Dopamine modulation of rod pathway signaling by suppression of GABACfeedback to rod-driven depolarizing bipolar cells

2015 ◽  
Vol 42 (6) ◽  
pp. 2258-2270 ◽  
Author(s):  
Benjamin J. Smith ◽  
Patrice D. Côté ◽  
François Tremblay
Keyword(s):  
Bipolar Cells ◽  
Dopamine Modulation ◽  
Rod Pathway

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.

scholarly journals Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells

2018 ◽  
Vol 120 (2) ◽  
pp. 867-879 ◽  
Author(s):  
Michael D. Flood ◽  
Johnnie M. Moore-Dotson ◽  
Erika D. Eggers
Keyword(s):  
Light Adaptation ◽  
Amacrine Cell ◽  
Amacrine Cells ◽  
Receptor Activation ◽  
Bipolar Cells ◽  
D1 Receptor ◽  
D1 Receptors ◽  
Light Responses ◽  
Dopamine Modulation ◽  
Rod Bipolar Cells

Dopamine modulation of retinal signaling has been shown to be an important part of retinal adaptation to increased background light levels, but the role of dopamine modulation of retinal inhibition is not clear. We previously showed that light adaptation causes a large reduction in inhibition to rod bipolar cells, potentially to match the decrease in excitation after rod saturation. In this study, we determined how dopamine D1 receptors in the inner retina contribute to this modulation. We found that D1 receptor activation significantly decreased the magnitude of inhibitory light responses from rod bipolar cells, whereas D1 receptor blockade during light adaptation partially prevented this decline. To determine what mechanisms were involved in the modulation of inhibitory light responses, we measured the effect of D1 receptor activation on spontaneous currents and currents evoked from electrically stimulating amacrine cell inputs to rod bipolar cells. D1 receptor activation decreased the frequency of spontaneous inhibition with no change in event amplitudes, suggesting a presynaptic change in amacrine cell activity in agreement with previous reports that rod bipolar cells lack D1 receptors. Additionally, we found that D1 receptor activation reduced the amplitude of electrically evoked responses, showing that D1 receptors can modulate amacrine cells directly. Our results suggest that D1 receptor activation can replicate a large portion but not all of the effects of light adaptation, likely by modulating release from amacrine cells onto rod bipolar cells. NEW & NOTEWORTHY We demonstrated a new aspect of dopaminergic signaling that is involved in mediating light adaptation of retinal inhibition. This D1 receptor-dependent mechanism likely acts through receptors located directly on amacrine cells, in addition to its potential role in modulating the strength of serial inhibition between amacrine cells. Our results also suggest that another D2/D4 receptor-dependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

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.

Developmental expression of protein kinase C immunoreactivity in rod bipolar cells of the rabbit retina

1996 ◽  
Vol 13 (5) ◽  
pp. 817-831 ◽  
Author(s):  
Giovanni Casini ◽  
Achille Grassi ◽  
Luigi Trasarti ◽  
Paola Bagnoli
Keyword(s):  
Protein Kinase C ◽  
Amacrine Cell ◽  
Plexiform Layer ◽  
Bipolar Cells ◽  
Cell Populations ◽  
Rabbit Retina ◽  
Kinase C ◽  
Eye Opening ◽  
Rod Bipolar Cells ◽  
Rod Pathway

AbstractRod bipolar cells constitute the second-order neuron in the rod pathway. Previous investigations of the rabbit retina have evaluated the development of other components of the rod pathway, namely the dopaminergic and All amacrine cell populations. To gain further insights into the maturation of this retinal circuitry, we studied the development of rod bipolar cells, identified with antibodies directed to the α isoform of protein kinase C (PKC), in the rabbit retina. Lightly immunostained PKC-immunoreactive (IR) somata are first observed at postnatal day (PND) 6 in the distal inner nuclear layer (INL). Immunostaining is also observed in the outer plexiform layer (OPL), indicating the presence of PKC-IR dendrites. PKC-IR axons are present in the INL oriented toward the inner plexiform layer (IPL). Several of them terminate with enlarged structures resembling growth cones. At PND 8, some immunostained terminal bulbs, characteristic of rod bipolar cells, are detected in the proximal IPL. PKC-IR cells at PND 11 (eye opening) display stronger immunostaining and more mature characteristics than at earlier ages. The dendritic arborizations of these cells in the OPL and their axon terminals in the IPL attain mature morphology at later ages (PND 30 or older). The density of PKC-IR cells shows a peak at PND 11 followed by a drastic decrease up to adulthood. The total number of PKC-IR cells increases from PND 6 to PND 11 and then it remains almost unchanged until adulthood. The mosaic of PKC-IR cells is nonrandom in some retinal locations at PND 6, but the overall regularity index at PND 6 is lower than at older ages. The present data provide a comprehensive evaluation of the development of rod bipolar cells in the postnatal rabbit retina and are consistent with those previously reported for dopaminergic and All amacrine cell populations, indicating that different components of the rod pathway follow a similar pattern of maturation, presumably allowing the rod pathway to be functional at eye opening.

scholarly journals Functional NMDA receptors are expressed by both AII and A17 amacrine cells in the rod pathway of the mammalian retina

