Contrast Adaptation in Subthreshold and Spiking Responses of Mammalian Y-Type Retinal Ganglion Cells

Retinal ganglion cells adapt their responses to the amplitude of fluctuations around the mean light level, or the contrast. But, in mammalian retina, it is not known whether adaptation arises exclusively at the level of synaptic inputs or whether there is also adaptation in the process of ganglion cell spike generation. Here, we made intracellular recordings from guinea pig Y-type ganglion cells and quantified changes in contrast sensitivity (gain) using a linear-nonlinear analysis. This analysis allowed us to measure adaptation in the presence of nonlinearities, such as the spike threshold, and to compare adaptation in subthreshold and spiking responses. At high contrast (0.30), relative to low contrast (0.10), gain reduced to 0.82 ± 0.016 (mean ± SEM) for the subthreshold response and to 0.61 ± 0.011 for the spiking response. Thus, there was an apparent reduction in gain between the subthreshold and spiking response of 0.74 ± 0.013. Control experiments suggested that the above effects could not be explained by an artifact of the intracellular recording conditions: extracellular recordings showed a gain change of 0.58 ± 0.022. For intracellular recordings, negative current reduced the spike output but did not affect the gain change in the subthreshold response: 0.80 ± 0.051. Thus, adaptation in the subthreshold response did not require spike-dependent conductances. We conclude that the contrast-dependent gain change in the spiking response can be explained by both a synaptic mechanism, as reflected by responses in the subthreshold potential, and an intrinsic mechanism in the ganglion cell related to spike generation

An accurate circuit-based description of retinal ganglion cell computation

https://doi.org/10.1186/1471-2202-16-S1-O

Functional circuitry of visual adaptation in the retina

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65522/1/jphysiol.2008.156638.pd

Distinct expressions of contrast gain control in parallel synaptic pathways converging on a retinal ganglion cell

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65990/1/jphysiol.2008.156224.pd

Paradox Research in Management Science: Looking Back to Move Forward

Paradox studies offer vital and timely insights into an array of organizational tensions. Yet this field stands at a critical juncture. Over the past 25 years, management scholars have drawn foundational insights from philosophy and psychology to apply a paradox lens to organizational phenomena. Yet extant studies selectively leverage ancient wisdom, adopting some key insights while abandoning others. Using a structured content analysis to review the burgeoning management literature, we surface six key themes, which represent the building blocks of a meta-theory of paradox. These six themes received varying attention in extant studies: paradox scholars emphasize types of paradoxes, collective approaches, and outcomes, but pay less attention to relationships within paradoxes, individual approaches, and dynamics. As this analysis suggests, management scholars have increasingly simplified the intricate, often messy phenomena of paradox. Greater simplicity renders phenomena understandable and testable, however, oversimplifying complex realities can foster reductionist and incomplete theories. We therefore propose a future research agenda targeted at enriching a meta-theory of paradox by reengaging these less developed themes. Doing so can sharpen the focus of this field, while revisiting its rich conceptual roots to capture the intricacies of paradox. This future research agenda leverages the potential of paradox across diverse streams of management science

Multiple Mechanisms for Contrast Adaptation in the Retina

AbstractThe retina adapts to average light intensity but also to the range of light intensities (contrast). A study by Baccus and Meister, in this issue of Neuron, identifies three ways that ganglion cells and interneurons adapt to high contrast: shorten integration time, reduce gain, and depolarize. Only the depolarization decays, over tens of seconds

Selective synaptic connections in the retinal pathway for night vision

The mammalian retina encodes visual information in dim light using rod photoreceptors and a specialized circuit: rods→rod bipolar cells→AII amacrine cell. The AII amacrine cell uses sign‐conserving electrical synapses to modulate ON cone bipolar cell terminals and sign‐inverting chemical (glycinergic) synapses to modulate OFF cone cell bipolar terminals; these ON and OFF cone bipolar terminals then drive the output neurons, retinal ganglion cells (RGCs), following light increments and decrements, respectively. The AII amacrine cell also makes direct glycinergic synapses with certain RGCs, but it is not well established how many types receive this direct AII input. Here, we investigated functional AII amacrine→RGC synaptic connections in the retina of the guinea pig (Cavia porcellus) by recording inhibitory currents from RGCs in the presence of ionotropic glutamate receptor (iGluR) antagonists. This condition isolates a specific pathway through the AII amacrine cell that does not require iGluRs: cone→ON cone bipolar cell→AII amacrine cell→RGC. These recordings show that AII amacrine cells make direct synapses with OFF Alpha, OFF Delta and a smaller OFF transient RGC type that co‐stratifies with OFF Alpha cells. However, AII amacrine cells avoid making synapses with numerous RGC types that co‐stratify with the connected RGCs. Selective AII connections ensure that a privileged minority of RGC types receives direct input from the night‐vision pathway, independent from OFF bipolar cell activity. Furthermore, these results illustrate the specificity of retinal connections, which cannot be predicted solely by co‐stratification of dendrites and axons within the inner plexiform layer.This study examined synaptic connections between retinal ganglion cells and the AII amacrine cell, which is a component of the night vision circuit in mammalian retina (rods → rod bipolar cells → AII amacrine cell). Using a physiological assay, combined with morphological analysis, we show that a direct inhibitory synapse from AII amacrine cells is limited to a privileged minority of ganglion cell types. More generally, co‐stratification did not reliably predict synaptic connection in the inner plexiform layer.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147115/1/cne24313.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147115/2/cne24313_am.pd

NMDA and AMPA receptors contribute similarly to temporal processing in mammalian retinal ganglion cells

Postsynaptic AMPA‐ and NMDA‐type glutamate receptors (AMPARs, NMDARs) are commonly expressed at the same synapses. AMPARs are thought to mediate the majority of fast excitatory neurotransmission whereas NMDARs, with their relatively slower kinetics and higher Ca 2+ permeability, are thought to mediate synaptic plasticity, especially in neural circuits devoted to learning and memory. In sensory neurons, however, the roles of AMPARs and NMDARs are less well understood. Here, we tested in the in vitro guinea pig retina whether AMPARs and NMDARs differentially support temporal contrast encoding by two ganglion cell types. In both OFF Alpha and Delta ganglion cells, contrast stimulation evoked an NMDAR‐mediated response with a characteristic J‐shaped I–V relationship. In OFF Delta cells, AMPAR‐ and NMDAR‐mediated responses could be modulated at low frequencies but were suppressed during 10 Hz stimulation, when responses were instead shaped by synaptic inhibition. With inhibition blocked, both AMPAR‐ and NMDAR‐mediated responses could be modulated at 10 Hz, indicating that NMDAR kinetics do not limit temporal encoding. In OFF Alpha cells, NMDAR‐mediated responses followed stimuli at frequencies up to ∼18 Hz. In both cell types, NMDAR‐mediated responses to contrast modulation at 9–18 Hz showed delays of <10 ms relative to AMPAR‐mediated responses. Thus, NMDARs combine with AMPARs to encode rapidly modulated glutamate release, and NMDAR kinetics do not limit temporal coding by OFF Alpha and Delta ganglion cells substantially. Furthermore, glutamatergic transmission is differentially regulated across bipolar cell pathways: in some, release is suppressed at high temporal frequencies by presynaptic inhibition.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109576/1/tjp6355.pd