Populations of wide-field amacrine cells in the mouse retina

The mammalian retina contains approximately 30 different morphological types of amacrine cells, receiving glutamatergic input from bipolar cells. In this study, we combined electrophysiological and pharmacological techniques in order to study the glutamate receptors expressed by different types of amacrine cells. Whole-cell currents were recorded from amacrine cells in vertical slices of the mouse retina. During the recordings the cells were filled with Lucifer Yellow/Neurobiotin allowing classification as wide-field or narrow-field amacrine cells. Amacrine cell recordings were also carried out in a transgenic mouse line whose glycinergic amacrine cells express enhanced green fluorescent protein (EGFP). Agonist-induced currents were elicited by exogenous application of NMDA, AMPA, and kainate (KA) while holding cells at −75 mV. Using a variety of specific agonists and antagonists (NBQX, AP5, cyclothiazide, GYKI 52466, GYKI 53655, SYM 2081) responses mediated by AMPA, KA, and NMDA receptors could be dissected. All cells (n= 300) showed prominent responses to non-NMDA agonists. Some cells expressed AMPA receptors exclusively and some cells expressed KA receptors exclusively. In the majority of cells both receptor types could be identified. NMDA receptors were observed in about 75% of the wide-field amacrine cells and in less than half of the narrow-field amacrine cells. Our results confirm that different amacrine cell types express distinct sets of ionotropic glutamate receptors, which may be critical in conferring their unique temporal responses to this diverse neuronal class.

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GABAc receptor mediated modulation of glutamatergic synaptic transmission to amacrine cells in the mouse retina

Neuroscience Research ◽

10.1016/s0168-0102(00)81038-x ◽

2000 ◽

Vol 38 ◽

pp. S32

Author(s):

K Matsui

Keyword(s):

Synaptic Transmission ◽

Amacrine Cells ◽

Mouse Retina ◽

Glutamatergic Synaptic Transmission ◽

Gabac Receptor

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Modulation by Zn2+ of GABA responses in bipolar cells of the mouse retina

Visual Neuroscience ◽

10.1017/s0952523800172098 ◽

2000 ◽

Vol 17 (2) ◽

pp. 273-281 ◽

Cited By ~ 20

Author(s):

M. KANEDA ◽

B. ANDRÁSFALVY ◽

A. KANEKO

Keyword(s):

Axon Terminal ◽

Inhibitory Action ◽

Phosphinic Acid ◽

Amacrine Cells ◽

Bipolar Cells ◽

Mouse Retina ◽

Induced Responses ◽

Inhibitory Interaction ◽

Cell Recording ◽

Recording Conditions

The localization of endogenous Zn2+ in the mouse retina was examined histochemically and the inhibitory action of Zn2+ on GABA-induced responses was studied in bipolar cells isolated from the mouse retina. Accumulation of endogenous Zn2+ was detected in photoreceptors, bipolar, and/or amacrine cells by either the bromopyridylazo-diethylaminophenol method or the dithizone method. Under whole-cell recording conditions, GABA induced a Cl− current in isolated bipolar cells. The current consisted of two components. The first component was inhibited completely by application of 100 μM bicuculline, suggesting that this is a GABAA-receptor mediated current. The second component was inhibited completely by 100 μM 3-aminopropyl-(methyl)-phosphinic acid, suggesting that this is a GABAC-receptor mediated current. GABAC receptors were present at a higher density on the axon terminal than on dendrites. Zn2+ inhibited both GABAA and GABAC receptors. GABAC receptors were more susceptible to Zn2+; the IC50 for the GABAA receptor was 67.4 μM and that for the GABAC receptor was 1.9 μM. These results suggest that Zn2+ modulates the inhibitory interaction between amacrine and bipolar cells, particularly that mediated by the GABAC receptor.

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Amacrine-to-amacrine cell inhibition: Spatiotemporal properties of GABA and glycine pathways

Visual Neuroscience ◽

10.1017/s0952523811000137 ◽

2011 ◽

Vol 28 (3) ◽

pp. 193-204 ◽

Cited By ~ 11

Author(s):

XIN CHEN ◽

HAIN ANN HSUEH ◽

FRANK S. WERBLIN

Keyword(s):

Amacrine Cell ◽

Ganglion Cells ◽

Amacrine Cells ◽

Peak Level ◽

Wide Field ◽

Gabaergic Inhibition ◽

Onset Latency ◽

Temporal Properties ◽

Glycinergic Inhibition ◽

Cell Inhibition

AbstractWe measured the spatial and temporal properties of GABAergic and glycinergic inhibition to amacrine cells in the whole-mount rabbit retina. The amacrine cells were parsed into two morphological classes: narrow-field cells with processes spreading less than 200 μm and wide-field cells with processes extending more than 300 μm. The inhibition was also parsed into two types: sustained glycine and transient GABA. Narrow-field amacrine cells receive 1) very transient GABAergic inhibition with a fast onset latency of 140 ± 16 ms decaying to 30% of the peak level within 208 ± 27 ms elicited broadly over a lateral distance of up to 1500 μm and 2) sustained glycinergic inhibition with a medium onset latency of 286 ± 23 ms that was elicited over a spatial area often broader than the processes of the narrow-field amacrine cells. Wide-field amacrine cells received sustained glycinergic inhibition but no broad transient GABAergic inhibition. Surprisingly, neither of these amacrine cell classes received sustained local GABAergic inhibition, commonly found in an earlier study of ganglion cells.

