TY - JOUR
T1 - Light evokes Ca2+ spikes in the axon terminal of a retinal bipolar cell
AU - Protti, Dario A.
AU - Flores-Herr, Nicolas
AU - Von Gersdorff, Henrique
N1 - Funding Information:
We are grateful to Dr. Heinz Wässle for his insightful comments; Drs. Kurt Backus, Andrew Boxall, Craig Jahr, Gary Matthews, and David Zenisek for critical reading of the manuscript; Dr. Erwin Neher for encouragement; Dr. Christophe Pouzat for analysis routines and helpful discussions; Dr. Isabel Llano for generous support and advice; and Brigitte Sinke for excellent technical assistance. This work was supported by the Max-Planck Society, the Alexander von Humboldt Foundation, the Human Frontiers Science Program, and an Alfred P. Sloan Research Scholar Award.
PY - 2000/1
Y1 - 2000/1
N2 - Bipolar cells in the vertebrate retina have been characterized as nonspiking interneurons. Using patch-clamp recordings from goldfish retinal slices, we find, however, that the morphologically well-defined Mb1 bipolar cell is capable of generating spikes. Surprisingly, in dark-adapted retina, spikes were reliably evoked by light flashes and had a long (1-2 s) refractory period. In light-adapted retina, most Mb1 cells did not spike. However, an L-type Ca2+ channel agonist could induce periodic spiking in these cells. Spikes were determined to be Ca2+ action potentials triggered at the axon terminal and were abolished by 2-amino-4-phosphonobutyric acid (APB), an agonist that mimics glutamate. Signaling via spikes in a specific class of bipolar cells may serve to accelerate and amplify small photoreceptor signals, thereby securing the synaptic transmission of dim and rapidly changing visual input.
AB - Bipolar cells in the vertebrate retina have been characterized as nonspiking interneurons. Using patch-clamp recordings from goldfish retinal slices, we find, however, that the morphologically well-defined Mb1 bipolar cell is capable of generating spikes. Surprisingly, in dark-adapted retina, spikes were reliably evoked by light flashes and had a long (1-2 s) refractory period. In light-adapted retina, most Mb1 cells did not spike. However, an L-type Ca2+ channel agonist could induce periodic spiking in these cells. Spikes were determined to be Ca2+ action potentials triggered at the axon terminal and were abolished by 2-amino-4-phosphonobutyric acid (APB), an agonist that mimics glutamate. Signaling via spikes in a specific class of bipolar cells may serve to accelerate and amplify small photoreceptor signals, thereby securing the synaptic transmission of dim and rapidly changing visual input.
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U2 - 10.1016/S0896-6273(00)80884-3
DO - 10.1016/S0896-6273(00)80884-3
M3 - Article
C2 - 10707985
AN - SCOPUS:0033630375
SN - 0896-6273
VL - 25
SP - 215
EP - 227
JO - Neuron
JF - Neuron
IS - 1
ER -