Modulation of an electrical synapse between solitary pairs of catfish horizontal cells by dopamine and second messengers.

DeVries, Steven H.; Schwartz, Eric A.

doi:10.1113/jphysiol.1989.sp017692

Cited by 264 publications

(211 citation statements)

References 41 publications

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“…In general, dopamine-mediated changes in coupling have been interpreted as reflecting the action of dopamine as a chemical messenger for light adaptation in the retina (Witkovsky, 2004). For coupling of fish horizontal cells , there is strong evidence for a modulatory role of dopamine (Lasater and Dowling, 1985), acting via the cAMPprotein kinase A (PKA) pathway (DeVries and Schwartz, 1989;Lasater, 1987) to change the conductance of the gap junction proteins (McMahon et al, 1989) and this work has been an important source of inspiration for similar investigations of AII amacrine cells.…”

Section: Tuning the Circuits: Modulation Of Electrical Coupling Betwementioning

confidence: 83%

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Hartveit

Veruki

2012

Brain Research

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Adaptation enables the visual system to operate across a large range of background light intensities. There is evidence that one component of this adaptation is mediated by modulation of gap junctions functioning as electrical synapses, thereby tuning and functionally optimizing specific retinal microcircuits and pathways. The AII amacrine cell is an interneuron found in most mammalian retinas and plays a crucial role for processing visual signals in starlight, twilight and daylight. AII amacrine cells are connected to each other by gap junctions, potentially serving as a substrate for signal averaging and noise reduction, and there is evidence that the strength of electrical coupling is modulated by the level of background light. Whereas there is extensive knowledge concerning the retinal microcircuits that involve the AII amacrine cell, it is less clear which signaling pathways and intracellular transduction mechanisms are involved in modulating the junctional conductance between electrically coupled AII amacrine cells. Here we review the current state of knowledge, with a focus on recent evidence that suggests that the modulatory control involves activity-dependent changes in the phosphorylation of the gap junction channels between AII amacrine cells, potentially linked to their intracellular Ca 2+ dynamics.

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Section: Tuning the Circuits: Modulation Of Electrical Coupling Betwementioning

confidence: 83%

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Hartveit

Veruki

2012

Brain Research

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“…In horizontal cells, NO decreases the affinity of AMPA/Kainate receptors, and increases the maximal current, a possible mechanism for preserving response range during light adaptation (McMahon and Schmidt, 1999). Furthermore, NO closes gap junctions between horizontal cells (DeVries and Schwartz, 1989;Pottek et al, 1997). NO stimulated increases in cGMP have also been reported to close the gap junction between amacrine cells and cone bipolar cells (Mills and Massey, 1995) and depress GABA A currents in amacrine cells (Wexler et al, 1998).…”

Section: Localization Of Cgmp and Nos In The Retinamentioning

confidence: 99%

Regulation of ON bipolar cell activity

Snellman

Kaur

Shen

et al. 2008

Progress in Retinal and Eye Research

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Synaptic transmission from photoreceptors to all types of ON bipolar cells is primarily mediated by the mGluR6 receptor. This receptor, which is apparently expressed uniquely in the nervous system by ON bipolar cells, couples negatively to a nonselective cation channel. This arrangement results in a sign reversal at photoreceptor/ON bipolar cell synapse, which is necessary in order to establish parallel ON and OFF pathways in the retina. The synapse is an important target for 2 nd messenger molecules that are known to modulate synaptic transmission elsewhere in the nervous system, 2 nd messengers that act on a time scale ranging from milliseconds to minutes. This review focuses on two of these molecules, Ca 2+ and cGMP, summarizing our current knowledge of how they modulate gain at the photoreceptor/ON bipolar cell synapse, as well as their proposed sites of action within the mGluR6 cascade. The implications of plasticity at this synapse for retinal function will also be examined.

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“…This effect results from elevation of cytoplasmic cAMP and is mediated by cAMP-dependent protein kinase (PKA). It uncouples gap junctions in horizontal cells (Lasater, 1987;DeVries & Schwartz, 1989) and AII amacrine cells (Hampson et al, 1992).…”

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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Modulation of an electrical synapse between solitary pairs of catfish horizontal cells by dopamine and second messengers.

Cited by 264 publications

References 41 publications

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Regulation of ON bipolar cell activity

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

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