Microcircuitry of the dark-adapted cat retina: functional architecture of the rod-cone network

Smith, Robert G.; Freed, MA; Sterling, Peter

doi:10.1523/jneurosci.06-12-03505.1986

Cited by 230 publications

(208 citation statements)

References 43 publications

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“…This apparent discrepancy with one of the results from tests of APB-treated monkeys (38) The symptom of night blindness cannot be entirely explained by the defect in signal transmission between rods and their ON bipolar cells, because rods have alternative electrical connections to the inner retina that bypass the ON bipolar cells (46). In the area centralis of the cat retina, anatomic studies have shown that each cone has electrical gap junctions with Ϸ48 neighboring rods (47). Rod signals can be transmitted to cones through these gap junctions and thence to cone bipolar cells and ganglion cells (48)(49)(50).…”

Section: Discussionmentioning

confidence: 98%

Night blindness and abnormal cone electroretinogram ON responses in patients with mutations in the GRM6 gene encoding mGluR6

Dryja

McGee²,

Berson³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

222

175

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We report three unrelated patients with mutations in the GRM6 gene that normally encodes the glutamate receptor mGluR6. This neurotransmitter receptor has been shown previously to be present only in the synapses of the ON bipolar cell dendrites, and it mediates synaptic transmission from rod and cone photoreceptors to this type of second-order neuron. Despite the synaptic defect, best visual acuities were normal or only moderately reduced (20͞15 to 20͞40). The patients were night blind from an early age, and when maximally dark-adapted, they could perceive lights only with an intensity equal to or slightly dimmer than that normally detected by the cone system (i.e., 2-3 log units above normal). Electroretinograms (ERGs) in response to single brief flashes of light had clearly detectable a-waves, which are derived from photoreceptors, and greatly reduced b-waves, which are derived from the second-order inner retinal neurons. ERGs in response to sawtooth flickering light indicated a markedly reduced ON response and a nearly normal OFF response. There was no subjective delay in the perception of suddenly appearing white vs. black objects on a gray background. These patients exemplify a previously unrecognized, autosomal recessive form of congenital night blindness associated with a negative ERG waveform. bipolar cell ͉ glutamate receptor ͉ retina

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Section: Discussionmentioning

confidence: 98%

Night blindness and abnormal cone electroretinogram ON responses in patients with mutations in the GRM6 gene encoding mGluR6

Dryja

McGee²,

Berson³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

222

175

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“…Interaction between the rod and cone pathways is extensive: rods and cones are electrically coupled (Raviola and Gilula, 1973;Smith et al, 1986;Schneeweis and Schnapf, 1995;Krizaj et al, 1998;Tsukamoto et al, 2001), and rod signals piggyback onto cone pathways at several stages in visual processing (for review, see Völgyi et al, 2004). This interaction of the two photoreceptor systems is essential for adaptation of photoreceptor sensitivity to different levels of ambient illumination.…”

Section: On the Distinctive Roles Of Horizontal Cell Somata And Axon mentioning

confidence: 99%

Rod and Cone Contributions to Horizontal Cell Light Responses in the Mouse Retina

Trümpler¹,

Dedek²,

Schubert³

et al. 2008

Journal of Neuroscience

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Mammalian B-type horizontal cells make contact with both photoreceptor types: the dendrites contact cone photoreceptors, whereas the axon terminal processes contact rods. Despite their distinct synaptic contacts, horizontal cell somata and axon terminals receive a mixture of rod and cone inputs. Interaction of the two photoreceptor systems is essential for adaptation of photoreceptor sensitivity to different levels of background illumination, and horizontal cells play a key role in this adaptation. In this study, we used transgenic mouse lines to examine the contributions of rod and cone photoreceptor inputs to horizontal cell light responses in the mouse retina: rod signals were isolated by recording intracellularly from horizontal cells in a mouse lacking the cone cyclic nucleotide-gated channel, which lacks cone function, and cone signals were assessed using the rhodopsin knock-out mouse, which is a model for pure cone function. We found that both horizontal cell compartments receive a mixture of inputs from both photoreceptor types. To determine whether these inputs arrive via the long axon connecting the compartments or by way of rod-cone gap junctional coupling, we assessed the rod and cone contributions to horizontal cell somatic and axon terminal light responses in the connexin36-deficient mouse retina, which lacks rodcone coupling. Our results confirm that rods and cones are coupled by connexin36, and suggest that signal transmission along the axon is unidirectional: signals are passed from horizontal cell soma to axon terminal but not from axon terminal to soma.

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“…Conecone coupling increases with light adaptation in the turtle (Copenhagen & Green, 1987), as does rod-cone coupling in salamander (Yang & Wu, 1989). These changes influence the functional efficacy of the output synapse (Smith et al, 1986) as well as rod input into the cone system.…”

Section: Introductionmentioning

confidence: 99%

Connexin 35/36 is phosphorylated at regulatory sites in the retina

Kothmann

Li²,

Burr

et al. 2007

Vis Neurosci

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Connexin 35/36 is the most widespread neuronal gap junction protein in the retina and central nervous system. Electrical and/or tracer coupling in a number of neuronal circuits that express this connexin are regulated by light adaptation. In many cases the regulation of coupling depends on signaling pathways that activate protein kinases such as PKA, and Cx35 has been shown to be regulated by PKA phosphorylation in cell culture systems. To examine whether phosphorylation might regulate Cx35/36 in the retina we developed phospho-specific polyclonal antibodies against the two regulatory phosphorylation sites of Cx35 and examined the phosphorylation state of this connexin in the retina. Western blot analysis with hybrid bass retinal membrane preparations showed Cx35 to be phosphorylated at both the Ser110 and Ser276 sites, and this labeling was eliminated by alkaline phosphatase digestion. The homologous sites of mouse and rabbit Cx36 were also phosphorylated in retinal membrane preparations. Quantitative confocal immunofluorescence analysis showed gap junctions identified with a monoclonal anti-Cx35 antibody to have variable levels of phosphorylation at both the Ser110 and Ser276 sites. Unusual gap junctions that could be identified by their large size (up to 32 μm 2 ) and location in the IPL showed a prominent shift in phosphorylation state from heavily phosphorylated in nighttime, dark-adapted retina to weakly phosphorylated in daytime, light-adapted retina. Both Ser110 and Ser276 sites showed significant changes in this manner. Under both lighting conditions other gap junctions varied from non-phosphorylated to heavily phosphorylated. We predict that changes in the phosphorylation states of these sites correlate with changes in the degree of coupling through Cx35/36 gap junctions. This leads to the conclusion that connexin phosphorylation mediates changes in coupling in some retinal networks. However, these changes are not global and likely occur in a cell type-specific or possibly a gap junction-specific manner.

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Microcircuitry of the dark-adapted cat retina: functional architecture of the rod-cone network

Cited by 230 publications

References 43 publications

Night blindness and abnormal cone electroretinogram ON responses in patients with mutations in the GRM6 gene encoding mGluR6

Night blindness and abnormal cone electroretinogram ON responses in patients with mutations in the GRM6 gene encoding mGluR6

Rod and Cone Contributions to Horizontal Cell Light Responses in the Mouse Retina

Connexin 35/36 is phosphorylated at regulatory sites in the retina

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