2016 ◽  
Vol 115 (1) ◽  
pp. 389-403 ◽  
Author(s):  
Yifan Zhou ◽  
Barbora Tencerová ◽  
Espen Hartveit ◽  
Margaret L. Veruki
Keyword(s):  
Nmda Receptors ◽  
Low Frequency ◽  
Amacrine Cells ◽  
Bipolar Cells ◽  
Evoked Responses ◽  
Patch Clamp Recording ◽  
Mammalian Retina ◽  
Frequency Stimulation ◽  
Rod Bipolar Cells ◽  
Rod Pathway

At many glutamatergic synapses, non- N-methyl-d-aspartate (NMDA) and NMDA receptors are coexpressed postsynaptically. In the mammalian retina, glutamatergic rod bipolar cells are presynaptic to two rod amacrine cells (AII and A17) that constitute dyad postsynaptic partners opposite each presynaptic active zone. Whereas there is strong evidence for expression of non-NMDA receptors by both AII and A17 amacrines, the expression of NMDA receptors by the pre- and postsynaptic neurons in this microcircuit has not been resolved. In this study, using patch-clamp recording from visually identified cells in rat retinal slices, we investigated the expression and functional properties of NMDA receptors in these cells with a combination of pharmacological and biophysical methods. Pressure application of NMDA did not evoke a response in rod bipolar cells, but for both AII and A17 amacrines, NMDA evoked responses that were blocked by a competitive antagonist (CPP) applied extracellularly and an open channel blocker (MK-801) applied intracellularly. NMDA-evoked responses also displayed strong Mg2+-dependent voltage block and were independent of gap junction coupling. With low-frequency application (60-s intervals), NMDA-evoked responses remained stable for up to 50 min, but with higher-frequency stimulation (10- to 20-s intervals), NMDA responses were strongly and reversibly suppressed. We observed strong potentiation when NMDA was applied in nominally Ca2+-free extracellular solution, potentially reflecting Ca2+-dependent NMDA receptor inactivation. These results indicate that expression of functional (i.e., conductance-increasing) NMDA receptors is common to both AII and A17 amacrine cells and suggest that these receptors could play an important role for synaptic signaling, integration, or plasticity in the rod pathway.

Type 3a and type 3b OFF cone bipolar cells provide for the alternative rod pathway in the mouse retina

2007 ◽  
Vol 502 (6) ◽  
pp. 1123-1137 ◽  
Author(s):  
Anja Mataruga ◽  
Elisabeth Kremmer ◽  
Frank Müller
Keyword(s):  
Bipolar Cells ◽  
Mouse Retina ◽  
Rod Pathway ◽  
Cone Bipolar Cells

scholarly journals Light adaptation alters the source of inhibition to the mouse retinal OFF pathway

2013 ◽  
Vol 110 (9) ◽  
pp. 2113-2128 ◽  
Author(s):  
Reece E. Mazade ◽  
Erika D. Eggers
Keyword(s):  
Bipolar Cell ◽  
Light Adaptation ◽  
Amacrine Cell ◽  
Bipolar Cells ◽  
Gabaergic Inhibition ◽  
Light Sensing ◽  
Wide Range ◽  
Rod Pathway ◽  
Aii Amacrine ◽  
Cone Bipolar Cells

Sensory systems must avoid saturation to encode a wide range of stimulus intensities. One way the retina accomplishes this is by using both dim-light-sensing rod and bright-light-sensing cone photoreceptor circuits. OFF cone bipolar cells are a key point in this process, as they receive both excitatory input from cones and inhibitory input from AII amacrine cells via the rod pathway. However, in addition to AII amacrine cell input, other inhibitory inputs from cone pathways also modulate OFF cone bipolar cell light signals. It is unknown how these inhibitory inputs to OFF cone bipolar cells change when switching between rod and cone pathways or whether all OFF cone bipolar cells receive rod pathway input. We found that one group of OFF cone bipolar cells (types 1, 2, and 4) receive rod-mediated inhibitory inputs that likely come from the rod-AII amacrine cell pathway, while another group of OFF cone bipolar cells (type 3) do not. In both cases, dark-adapted rod-dominant light responses showed a significant contribution of glycinergic inhibition, which decreased with light adaptation and was, surprisingly, compensated by an increase in GABAergic inhibition. As GABAergic input has distinct timing and spatial spread from glycinergic input, a shift from glycinergic to GABAergic inhibition could significantly alter OFF cone bipolar cell signaling to downstream OFF ganglion cells. Larger GABAergic input could reflect an adjustment of OFF bipolar cell spatial inhibition, which may be one mechanism that contributes to retinal spatial sensitivity in the light.

Cone bipolar cells as interneurons in the rod, pathway of the rabbit retina

1994 ◽  
Vol 347 (1) ◽  
pp. 139-149 ◽  
Author(s):  
Enrica Strettoi ◽  
Ramon F. Dacheux ◽  
Elio Raviola
Keyword(s):  
Bipolar Cells ◽  
Rabbit Retina ◽  
Rod Pathway ◽  
Cone Bipolar Cells
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