Corrigendum: Gap Junctions in A8 Amacrine Cells Are Made of Connexin36 but Are Differently Regulated Than Gap Junctions in AII Amacrine Cells

Gap junctions are commonplace in retina, often between cells of the same morphological type, but sometimes linking different cell types. The strength of coupling between cells derives from the properties of the connexins, but also is regulated by the intracellular environment of each cell. We measured the relative coupling of two different gap junctions made by AII amacrine cells of the rabbit retina. Permeability to the tracer Neurobiotin was measured at different concentrations of the neuromodulators dopamine, nitric oxide, or cyclic adenosine monophosphate (cAMP) analogs. Diffusion coefficients were calculated separately for the gap junctions between pairs of AII amacrine cells and for those connecting AII amacrine cells with ON cone bipolar cells. Increased dopamine caused diffusion rates to decline more rapidly across the AII–AII gap junctions than across the AII–bipolar cell gap junctions. The rate of decline at these sites was well fit by a model proposing that dopamine modulates two independent gates in AII–AII channels, but only a single gate on the AII side of the AII–bipolar channel. However, a membrane-permeant cAMP agonist modulated both types of channel equally. Therefore, the major regulator of channel closure in this network is the local cAMP concentration within each cell, as regulated by dopamine, rather than different cAMP sensitivity of their respective gates. In contrast, nitric oxide preferentially reduced AII–bipolar cell permeabilities. Coupling from AII amacrine cells to the different bipolar cell subtypes was differentially affected by dopamine, indicating that light adaptation actingviadopamine release alters network coupling properties in multiple ways.

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Gap junctions between AII amacrine cells and calbindin-positive bipolar cells in the rabbit retina

Visual Neuroscience ◽

10.1017/s0952523899166173 ◽

1999 ◽

Vol 16 (6) ◽

pp. 1181-1189 ◽

Cited By ~ 25

Author(s):

STEPHEN C. MASSEY ◽

STEPHEN L. MILLS

Keyword(s):

Gap Junctions ◽

Bipolar Cell ◽

Amacrine Cells ◽

Positive Cone ◽

Bipolar Cells ◽

Cell Network ◽

Ribbon Synapses ◽

Aii Amacrine Cells ◽

Aii Amacrine ◽

Cone Bipolar Cells

Electrical synapses or gap junctions occur between many retinal neurons. However, in most cases, the gap junctions have not been visualized directly. Instead, their presence has been inferred from tracer spread throughout the network of cells. Thus, tracer coupling is taken as a marker for the presence of gap junctions between coupled cells. AII amacrine cells are critical interneurons in the rod pathway of the mammalian retina. Rod bipolar cell output passes to AII amacrine cells, which in turn make conventional synapses with OFF cone bipolar cells and gap junctions with ON cone bipolar cells. Injections of biotinylated tracers into AII amacrine cells reveals coupling between the AII amacrine cell network and heterologous coupling with a variety of ON cone bipolar cells, including the calbindin-positive cone bipolar cell. To directly visualize gap junctions in this network, we prepared material for electron microscopy that was double labeled with antibodies to calretinin and calbindin to label AII amacrine cells and calbindin-positive cone bipolar cells, respectively. AII amacrine cells were postsynaptic to large vesicle-laden rod bipolar terminals, as previously reported. Gap junctions were identified between AII amacrine cells and calbindin-positive cone bipolar cell terminals identified by the presence of immunostaining and ribbon synapses. This represents direct confirmation of gap junctions between two different yet positively identified cells, which are tracer coupled, and provides additional evidence that tracer coupling with Neurobiotin indicates the presence of gap junctions. These results also definitively establish the presence of gap junctions between AII amacrine cells and calbindin bipolar cells which can therefore carry rod signals to the ON alpha ganglion cell.

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Gap Junctions in A8 Amacrine Cells Are Made of Connexin36 but Are Differently Regulated Than Gap Junctions in AII Amacrine Cells

Frontiers in Molecular Neuroscience ◽

10.3389/fnmol.2019.00099 ◽

2019 ◽

Vol 12 ◽

Cited By ~ 5

Author(s):

Shubhash C. Yadav ◽

Stephan Tetenborg ◽

Karin Dedek

Keyword(s):

Gap Junctions ◽

Amacrine Cells ◽

Aii Amacrine Cells ◽

Aii Amacrine

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Increased phosphorylation of Cx36 gap junctions in the AII amacrine cells of RD retina

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2015.00390 ◽

2015 ◽

Vol 9 ◽

Cited By ~ 12

Author(s):

