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The Journal of Neuroscience, July 30, 2008, 28(31):7919-7928; doi:10.1523/JNEUROSCI.0784-08.2008

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Cellular/Molecular
Diverse Mechanisms Underlie Glycinergic Feedback Transmission onto Rod Bipolar Cells in Rat Retina

Andrés E. Chávez and Jeffrey S. Diamond

Synaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-3701

Correspondence should be addressed to Dr. Jeffrey S. Diamond, Synaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Building 35, Room 3C-1000, Bethesda, MD 20892-3701. Email: diamondj{at}ninds.nih.gov

Synaptic inhibition shapes visual signaling in the inner retina, but the physiology of most amacrine cells, the interneurons that mediate this inhibition, is poorly understood. Discerning the function of most individual amacrine cell types is a daunting task, because few molecular or morphological markers specifically distinguish between approximately two dozen different amacrine cell types. Here, we examine a functional subset of amacrine cells by pharmacologically isolating glycinergic inhibition and evoking feedback IPSCs in a single cell type, the rod bipolar cell (RBC), with brief glutamate applications in the inner plexiform layer. We find that glycinergic amacrine cells innervating RBCs receive excitatory inputs from ON and OFF bipolar cells primarily via NMDA receptors (NMDARs) and Ca²⁺-impermeable AMPA-type glutamate receptors. Glycine release from amacrine cells is triggered by Ca²⁺ influx through both voltage-gated Ca²⁺ (Ca_v) channels and NMDARs. These intracellular Ca²⁺signals are amplified by Ca²⁺-induced Ca²⁺ release via both ryanodine and IP₃ receptors, which are activated independently by Ca²⁺ influx through Ca_v channels and NMDARs, respectively. Glycinergic feedback signaling depends strongly, although not completely, on voltage-gated Na⁺ channels, and the spatial extent of feedback inhibition is expanded by gap junction connections between glycinergic amacrine cells. These results indicate that a diversity of mechanisms underlie glycinergic feedback inhibition onto RBCs, yet they highlight several physiological themes that appear to distinguish amacrine cell function.

Key words: amacrine; AMPA receptor; Ca²⁺-induced Ca²⁺ release; calcium channels; feedback; gap junction; glutamate receptor; glycine; interneuron; retina; retinal bipolar cell

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Received Feb. 21, 2008; revised June 18, 2008; accepted June 20, 2008.

Correspondence should be addressed to Dr. Jeffrey S. Diamond, Synaptic Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Building 35, Room 3C-1000, Bethesda, MD 20892-3701. Email: diamondj{at}ninds.nih.gov

This article has been cited by other articles:

				J. Snellman, D. Zenisek, and S. Nawy Switching between transient and sustained signalling at the rod bipolar-AII amacrine cell synapse of the mouse retina J. Physiol., June 1, 2009; 587(11): 2443 - 2455. [Abstract] [Full Text] [PDF]

				T. L. Kalbaugh, J. Zhang, and J. S. Diamond Coagonist Release Modulates NMDA Receptor Subtype Contributions at Synaptic Inputs to Retinal Ganglion Cells J. Neurosci., February 4, 2009; 29(5): 1469 - 1479. [Abstract] [Full Text] [PDF]

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