Lin, Wiggs, Janey, Wu, Samuel, Stowell, Cheri, Burgoyne, Claude F., Tamm, Ernst R., and Ethier, C. Ross

Published
2017
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20. Neuromodulation: Actions of Dopamine, Retinoic Acid, Nitric Oxide, and Other Substances on Retinal Horizontal Cells

Author

McMahon,Douglas G, Dowling,John E, McMahon,Douglas G, and Dowling,John E

Abstract

Douglas G McMahon,1 John E Dowling2 1Department of Biological Sciences, Vanderbilt University, Nashville, TN, 37235, USA; 2Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA, 02138, USACorrespondence: Douglas G McMahon, Department of Biological Sciences, Vanderbilt University, Nashville, TN, 37235, USA, Email douglas.g.mcmahon@vanderbilt.eduAbstract: Whereas excitation and inhibition of neurons are well understood, it is clear that neuromodulatory influences on neurons and their synapses play a major role in shaping neural activity in the brain. Memory and learning, emotional and other complex behaviors, as well as cognitive disorders have all been related to neuromodulatory mechanisms. A number of neuroactive substances including monoamines such as dopamine and neuropeptides have been shown to act as neuromodulators, but other substances thought to play very different roles in the body and brain act as neuromodulators, such as retinoic acid. We still understand little about how neuromodulatory substances exert their effects, and the present review focuses on how two such substances, dopamine and retinoic acid, exert their effects. The emphasis is on the underlying neuromodulatory mechanisms down to the molecular level that allow the second order bipolar cells and the output neurons of the retina, the ganglion cells, to respond to different environmental (ie lighting) conditions. The modulation described affects a simple circuit in the outer retina, involves several neuroactive substances and is surprisingly complex and not fully understood.Keywords: neural network adaptation, vision, synaptic modulation, gap junctions, glutamate receptors, GABA receptors

Published
2023

21. Circadian Rhythms and Vision in Zebrafish

Author

Emran, Farida, Dowling, John E., Marshall, N. Justin, Series editor, Collin, Shaun P, Series editor, Tosini, Gianluca, editor, Iuvone, P. Michael, editor, McMahon, Douglas G., editor, and Collin, Shaun P., editor

Published
2014
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