Elena Ivanova ◽

Christopher W. Yee ◽

Botir T. Sagdullaev

Keyword(s):

Gap Junctions ◽

Amacrine Cells ◽

Aii Amacrine Cells ◽

Aii Amacrine

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Light-induced modulation of coupling between AII amacrine cells in the rabbit retina

Visual Neuroscience ◽

10.1017/s0952523800012220 ◽

1997 ◽

Vol 14 (3) ◽

pp. 565-576 ◽

Cited By ~ 107

Author(s):

Stewart A. Bloomfield ◽

Daiyan Xin ◽

Tristan Osborne

Keyword(s):

Receptive Field ◽

Gap Junctions ◽

Electrical Coupling ◽

Amacrine Cells ◽

Bipolar Cells ◽

Field Size ◽

Background Illumination ◽

Aii Amacrine Cells ◽

Aii Amacrine ◽

Cone Bipolar Cells

AbstractThe rod-driven, AII amacrine cells in the mammalian retina maintain homologous gap junctions with one another as well as heterologous gap junctions with on-cone bipolar cells. We used background illumination to study whether changes in the adaptational state of the retina affected the permeabilities of these two sets of gap junctions. To access changes in permeability, we injected single AII amacrine cells with the biotinylated tracer, Neurobiotin, and measured the extent of tracer coupling to neighboring AII cells and neighboring cone bipolar cells. We also measured the center-receptive field size of All cells to assess concomitant changes in electrical coupling. Our results indicate that in well dark-adapted retinas, AII cells form relatively small networks averaging 20 amacrine cells and covering about 75 μm. The size of these networks matched closely to the size of AII cell on-center receptive fields. However, over most of their operating range, AII cells formed dramatically larger networks, averaging 326 amacrine cells, which corresponded to an increased receptive-field size. As the retina was light adapted beyond the operating range of the AII cells, they uncoupled to form networks comparable in size to those seen in well dark-adapted retinas. Our results, then, indicate that the adaptational state of the retina has a profound effect on the extent of electrical coupling between AII amacrine cells. Although we observed light-induced changes in the number of tracer-coupled cone bipolar cells, these appeared to be an epiphenomenon of changes in homologous coupling between AII amacrine cells. Therefore, in contrast to the robust changes in AII–AII coupling produced by background illumination, our data provided no evidence of a light-induced modulation of coupling between AII cells and on-cone bipolar cells.

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Meclofenamic Acid Blocks Electrical Synapses of Retinal AII Amacrine and on-Cone Bipolar Cells

Journal of Neurophysiology ◽

10.1152/jn.00112.2009 ◽

2009 ◽

Vol 101 (5) ◽

pp. 2339-2347 ◽

Cited By ~ 41

Author(s):

Margaret Lin Veruki ◽

Espen Hartveit

Keyword(s):

Amacrine Cells ◽

Bipolar Cells ◽

Electrical Synapse ◽

Dependent Manner ◽

Electrical Synapses ◽

Meclofenamic Acid ◽

Aii Amacrine Cells ◽

Rod Pathway ◽

Aii Amacrine ◽

Cone Bipolar Cells

Gap junction channels constitute specialized intercellular contacts that can serve as electrical synapses. In the rod pathway of the retina, electrical synapses between AII amacrine cells express connexin 36 (Cx36) and electrical synapses between AII amacrines and on-cone bipolar cells express Cx36 on the amacrine side and Cx36 or Cx45 on the bipolar side. For physiological investigations of the properties and functions of these electrical synapses, it is highly desirable to have access to potent pharmacological blockers with selective and reversible action. Here we use dual whole cell voltage-clamp recordings of pairs of AII amacrine cells and pairs of AII amacrine and on-cone bipolar cells in rat retinal slices to directly measure the junctional conductance ( Gj) between electrically coupled cells and to study the effect of the drug meclofenamic acid (MFA) on Gj. Consistent with previous tracer coupling studies, we found that MFA reversibly blocked the electrical synapse currents in a concentration-dependent manner, with complete block at 100 μM. Whereas MFA evoked a detectable decrease in Gj within minutes of application, the time to complete block of Gj was considerably longer, typically 20–40 min. After washout, Gj recovered to 20–90% of the control level, but the time to maximum recovery was typically >1 h. These results suggest that MFA can be a useful drug to investigate the physiological functions of electrical synapses in the rod pathway, but that the slow kinetics of block and reversal might compromise interpretation of the results and that explicit monitoring of Gj is desirable.

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