scholarly journals Dark-adapted response threshold of OFF ganglion cells is not set by OFF bipolar cells in the mouse retina

2012 ◽  
Vol 107 (10) ◽  
pp. 2649-2659 ◽  
Author(s):  
A. Cyrus Arman ◽  
Alapakkam P. Sampath
Keyword(s):  
Ganglion Cells ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Response Threshold ◽  
Mouse Retina ◽  
Signal Flow ◽  
Visual Threshold ◽  
Aii Amacrine Cells ◽  
Aii Amacrine ◽  
Cone Bipolar Cells

The nervous system frequently integrates parallel streams of information to encode a broad range of stimulus strengths. In mammalian retina it is generally believed that signals generated by rod and cone photoreceptors converge onto cone bipolar cells prior to reaching the retinal output, the ganglion cells. Near absolute visual threshold a specialized mammalian retinal circuit, the rod bipolar pathway, pools signals from many rods and converges on depolarizing (AII) amacrine cells. However, whether subsequent signal flow to OFF ganglion cells requires OFF cone bipolar cells near visual threshold remains unclear. Glycinergic synapses between AII amacrine cells and OFF cone bipolar cells are believed to relay subsequently rod-driven signals to OFF ganglion cells. However, AII amacrine cells also make glycinergic synapses directly with OFF ganglion cells. To determine the route for signal flow near visual threshold, we measured the effect of the glycine receptor antagonist strychnine on response threshold in fully dark-adapted retinal cells. As shown previously, we found that response threshold for OFF ganglion cells was elevated by strychnine. Surprisingly, strychnine did not elevate response threshold in any subclass of OFF cone bipolar cell. Instead, in every OFF cone bipolar subclass strychnine suppressed tonic glycinergic inhibition without altering response threshold. Consistent with this lack of influence of strychnine, we found that the dominant input to OFF cone bipolar cells in darkness was excitatory and the response threshold of the excitatory input varied by subclass. Thus, in the dark-adapted mouse retina, the high absolute sensitivity of OFF ganglion cells cannot be explained by signal transmission through OFF cone bipolar cells.

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

2009 ◽  
Vol 101 (5) ◽  
pp. 2339-2347 ◽  
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.

Unique functional properties of the APB sensitive and insensitive rod pathways signaling light decrements in mouse retinal ganglion cells

2006 ◽  
Vol 23 (1) ◽  
pp. 127-135 ◽  
Author(s):  
GUO-YONG WANG
Keyword(s):  
Functional Properties ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Mouse Retina ◽  
Clear Cut ◽  
Types Of Information ◽  
Rod Bipolar Cells ◽  
Rod Pathway ◽  
Cone Bipolar Cells

Light decrements are mediated by two distinct groups of rod pathways in the dark-adapted retina that can be differentiated on the basis of their sensitivity to the glutamate agonist DL-2-amino-phosphonobutyric (APB). By means of the APB sensitive pathway, rods transmit light decrementsviarod bipolar cells to AII amacrine cells, then to Off cone bipolar cells, which in turn innervate the dendrites of Off ganglion cells. APB hyperpolarizes rod bipolar cells, thus blocking this rod pathway. With APB insensitive pathways, rods either directly synapse onto Off cone bipolar cells, or rods pass light decrement signal to cones by gap junctions. In the present study, whole-cell patch-clamp recordings were made from ganglion cells in the dark-adapted mouse retina to investigate the functional properties of APB sensitive and insensitive rod pathways. The results revealed several clear-cut differences between the APB sensitive and APB insensitive rod pathways. The latency of Off responses to a flashing spot of light was significantly shorter for the APB insensitive pathways than those for the APB sensitive pathway. Moreover, Off responses of the APB insensitive pathways were found to be capable of following substantially higher stimulus frequencies. Nitric oxide was found to selectively block Off responses in the APB sensitive rod pathway. Collectively, these results provide evidence that the APB sensitive and insensitive rod pathways can convey different types of information signaling light decrements in the dark-adapted retina.

