A17: A broad-field amacrine cell in the rod system of the cat

Journal of Neurophysiology (Impact Factor: 2.89). 10/1985; 54(3):592-614.
Source: PubMed


A17 amacrine cells of the cat retina have been penetrated with horseradish peroxidase (HRP)-filled microelectrodes and their light responses recorded. These cells depolarize in sustained fashion to steps of light. Viewed in retinal wholemounts, HRP-injected cells have a spokelike radiating splay of very fine dendrites (0.1 micron diam) passing diffusely through all strata of the inner plexiform layer (IPL) to run primarily in strata 4 and 5. There are as many as 1,000 large, regularly spaced beads borne on the 500- to 1,200-micron diameter dendritic field. Cell body sizes range from 9 to 13 micron. In the electron microscope, the dendritic beads in sublamina b of the IPL are seen to synapse reciprocally with rod bipolar axon terminals. Dendritic beads in sublamina a rarely make synapses, but between the beads in this layer, input from at least three distinctive amacrine profiles occurs. Though diffuse at the light microscopic level, A17 thus appears to be structurally bistratified, with amacrine input in sublamina a and bipolar input in sublamina b. It is likely that A17 can be identified with AI. A17 signals are driven almost exclusively by rods. The spectral sensitivity peaks at 507 nm, identical with that of pigment epithelial cells. Light adaptation abolishes all but a small hyperpolarizing component of the signal. The overall intensity-response range is similar to that of AII amacrine cells. When receptive fields of A17 cells are mapped with slit stimuli, a broad, single-component curve is measured approximately covering the dendritic field. The receptive field is well described by a linear electrical model with a mean space constant of 259 +/- 97 micron (SD). On the other hand, responses to centered slit stimuli of varying width yielded space constants of only 38 +/- 29 micron. A17 amacrines are thus broad-field components of the cat's rod system but with very little capacity for spatial integration. Receptive-field measurements are not supportive of the notion of isolated dendritic regions.

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    • "The two vertebrate wide-field amacrine cells best studied physiologically are the A17 and A1, and they follow the classical pattern of collecting information over a restricted region of visual space. The A17 amacrine cell is an axonless, wide-field cell that performs important functions for visual processing under dim (scotopic) lighting conditions (Grimes et al. 2010; Hartveit 1999; Menger and Wässle 2000; Nelson and Kolb 1985). Despite its diffuse dendritic arbor, the A17 cell is involved primarily in local computations by forming reciprocal synapses, providing local inhibition back onto rod bipolar cell terminals from which the A17 receives its input. "
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    ABSTRACT: At early stages of visual processing, receptive fields are typically described as subtending local regions of space and thus performing computations on a narrow spatial scale. Nevertheless, stimulation well outside of the classical receptive field can exert clear and significant effects on visual processing. Given the distances over which they occur, the retinal mechanisms responsible for these long-range effects would certainly require signal propagation via active membrane properties. Here, the physiology of a wide-field amacrine cell-the wiry cell-in macaque monkey retina is explored, revealing receptive fields that represent a striking departure from the classic structure. A single wiry cell integrates signals over wide regions of retina, 5-10 times larger than the classic receptive fields of most retinal ganglion cells. Wiry cells integrate signals over space much more effectively than predicted from passive signal propagation and spatial integration is strongly attenuated during blockade of NMDA spikes but integration is insensitive to blockade of NaV channels with TTX. Thus, these cells appear well suited for contributing to the long-range interactions of visual signals that characterize many aspects of visual perception. Copyright © 2015, Journal of Neurophysiology.
    Full-text · Article · Jul 2015 · Journal of Neurophysiology
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    • "At dim light levels, visual information from rod photoreceptors is conveyed to rod bipolar cells (RBCs), which relay the signal to amacrine cells in the inner retina (reviewed by Wä ssle, 2004). Specifically, RBCs contact GABAergic A17 amacrine cells (A17s) (Nelson and Kolb, 1985), which provide local feedback inhibition onto the rod bipolar cell axon terminals to modulate their release of glutamate (Chá vez et al., 2006; Chun et al., 1993; Hartveit, 1999). In addition, RBC axon terminals also receive GABAergic drive from other widefield amacrine cells (Chá vez et al., 2010; McGuire et al., 1984). "
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    ABSTRACT: Presynaptic inhibition onto axons regulates neuronal output, but how such inhibitory synapses develop and are maintained in vivo remains unclear. Axon terminals of glutamatergic retinal rod bipolar cells (RBCs) receive GABAA and GABAC receptor-mediated synaptic inhibition. We found that perturbing GABAergic or glutamatergic neurotransmission does not prevent GABAergic synaptogenesis onto RBC axons. But, GABA release is necessary for maintaining axonal GABA receptors. This activity-dependent process is receptor subtype specific: GABAC receptors are maintained, whereas GABAA receptors containing α1, but not α3, subunits decrease over time in mice with deficient GABA synthesis. GABAA receptor distribution on RBC axons is unaffected in GABAC receptor knockout mice. Thus, GABAA and GABAC receptor maintenance are regulated separately. Although immature RBCs elevate their glutamate release when GABA synthesis is impaired, homeostatic mechanisms ensure that the RBC output operates within its normal range after eye opening, perhaps to regain proper visual processing within the scotopic pathway.
    Full-text · Article · Apr 2013 · Neuron
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    • "Dim stimuli elicited wide-field, GABA receptor-mediated inhibition. GABAergic amacrine cells are components of the rod signaling pathway (Nelson and Kolb, 1985), accounting for the higher light sensitivity of this inhibition. Bright stimuli elicited narrow-field, EAATmediated inhibition that was less light sensitive. "
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    ABSTRACT: Excitatory amino acid transporters (EAATs) terminate signaling in the CNS by clearing released glutamate. Glutamate also evokes an EAAT-mediated Cl(-) current, but its role in CNS signaling is poorly understood. We show in mouse retina that EAAT-mediated Cl(-) currents that were evoked by light inhibit rod pathway signaling. EAATs reside on rod bipolar cell axon terminals where GABA and glycine receptors also mediate light-evoked inhibition. We found that the mode of inhibition depended on light intensity. Dim light evoked GABAergic and glycinergic inhibition with rapid kinetics and a large spatial extent. Bright light evoked predominantly EAAT-mediated inhibition with slow kinetics and a small spatial extent. The switch to EAAT-mediated signaling in bright light supplements receptor-mediated signaling to expand the dynamic range of inhibition and contributes to the transition from rod to cone signaling by suppressing rod pathway signaling in bright light conditions.
    Full-text · Article · Mar 2012 · The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
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