scholarly journals Decreased vascular supply leads to higher numbers of NADPH diaphorase amacrine cells in the degenerating mouse retina

2017 ◽  
Vol 1 (2) ◽  
Author(s):  
Christian-Albrecht May
Keyword(s):  
Amacrine Cells ◽  
Vascular Supply ◽  
Nadph Diaphorase ◽  
Mouse Retina

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

2000 ◽  
Vol 17 (2) ◽  
pp. 273-281 ◽  
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.

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

2018 ◽  
Vol 28 (17) ◽  
pp. 2739-2751.e3 ◽  
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

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

eLife ◽  
2018 ◽  
Vol 7 ◽  
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.

Spontaneous Oscillatory Activity of Starburst Amacrine Cells in the Mouse Retina

2005 ◽  
Vol 94 (3) ◽  
pp. 1770-1780 ◽  
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.

Identification and characterization of SMI32-immunoreactive amacrine cells in the mouse retina

2007 ◽  
Vol 424 (3) ◽  
pp. 199-202 ◽  
Author(s):  
Eun-Jin Lim ◽  
In-Beom Kim ◽  
Su-Ja Oh ◽  
Myung-Hoon Chun
Keyword(s):  
Amacrine Cells ◽  
Mouse Retina ◽  
Identification And Characterization

Ectopic localization of putative AII amacrine cells in the outer plexiform layer of the developing FVB/N mouse retina

2004 ◽  
Vol 315 (3) ◽  
pp. 407-412 ◽  
Author(s):  
Sung-Jin Park ◽  
Eun-Jin Lim ◽  
Su-Ja Oh ◽  
Jin-Woong Chung ◽  
Dennis W. Rickman ◽  
...  
Keyword(s):  
Plexiform Layer ◽  
Amacrine Cells ◽  
Outer Plexiform Layer ◽  
Mouse Retina ◽  
Aii Amacrine Cells ◽  
Aii Amacrine

scholarly journals Laminin deficits induce alterations in the development of dopaminergic neurons in the mouse retina

2007 ◽  
Vol 24 (4) ◽  
pp. 549-562 ◽  
Author(s):  
VIKTÓRIA DÉNES ◽  
PAUL WITKOVSKY ◽  
MANUEL KOCH ◽  
DALE D. HUNTER ◽  
GERMÁN PINZÓN-DUARTE ◽  
...  
Keyword(s):  
Amacrine Cells ◽  
Cell Types ◽  
Mouse Retina ◽  
Null Mouse ◽  
Type I ◽  
Intermediate Cell ◽  
Retinal Ganglion ◽  
Wild Type ◽  
Müller Glial Cell ◽  
Process Outgrowth

Genetically modified mice lacking the β2 laminin chain (β2null), the γ3 laminin chain (γ3 null), or both β2/γ3 chains (compound null) were produced. The development of tyrosine hydroxylase (TH) immunoreactive neurons in these mouse lines was studied between birth and postnatal day (P) 20. Compared to wild type mice, no alterations were seen in γ3 null mice. In β2 null mice, however, the large, type I TH neurons appeared later in development, were at a lower density and had reduced TH immunoreactivity, although TH process number and size were not altered. In the compound null mouse, the same changes were observed together with reduced TH process outgrowth. Surprisingly, in the smaller, type II TH neurons, TH immunoreactivity was increased in laminin-deficient compared to wild type mice. Other retinal defects we observed were a patchy disruption of the inner limiting retinal basement membrane and a disoriented growth of Müller glial cells. Starburst and AII type amacrine cells were not apparently altered in laminin-deficient relative to wild type mice. We postulate that laminin-dependent developmental signals are conveyed to TH amacrine neurons through intermediate cell types, perhaps the Müller glial cell and/or the retinal ganglion cell.

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