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Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina
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| Zeitschriftentitel: | Journal of Neurophysiology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | Journal of Neurophysiology, 112, 2014, 6, S. 1491-1504 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
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| Schlagwörter: |
| author_facet |
Choi, Hannah Zhang, Lei Cembrowski, Mark S. Sabottke, Carl F. Markowitz, Alexander L. Butts, Daniel A. Kath, William L. Singer, Joshua H. Riecke, Hermann Choi, Hannah Zhang, Lei Cembrowski, Mark S. Sabottke, Carl F. Markowitz, Alexander L. Butts, Daniel A. Kath, William L. Singer, Joshua H. Riecke, Hermann |
|---|---|
| author |
Choi, Hannah Zhang, Lei Cembrowski, Mark S. Sabottke, Carl F. Markowitz, Alexander L. Butts, Daniel A. Kath, William L. Singer, Joshua H. Riecke, Hermann |
| spellingShingle |
Choi, Hannah Zhang, Lei Cembrowski, Mark S. Sabottke, Carl F. Markowitz, Alexander L. Butts, Daniel A. Kath, William L. Singer, Joshua H. Riecke, Hermann Journal of Neurophysiology Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina Physiology General Neuroscience |
| author_sort |
choi, hannah |
| spelling |
Choi, Hannah Zhang, Lei Cembrowski, Mark S. Sabottke, Carl F. Markowitz, Alexander L. Butts, Daniel A. Kath, William L. Singer, Joshua H. Riecke, Hermann 0022-3077 1522-1598 American Physiological Society Physiology General Neuroscience http://dx.doi.org/10.1152/jn.00437.2014 <jats:p> In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. We tested and confirmed this hypothesis experimentally by recording from AIIs in a slice preparation of rd1 retina. Additionally, recordings from ganglion cells in a whole mount preparation of rd1 retina demonstrated that activity in AIIs was propagated unchanged to elicit bursts of action potentials in ganglion cells. We conclude that oscillations are not an emergent property of a degenerated retinal network. Rather, they arise largely from the intrinsic properties of a single retinal interneuron, the AII amacrine cell. </jats:p> Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina Journal of Neurophysiology |
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American Physiological Society, 2014 |
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American Physiological Society, 2014 |
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American Physiological Society |
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Journal of Neurophysiology |
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| title |
Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_unstemmed |
Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_full |
Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_fullStr |
Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_full_unstemmed |
Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_short |
Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_sort |
intrinsic bursting of aii amacrine cells underlies oscillations in the rd1 mouse retina |
| topic |
Physiology General Neuroscience |
| url |
http://dx.doi.org/10.1152/jn.00437.2014 |
| publishDate |
2014 |
| physical |
1491-1504 |
| description |
<jats:p> In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. We tested and confirmed this hypothesis experimentally by recording from AIIs in a slice preparation of rd1 retina. Additionally, recordings from ganglion cells in a whole mount preparation of rd1 retina demonstrated that activity in AIIs was propagated unchanged to elicit bursts of action potentials in ganglion cells. We conclude that oscillations are not an emergent property of a degenerated retinal network. Rather, they arise largely from the intrinsic properties of a single retinal interneuron, the AII amacrine cell. </jats:p> |
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| author | Choi, Hannah, Zhang, Lei, Cembrowski, Mark S., Sabottke, Carl F., Markowitz, Alexander L., Butts, Daniel A., Kath, William L., Singer, Joshua H., Riecke, Hermann |
| author_facet | Choi, Hannah, Zhang, Lei, Cembrowski, Mark S., Sabottke, Carl F., Markowitz, Alexander L., Butts, Daniel A., Kath, William L., Singer, Joshua H., Riecke, Hermann, Choi, Hannah, Zhang, Lei, Cembrowski, Mark S., Sabottke, Carl F., Markowitz, Alexander L., Butts, Daniel A., Kath, William L., Singer, Joshua H., Riecke, Hermann |
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| description | <jats:p> In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. We tested and confirmed this hypothesis experimentally by recording from AIIs in a slice preparation of rd1 retina. Additionally, recordings from ganglion cells in a whole mount preparation of rd1 retina demonstrated that activity in AIIs was propagated unchanged to elicit bursts of action potentials in ganglion cells. We conclude that oscillations are not an emergent property of a degenerated retinal network. Rather, they arise largely from the intrinsic properties of a single retinal interneuron, the AII amacrine cell. </jats:p> |
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| spelling | Choi, Hannah Zhang, Lei Cembrowski, Mark S. Sabottke, Carl F. Markowitz, Alexander L. Butts, Daniel A. Kath, William L. Singer, Joshua H. Riecke, Hermann 0022-3077 1522-1598 American Physiological Society Physiology General Neuroscience http://dx.doi.org/10.1152/jn.00437.2014 <jats:p> In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. We tested and confirmed this hypothesis experimentally by recording from AIIs in a slice preparation of rd1 retina. Additionally, recordings from ganglion cells in a whole mount preparation of rd1 retina demonstrated that activity in AIIs was propagated unchanged to elicit bursts of action potentials in ganglion cells. We conclude that oscillations are not an emergent property of a degenerated retinal network. Rather, they arise largely from the intrinsic properties of a single retinal interneuron, the AII amacrine cell. </jats:p> Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina Journal of Neurophysiology |
| spellingShingle | Choi, Hannah, Zhang, Lei, Cembrowski, Mark S., Sabottke, Carl F., Markowitz, Alexander L., Butts, Daniel A., Kath, William L., Singer, Joshua H., Riecke, Hermann, Journal of Neurophysiology, Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina, Physiology, General Neuroscience |
| title | Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_full | Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_fullStr | Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_full_unstemmed | Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_short | Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| title_sort | intrinsic bursting of aii amacrine cells underlies oscillations in the rd1 mouse retina |
| title_unstemmed | Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina |
| topic | Physiology, General Neuroscience |
| url | http://dx.doi.org/10.1152/jn.00437.2014 |