Abstract
How neurons in the eye feed signals back to photoreceptors to optimize sensitivity to patterns of light appears to be mediated by one or more unconventional mechanisms. Via these mechanisms, horizontal cells control photoreceptor synaptic gain and enhance key aspects of temporal and spatial center-surround receptive field antagonism. After the transduction of light energy into an electrical signal in photoreceptors, the next key task in visual processing is the transmission of an optimized signal to the follower neurons in the retina. For this to happen, the release of the excitatory neurotransmitter glutamate from photoreceptors is carefully regulated via horizontal cell feedback, which acts as a thermostat to keep the synaptic transmission in an optimal range during changes to light patterns and intensities. Novel findings of a recently described model that casts a classical neurotransmitter system together with ion transport mechanisms to adjust the alkaline milieu outside the synapse are reviewed. This novel inter-neuronal messaging system carries feedback signals using two separate, but interwoven regulated systems. The complex interplay between these two signaling modalities, creating synaptic modulation-at-a-distance, has obscured it’s being defined. The foundations of our understanding of the feedback mechanism from horizontal cells to photoreceptors have been long established: Horizontal cells have broad receptive fields, suitable for providing surround inhibition, their membrane potential, a function of stimulus intensity and size, regulates inhibition of photoreceptor voltage-gated Ca2+ channels, and strong artificial pH buffering eliminates this action. This review compares and contrasts models of how these foundations are linked, focusing on a recent report in mammals that shows tonic horizontal cell release of GABA activating Cl− and HCO3− permeable GABA autoreceptors. The membrane potential of horizontal cells provides the driving force for GABAR-mediated HCO3− efflux, alkalinizing the cleft when horizontal cells are hyperpolarized by light or adding to their depolarization in darkness and contributing to cleft acidification via NHE-mediated H+ efflux. This model challenges interpretations of earlier studies that were considered to rule out a role for GABA in feedback to cones.
Highlights
How neurons in the eye feed signals back to photoreceptors to optimize sensitivity to patterns of light appears to be mediated by one or more unconventional mechanisms
While HCO−3 efflux from horizontal cells during hyperpolarization accounts for the disinhibition of photoreceptor CaV channels caused by increased alkalinity, do horizontal cell depolarization produce inward flux of HCO−3 or reduce the outward driving force on HCO−3 efflux sufficiently to account for the inhibition of photoreceptor CaV channels? The outward rectification provided by BK channels (Sun et al, 2017), which activate steeply positive to −30 mV, prevents horizontal cell depolarization positive to equilibrium potential for HCO−3 (E−HCO3), a value typically in the range of −15 to −20 mV for cells (Bolton and Vaughan-Jones, 1977)
To aid the comparison of this new GABA-pH hybrid model with earlier reports, Figure 12 summarizes the key membrane properties of photoreceptors and horizontal cells at the synaptic cleft that are central to the model
Summary
Received: 15 August 2020 Accepted: 24 September 2020 Published: 04 November 2020. Citation: Barnes S, Grove JCR, McHugh CF, Hirano AA and Brecha NC (2020) Horizontal Cell Feedback to Cone Photoreceptors in Mammalian. After the transduction of light energy into an electrical signal in photoreceptors, the key task in visual processing is the transmission of an optimized signal to the follower neurons in the retina For this to happen, the release of the excitatory neurotransmitter glutamate from photoreceptors is carefully regulated via horizontal cell feedback, which acts as a thermostat to keep the synaptic transmission in an optimal range during changes to light patterns and intensities. Novel findings of a recently described model that casts a classical neurotransmitter system together with ion transport mechanisms to adjust the alkaline milieu outside the synapse are reviewed This novel inter-neuronal messaging system carries feedback signals using two separate, but interwoven regulated systems.
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