Microcircuits for Night Vision in Mouse Retina

Tsukamoto, Yoshihiko; Morigiwa, Katsuko; Ueda, Mari; Sterling, Peter

doi:10.1523/jneurosci.21-21-08616.2001

Cited by 310 publications

(444 citation statements)

References 42 publications

(51 reference statements)

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“…If this pool were evenly distributed across the 34 ribbon-style active zones (Figure 1), each active zone would possess ≈ 0.88 fF worth of releasable vesicles. Assuming a conversion factor of 25 aF/vesicle, obtained from the specific membrane capacitance of 9 fFμm -2 (Gentet et al, 2000) and a vesicle diameter of ≈ 30 nm (von Gersdorff et al, 1996;Spiwoks-Becker et al, 2001;Tsukamoto et al, 2001), the releasable pool of the mouse rod bipolar cell would correspond to nearly 1,200 vesicles or ≈ 35 vesicles per ribbon-style active zone. This is consistent with the predicted size of the releasable pool per ribbon synapse in the rat rod bipolar cell based upon data obtained from paired recordings (Singer & Diamond, 2006).…”

Section: Discussionmentioning

confidence: 99%

Synaptic vesicle dynamics in mouse rod bipolar cells

Wan¹,

Vila²,

Zhou³

et al. 2008

Vis Neurosci

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To better understand synaptic signaling at the mammalian rod bipolar cell terminal and pave the way for applying genetic approaches to the study of visual information processing in the mammalian retina, synaptic vesicle dynamics and intraterminal calcium were monitored in terminals of acutely isolated mouse rod bipolar cells and the number of ribbon-style active zones quantified. We identified a releasable pool, corresponding to a maximum of ≈ 35 vesicles/ribbon-style active zone. Following depletion, this pool was refilled with a time constant of ≈ 7 s. The presence of a smaller, rapidlyreleasing pool and a small, fast component of refilling were also suggested. Following calcium channel closure, membrane surface area was restored to baseline with a time constant that ranged from 2 to 21 seconds, depending upon the magnitude of the preceding Ca 2+ transient. In addition, a brief, calcium-dependent delay often preceded the start of onset of membrane recovery. Thus, several aspects of synaptic vesicle dynamics appear to be conserved between rod-dominant bipolar cells of fish and mammalian rod bipolar cells. A major difference is that the number of vesicles available for release is significantly smaller in the mouse rod bipolar cell, both as a function of the total number per neuron and on a per active zone basis.

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Section: Discussionmentioning

confidence: 99%

Synaptic vesicle dynamics in mouse rod bipolar cells

Wan¹,

Vila²,

Zhou³

et al. 2008

Vis Neurosci

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“…AII amacrines are also postsynaptic to (some) OFF-cone bipolar cells at dyad synapses in the outer part of the IPL where the other postsynaptic element is typically the dendritic process of a ganglion cell or that of another amacrine cell (McGuire et al, 1984;Strettoi et al 1992Strettoi et al , 1994Tsukamoto et al, 2001). The synaptic input from OFF-cone bipolar cells is located at the lobular appendages in sublamina a of the IPL.…”

Section: The Aii Amacrine Cell In the Mammalian Retinamentioning

confidence: 99%

“…Although it has not been examined extensively, electrophysiological recordings suggest that the input is mediated by iGluRs (Veruki et al, 2003; see also Xin and Bloomfield, 1999). The AII amacrine lobular appendages can also be presynaptic to the axon terminals of OFFcone bipolar cells from which they receive input and to dendrites of OFF-ganglion cells (McGuire et al, 1984;Strettoi et al, 1992Strettoi et al, , 1994Tsukamoto et al, 2001). At the EM level, the lobular appendages contain synaptic vesicles (Strettoi et al, 1992) and there is evidence that the transmission is glycinergic (Pourcho and Goebel, 1985;Sassoè-Pognetto et al, 1994).…”

Section: The Aii Amacrine Cell In the Mammalian Retinamentioning

confidence: 99%

“…As for the homologous junctions between AII amacrines, the first evidence for electrical synapses between AII amacrines and ON-cone bipolar cells also came from ultrastructural studies in cat retina (Famiglietti and Kolb, 1975;Kolb, 1979;Kolb and Famiglietti 1974), but has since been verified for several other mammalian retinas (Chun et al, 1993;Massey and Mills, 1999b;Tsukamoto et al, 2001;Wässle et al, 1995).…”

Section: Heterologous Gap Junctions Between Aii Amacrines and On-conementioning

confidence: 99%

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Electrical synapses between AII amacrine cells in the retina: Function and modulation