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

1999 ◽  
Vol 16 (6) ◽  
pp. 1181-1189 ◽  
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.

scholarly journals Parvalbumin-immunoreactive amacrine cells of macaque retina

2009 ◽  
Vol 26 (3) ◽  
pp. 287-296 ◽  
Author(s):  
KATHRYN E. KLUMP ◽  
AI-JUN ZHANG ◽  
SAMUEL M. WU ◽  
DAVID W. MARSHAK
Keyword(s):  
Light Intensity ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Morphological Type ◽  
Golgi Method ◽  
Bipolar Cells ◽  
Spatial Density ◽  
Ultrastructural Studies ◽  
Aii Amacrine Cells ◽  
Aii Amacrine

AbstractA number of authors have observed amacrine cells containing high levels of immunoreactive parvalbumin in primate retinas. The experiments described here were designed to identify these cells morphologically, to determine their neurotransmitter, to record their light responses, and to describe the other cells that they contact. Macaque retinas were fixed in paraformaldehyde and labeled with antibodies to parvalbumin and one or two other markers, and this double- and triple-labeled material was analyzed by confocal microscopy. In their morphology and dendritic stratification patterns, the parvalbumin-positive cells closely resembled the knotty type 2 amacrine cells described using the Golgi method in macaques. They contained immunoreactive glycine transporter, but not immunoreactive γ-aminobutyric acid, and therefore, they use glycine as their neurotransmitter. Their spatial density was relatively high, roughly half that of AII amacrine cells. They contacted lobular dendrites of AII cells, and they are expected to be presynaptic to AII cells based on earlier ultrastructural studies. They also made extensive contacts with axon terminals of OFF midget bipolar cells whose polarity cannot be predicted with certainty. A macaque amacrine cell of the same morphological type depolarized at the onset of increments in light intensity, and it was well coupled to other amacrine cells. Previously, we described amacrine cells like these that contacted OFF parasol ganglion cells and OFF starburst amacrine cells. Taken together, these findings suggest that one function of these amacrine cells is to inhibit the transmission of signals from rods to OFF bipolar cells via AII amacrine cells. Another function may be inhibition of the OFF pathway following increments in light intensity.

Coupling from AII amacrine cells to ON cone bipolar cells is bidirectional

2001 ◽  
Vol 437 (4) ◽  
pp. 408-422 ◽  
Author(s):  
E. Brady Trexler ◽  
Wei Li ◽  
Stephen L. Mills ◽  
Stephen C. Massey
Keyword(s):  
Amacrine Cells ◽  
Bipolar Cells ◽  
Aii Amacrine Cells ◽  
Aii Amacrine ◽  
Cone Bipolar Cells

AMPA-selective glutamate receptor subunits GluR2 and GluR4 in the cat retina: An immunocytochemical study

1999 ◽  
Vol 16 (6) ◽  
pp. 1105-1114 ◽  
Author(s):  
PU QIN ◽  
ROBERTA G. POURCHO
Keyword(s):  
Ganglion Cells ◽  
Plexiform Layer ◽  
Amacrine Cells ◽  
Cell Types ◽  
Bipolar Cells ◽  
Horizontal Cells ◽  
Inner Plexiform Layer ◽  
Cat Retina ◽  
Aii Amacrine Cells ◽  
Aii Amacrine

AMPA-selective glutamate receptors play a major role in glutamatergic neurotransmission in the retina and are expressed in a variety of neuronal subpopulations. In the present study, immunocytochemical techniques were used to visualize the distribution of GluR2 and GluR4 subunits in the cat retina. Results were compared with previous localizations of GluR1 and GluR2/3. Staining for GluR2 was limited to a small number of amacrine and ganglion cells whereas GluR4 staining was present in A-type horizontal cells, many amacrine cells including type AII amacrine cells, and the majority of the cells in the ganglion cell layer. Analysis of synaptic relationships in the outer plexiform layer showed the GluR4 subunit to be concentrated at the contacts of cone photoreceptors with A-horizontal cells. In the inner plexiform layer, both GluR2 and GluR4 were postsynaptic to cone bipolar cells at dyad contacts although GluR2 staining was limited to one of the postsynaptic elements whereas GluR4 immunoreactivity was often seen in both postsynaptic elements. Unlike GluR2, GluR4 was also postsynaptic to rod bipolar cells where it could be visualized in processes of AII amacrine cells. The data indicate that GluR3 and GluR4 subunits are colocalized in a number of cell types including A-type horizontal cells, AII amacrine cells, and alpha ganglion cells, but whether they are combined in the same multimeric receptors remains to be determined.

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

1997 ◽  
Vol 14 (3) ◽  
pp. 565-576 ◽  
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.

