The neural circuit mechanisms underlying the retinal response to motion reversal.

TitleThe neural circuit mechanisms underlying the retinal response to motion reversal.
Publication TypeJournal Article
Year of Publication2014
AuthorsChen, EY, Chou, J, Park, J, Schwartz, G, Berry, MJ
JournalJ Neurosci
Date Published2014 Nov 19
KeywordsAmbystoma, Animals, Computer Simulation, GABA Antagonists, Motion, Nerve Net, Patch-Clamp Techniques, Photic Stimulation, Receptors, GABA, Retina, Retinal Bipolar Cells, Retinal Ganglion Cells, Visual Pathways, Visual Perception

<p>To make up for delays in visual processing, retinal circuitry effectively predicts that a moving object will continue moving in a straight line, allowing retinal ganglion cells to anticipate the object's position. However, a sudden reversal of motion triggers a synchronous burst of firing from a large group of ganglion cells, possibly signaling a violation of the retina's motion prediction. To investigate the neural circuitry underlying this response, we used a combination of multielectrode array and whole-cell patch recordings to measure the responses of individual retinal ganglion cells in the tiger salamander to reversing stimuli. We found that different populations of ganglion cells were responsible for responding to the reversal of different kinds of objects, such as bright versus dark objects. Using pharmacology and designed stimuli, we concluded that ON and OFF bipolar cells both contributed to the reversal response, but that amacrine cells had, at best, a minor role. This allowed us to formulate an adaptive cascade model (ACM), similar to the one previously used to describe ganglion cell responses to motion onset. By incorporating the ON pathway into the ACM, we were able to reproduce the time-varying firing rate of fast OFF ganglion cells for all experimentally tested stimuli. Analysis of the ACM demonstrates that bipolar cell gain control is primarily responsible for generating the synchronized retinal response, as individual bipolar cells require a constant time delay before recovering from gain control.</p>

Alternate JournalJ Neurosci
PubMed ID25411485
PubMed Central IDPMC4236393
Grant ListR01 EY017934 / EY / NEI NIH HHS / United States
EY017934 / EY / NEI NIH HHS / United States