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.
"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). "
[Show abstract][Hide abstract] 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.
"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. "
[Show abstract][Hide abstract] 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.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 03/2012; 32(13):4360-71. DOI:10.1523/JNEUROSCI.5645-11.2012 · 6.34 Impact Factor
"Evidence that A17s fire action potentials is inconsistent across species, with small (~10 mV) spikes evident in somatic recordings from rabbit (Bloomfield, 1996) but not cat or rat (Menger and Wässle, 2000; Nelson and Kolb, 1985). To maximize our chances to observe spikes in rat A17s, we partially relieved Na v channel inactivation by injecting a negative current step (−200 pA for 200 ms), thereby hyperpolarizing the membranes by more than 30 mV relative to rest, prior to delivering large, positive current steps (up to +1000 pA for 200 ms; Figure 4F). "
[Show abstract][Hide abstract] ABSTRACT: Most neurons are highly polarized cells with branched dendrites that receive and integrate synaptic inputs and extensive axons that deliver action potential output to distant targets. By contrast, amacrine cells, a diverse class of inhibitory interneurons in the inner retina, collect input and distribute output within the same neuritic network. The extent to which most amacrine cells integrate synaptic information and distribute their output is poorly understood. Here, we show that single A17 amacrine cells provide reciprocal feedback inhibition to presynaptic bipolar cells via hundreds of independent microcircuits operating in parallel. The A17 uses specialized morphological features, biophysical properties, and synaptic mechanisms to isolate feedback microcircuits and maximize its capacity to handle many independent processes. This example of a neuron employing distributed parallel processing rather than spatial integration provides insights into how unconventional neuronal morphology and physiology can maximize network function while minimizing wiring cost.
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