Hartveit

Veruki

2012

Brain Research

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Adaptation enables the visual system to operate across a large range of background light intensities. There is evidence that one component of this adaptation is mediated by modulation of gap junctions functioning as electrical synapses, thereby tuning and functionally optimizing specific retinal microcircuits and pathways. The AII amacrine cell is an interneuron found in most mammalian retinas and plays a crucial role for processing visual signals in starlight, twilight and daylight. AII amacrine cells are connected to each other by gap junctions, potentially serving as a substrate for signal averaging and noise reduction, and there is evidence that the strength of electrical coupling is modulated by the level of background light. Whereas there is extensive knowledge concerning the retinal microcircuits that involve the AII amacrine cell, it is less clear which signaling pathways and intracellular transduction mechanisms are involved in modulating the junctional conductance between electrically coupled AII amacrine cells. Here we review the current state of knowledge, with a focus on recent evidence that suggests that the modulatory control involves activity-dependent changes in the phosphorylation of the gap junction channels between AII amacrine cells, potentially linked to their intracellular Ca 2+ dynamics.

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“…This change in transmitter release is detected by two major categories of bipolar cells in the retina, depolarizing (DBCs) and hyperpolarizing bipolar cells (HBCs). The HBCs are contacted mainly but not exclusively by cone rather than rod photoreceptors (Tsukamoto et al, 2001), and have ionotropic glutamate receptors on their dendrites that lead to sign conserving, hyperpolarizing responses to light onset, and depolarizing responses to light offset. In contrast, the DBCs in both rod and cone pathways have G-protein-coupled metabotropic glutamate receptors (mGluR6) that lead, via a biochemical cascade, to sign inverting responses such that onset of a light stimulus causes the cells to depolarize and offset, to hyperpolarize.…”

Section: Introductionmentioning

confidence: 99%

Postreceptoral contributions to the light-adapted ERG of mice lacking b-waves

Shirato

Maeda

Miura

et al. 2008

Experimental Eye Research

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The purpose of this study was to determine the contributions of postreceptoral neurons to the lightadapted ERG of the Nob mouse, a model for complete-type congenital stationary night blindness (CSNB1) that lacks a b-wave from depolarizing bipolar cells. Ganzfeld ERGs were recorded from anesthetized adult control mice, control mice injected intravitreally with L-2-amino-4-phosphonobutyric acid (Control APB mice) to remove On pathway activity, and Nob mice. ERGs also were recorded after PDA (cis-2, 3-piperidine-dicarboxylic acid, 3-5 mM) was injected to block transmission to hyperpolarizing (Off) bipolar and horizontal cells, and all 3rd order neurons. Stimuli were brief (< 4 ms, 0.4 -2.5 log sc td s) and long (200 ms, 2.5 -4.6 log sc td) LED flashes (λmax = 513 nm, on a rod suppressing background (2.6 log sc td). Sinusoidal modulation of the LEDs (mean, 2.6 log sc td; contrast, 100%; 3 to 36 Hz) was used to study flicker ERGs.Brief-flash ERGs of Nob mice presented as long-lasting negative waves with a positive-going intrusion that started about 50 ms after the flash and peaked around 120 ms. Control APB mice had similar responses, and in both cases, PDA removed the positive-going intrusion. For long flashes, PDA removed a small, slow "d-wave" after light offset. With sinusoidal stimulation, the fundamental (F1) amplitude of control mice ERG peaked at 8 Hz (~70 μV). For Nob mice the peak was ~20 μV at 6 Hz before PDA and ~10 μV at 3 Hz or lower after PDA. F1 responses were present up to 21 Hz in control and Nob eyes and 15 Hz in Nob eyes after PDA. Between 3 and 6 Hz, F1 phase was 170°-210° more delayed in Nob than control mice; phase was hardly altered by PDA. With vector analysis, a substantial postreceptoral input to the Nob flicker ERG was revealed. In control mice, the second harmonic (F2) response showed peaks of ~10 μV at 3 Hz and 13 Hz. Nob mice showed almost no F2. In summary, in this study it was found that in Nob mice, postreceptoral neurons from the Off pathway make a positive-going contribution to the light-adapted flash ERG, and contribute substantially to sinusoidal flicker ERG.

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Microcircuits for Night Vision in Mouse Retina

Cited by 310 publications

References 42 publications

Synaptic vesicle dynamics in mouse rod bipolar cells

Synaptic vesicle dynamics in mouse rod bipolar cells

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Postreceptoral contributions to the light-adapted ERG of mice lacking b-waves

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