Functional Organization of Cone Bipolar Cells in the Rat Retina

1997 ◽  
Vol 77 (4) ◽  
pp. 1716-1730 ◽  
Author(s):  
Espen Hartveit
Keyword(s):  
Receptor Antagonist ◽  
Functional Organization ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Short Latency ◽  
Rat Retina ◽  
Long Latency ◽  
Aii Amacrine Cells ◽  
Aii Amacrine ◽  
Cone Bipolar Cells

Hartveit, Espen. Functional organization of cone bipolar cells in the rat retina. J. Neurophysiol. 77: 1716–1730, 1997. The responses of cone bipolar cells in slices of rat retina to ionotropic glutamate receptor agonists were recorded with the whole cell voltage-clamp technique in the presence of 5 mM Co2+ and nominally 0 mM Ca2+ extracellularly. Application of the non- N-methyl-d-aspartate (non-NMDA) receptor agonists kainate and (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate had a series of effects on cone bipolar cells (types 1–9), and the different cell types could be classified as on- or off-type cells according to which type(s) of responses they displayed. First, direct responses were observed in cell types 1–4 as short-latency inward currents at −70 mV with reversal potentials ( E revs) close to 0 mV, characteristic of nonselective cation channels. Second, some cells, among types 5–9, did not display short-latency inward currents to kainate at −70 mV. Other type 5–8 cells displayed short-latency kainate responses, but the currents could not be reversed ( E rev of +40 mV or greater). I suggest that these responses are conveyed to the cone bipolar cells through gap junctions, most likely with AII amacrine cells. The lack of reversal is likely due to a substantial voltage drop across the gap junctions resulting in an inadequate voltage control of AII amacrine cells when the recording pipette is on the cone bipolar cell. Kainate responses recorded directly from AII amacrine cells had E rev ∼ 0 mV. Third, long-latency indirect responses selective for chloride ions ( E rev ∼ chloride equilibrium potential) were observed in many cone bipolar cells during longer-lasting application of kainate. The long-latency response component was suppressed by coapplication of the γ-aminobutyric acid-A (GABAA) receptor antagonist picrotoxin and the GABAC receptor antagonist 3-aminopropyl(methyl)phosphinic acid. This long-latency component was absent in axotomized bipolar cells, suggesting that it was due to external Ca2+-independent release of GABA onto the axon terminals of the cone bipolar cells. All kainate-evoked response components were blocked by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. Application of NMDA evoked no response in cone bipolar cells. These results suggest that cone bipolar cells types 1–4 are off cone bipolar cells, whereas cone bipolar cells types 5–9 are on cone bipolar cells.

scholarly journals The somal patterning of the AII amacrine cell mosaic in the mouse retina is indistinguishable from random simulations matched for density and constrained by soma size

2018 ◽  
Vol 35 ◽  
Author(s):  
PATRICK W. KEELEY ◽  
BENJAMIN E. REESE
Keyword(s):  
Amacrine Cell ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Horizontal Cells ◽  
Mouse Retina ◽  
Retinal Neurons ◽  
Soma Size ◽  
Aii Amacrine Cells ◽  
Aii Amacrine ◽  
Cholinergic Amacrine Cells

AbstractThe orderly spacing of retinal neurons is commonly regarded as a characteristic feature of retinal nerve cell populations. Exemplars of this property include the horizontal cells and the cholinergic amacrine cells, where individual cells minimize the proximity to like-type neighbors, yielding regularity in the patterning of their somata. Recently, two types of retinal bipolar cells in the mouse retina were shown to exhibit an order in their somal patterning no different from density-matched simulations constrained by soma size but being otherwise randomly distributed. The present study has now extended this finding to a type of retinal amacrine cell, the AII amacrine cell. Voronoi domain analysis revealed the patterning in the population of AII amacrine somata to be no different from density-matched and soma-size-constrained random simulations, while analysis of the density recovery profile showed AII amacrine cells to exhibit a minimal intercellular spacing identical to that for those random simulations: AII amacrine somata were positioned side-by-side as often as chance would predict. Regularity indexes and packing factors (PF) were far lower than those achieved by either the horizontal cells or cholinergic amacrine cells, with PFs also being comparable to those derived from the constrained random simulations. These results extend recent findings that call into question the widespread assumption that all types of retinal neurons are assembled as regular somal arrays, and have implications for the way in which AII amacrine cells must distribute their processes to ensure a uniform coverage of the retinal surface.

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