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Synaptic Transfer between Rod and Cone Pathways Mediated by AII Amacrine Cells in the Mouse Retina

Current Biology ◽

10.1016/j.cub.2018.06.063 ◽

2018 ◽

Vol 28 (17) ◽

pp. 2739-2751.e3 ◽

Cited By ~ 17

Author(s):

Cole W. Graydon ◽

Evan E. Lieberman ◽

Nao Rho ◽

Kevin L. Briggman ◽

Joshua H. Singer ◽

...

Keyword(s):

Amacrine Cells ◽

Mouse Retina ◽

Aii Amacrine Cells ◽

Aii Amacrine

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Formation of retinal direction-selective circuitry initiated by starburst amacrine cell homotypic contact

eLife ◽

10.7554/elife.34241 ◽

2018 ◽

Vol 7 ◽

Cited By ~ 13

Author(s):

Thomas A Ray ◽

Suva Roy ◽

Christopher Kozlowski ◽

Jingjing Wang ◽

Jon Cafaro ◽

...

Keyword(s):

Synapse Formation ◽

Ganglion Cells ◽

Plexiform Layer ◽

Surface Protein ◽

Amacrine Cells ◽

Direction Selectivity ◽

Mouse Retina ◽

Inner Plexiform Layer ◽

Starburst Amacrine Cells ◽

Developing Neurons

A common strategy by which developing neurons locate their synaptic partners is through projections to circuit-specific neuropil sublayers. Once established, sublayers serve as a substrate for selective synapse formation, but how sublayers arise during neurodevelopment remains unknown. Here, we identify the earliest events that initiate formation of the direction-selective circuit in the inner plexiform layer of mouse retina. We demonstrate that radially migrating newborn starburst amacrine cells establish homotypic contacts on arrival at the inner retina. These contacts, mediated by the cell-surface protein MEGF10, trigger neuropil innervation resulting in generation of two sublayers comprising starburst-cell dendrites. This dendritic scaffold then recruits projections from circuit partners. Abolishing MEGF10-mediated contacts profoundly delays and ultimately disrupts sublayer formation, leading to broader direction tuning and weaker direction-selectivity in retinal ganglion cells. Our findings reveal a mechanism by which differentiating neurons transition from migratory to mature morphology, and highlight this mechanism’s importance in forming circuit-specific sublayers.

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Spontaneous Oscillatory Activity of Starburst Amacrine Cells in the Mouse Retina

Journal of Neurophysiology ◽

10.1152/jn.00279.2005 ◽

2005 ◽

Vol 94 (3) ◽

pp. 1770-1780 ◽

Cited By ~ 20

Author(s):

Jerome Petit-Jacques ◽

Béla Völgyi ◽

Bernardo Rudy ◽

Stewart Bloomfield

Keyword(s):

Feedback Inhibition ◽

Glutamate Release ◽

Amacrine Cells ◽

Bipolar Cells ◽

Kainate Receptors ◽

Oscillatory Activity ◽

Mouse Retina ◽

Inner Plexiform Layer ◽

Experimental Conditions ◽

Starburst Amacrine Cells

Using patch-clamp techniques, we investigated the characteristics of the spontaneous oscillatory activity displayed by starburst amacrine cells in the mouse retina. At a holding potential of –70 mV, oscillations appeared as spontaneous, rhythmic inward currents with a frequency of ∼3.5 Hz and an average maximal amplitude of ∼120 pA. Application of TEA, a potassium channel blocker, increased the amplitude of oscillatory currents by >70% but reduced their frequency by ∼17%. The TEA effects did not appear to result from direct actions on starburst cells, but rather a modulation of their synaptic inputs. Oscillatory currents were inhibited by 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), an antagonist of AMPA/kainate receptors, indicating that they were dependent on a periodic glutamatergic input likely from presynaptic bipolar cells. The oscillations were also inhibited by the calcium channel blockers cadmium and nifedipine, suggesting that the glutamate release was calcium dependent. Application of AP4, an agonist of mGluR6 receptors on on-center bipolar cells, blocked the oscillatory currents in starburst cells. However, application of TEA overcame the AP4 blockade, suggesting that the periodic glutamate release from bipolar cells is intrinsic to the inner plexiform layer in that, under experimental conditions, it can occur independent of photoreceptor input. The GABA receptor antagonists picrotoxin and bicuculline enhanced the amplitude of oscillations in starburst cells prestimulated with TEA. Our results suggest that this enhancement was due to a reduction of a GABAergic feedback inhibition from amacrine cells to bipolar cells and the resultant increased glutamate release. Finally, we found that some ganglion cells and other types of amacrine cell also displayed rhythmic activity, suggesting that oscillatory behavior is expressed by a number of inner retinal neurons.

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