A Dopamine- and Protein Kinase A-Dependent Mechanism for Network Adaptation in Retinal Ganglion Cells

Vaquero, Cecilia F.; Pignatelli, Angela; Partida, Gloria J.; Ishida, Andrew T.

doi:10.1523/jneurosci.21-21-08624.2001

Cited by 58 publications

(69 citation statements)

References 82 publications

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“…In this respect, HCN4 channels are interesting to investigate because their voltage sensitivity is altered to a greater extent by cAMP than in any of the other mammalian HCN isoforms (e.g., Ludwig et al, 1998;Santoro et al, 2000). This would predict that the contribution of I h to resting membrane potential and resistance (Lee and Ishida, 2007) and to rebound excitation (Tabata and Ishida, 1996;Lee et al, 2003;Lee and Ishida, 2007) is increased by conditions that elevate intracellular cAMP levels (Vaquero et al, 2001;Nir et al, 2002;Dunn et al, 2006;Mills et al 2007). However, properties of the net current are shaped by the presence of other HCN isoforms (Franz et al, 2000;Santoro et al, 2000;Altomare et al, 2001;Chen et al, 2001).…”

Section: Presence Of Camp-sensitive Channels In Ganglion Cellsmentioning

confidence: 99%

HCN4-like immunoreactivity in rat retinal ganglion cells

Partida

Lee

et al. 2008

Vis Neurosci

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Antisera directed against hyperpolarization-activated, cyclic nucleotide-sensitive ("HCN") channels bind to somata in the ganglion cell layer of rat and rabbit retinas, and mRNA for different HCN channel isoforms has been detected in the ganglion cell layer of mouse retina. However, previous studies neither provided evidence that any of the somata are ganglion cells (as opposed to displaced amacrine cells) nor quantified these cells. We therefore tested whether isoform-specific anti-HCN channel antisera bind to ganglion cells labeled by retrograde transport of fluorophorecoupled dextran. In flat-mounted adult rat retinas, the number of dextran-backfilled ganglion cells agreed with cell densities reported in previous studies, and anti-HCN4 antisera bound to the somata of approximately 40% of these cells. The diameter of these somata ranged from 7 to 30 μm. Consistent with localization to cell membranes, the immunoreactivity formed a thin line that circumscribed individual somata. Optic fiber layer axon fascicles, and the proximal dendrites of some ganglion cells, also displayed binding of anti-HCN4 antisera. These results suggest that the response of some mammalian retinal ganglion cells to hyperpolarization may be modulated by changes in intracellular cAMP levels, and could thus be more complex than expected from previous voltage and current recordings.

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Section: Presence Of Camp-sensitive Channels In Ganglion Cellsmentioning

confidence: 99%

HCN4-like immunoreactivity in rat retinal ganglion cells

Partida

Lee

et al. 2008

Vis Neurosci

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“…However, the possibility remains that these receptors are present, but not involved in regulation of gap junctional conductance. For example, D 1 receptors influence ganglion cell excitability (Vaquero et al, 2001;Hayashida & Ishida, 2004).…”

Section: Regulation Of Gap Junctional Channels In the Off α Ganglion mentioning

confidence: 99%

Dopaminergic modulation of tracer coupling in a ganglion-amacrine cell network

et al. 2007

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Many retinal ganglion cells are coupled via gap junctions with neighboring amacrine cells and ganglion cells. We investigated the extent and dynamics of coupling in one such network, the OFF α ganglion cell of rabbit retina and its associated amacrine cells. We also observed the relative spread of Neurobiotin injected into a ganglion cell in the presence of modulators of gap junctional permeability. We found that gap junctions between amacrine cells were closed via stimulation of a D 1 dopamine receptor, while the gap junctions between ganglion cells were closed via stimulation of a D 2 dopamine receptor. The pairs of hemichannels making up the heterologous gap junctions between the ganglion and amacrine cells were modulated independently, so that elevations of cAMP in the ganglion cell open the ganglion cell hemichannels, while elevations of cAMP in the amacrine cell close its hemichannels. We also measured endogenous dopamine release from an eyecup preparation and found a basal release from the dark-adapted retina of approximately 2 pmol/min during the day. Maximal stimulation with light increased the rate of dopamine release from rabbit retina by 66%. The results suggest that coupling between members of the OFF α ganglion cell/ amacrine cell network is differentially modulated with changing levels of dopamine.

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“…The present results suggest that not only is the release of dopamine a subject of light-dark adaptation but also the dopaminergic receptor-expressing glutamatergic cells, responding in light with glutamate release after dopamine exposure, do not respond to dopaminergic stimulation in the dark. Different intracellular levels of cAMP in retinal cells of light-and darkadapted animals (Vaquero et al, 2001) may play a role in this different responsiveness of glutamatergic cells.…”

Section: Mechanism Of Glial Cell Morphological Alterationsmentioning

confidence: 99%

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

Uckermann¹,

Vargová²,

Ulbricht³

et al. 2004

J. Neurosci.

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Neuronal activity is accompanied by transmembranous ion fluxes that cause cell volume changes. In whole mounts of the guinea pig retina, application of glutamate resulted in fast swelling of neuronal cell bodies in the ganglion cell layer (GCL) and the inner nuclear layer (INL) (by ϳ40%) and a concomitant decrease of the thickness of glial cell processes in the inner plexiform layer (IPL) (by ϳ40%) that was accompanied by an elongation of the glial cells, by a thickening of the whole retinal tissue, and by a shrinkage of the extracellular space (by ϳ18%). The half-maximal effect of glutamate was observed at ϳ250 M, after ϳ4 min. The swelling was caused predominantly by AMPAkainate receptor-mediated influx of Na ϩ into retinal neurons. Similar but transient morphological alterations were induced by high K ϩ and dopamine, which caused release of endogenous glutamate and subsequent activation of AMPA-kainate receptors. Apparently, retinal glutamatergic transmission is accompanied by neuronal cell swelling that causes compensatory morphological alterations of glial cells. The effect of dopamine was elicitable only during light adaptation but not in the dark, and glutamate and high K ϩ induced stronger effects in the dark than in the light. This suggests that not only the endogenous release of dopamine but also the responsiveness of glutamatergic neurons to dopamine is regulated by light-dark adaptation. Similar morphological alterations (neuronal swelling and decreased glial process thickness) were observed in whole mounts isolated immediately after experimental retinal ischemia, suggesting an involvement of AMPA-kainate receptor activation in putative neurotoxic cell swelling in the postischemic retina.Key words: glutamate; dopamine; ATP; neuroglia; circadian phase; ischemia; retina IntroductionGlial cells play crucial roles in supporting neuronal survival and information processing (Newman and Reichenbach, 1996): they regulate the extracellular homeostasis of relevant ions including K ϩ , control the water content of the extracellular space, and mediate the rapid termination of neuronal activity by transmitter uptake from the synaptic cleft (Matsui et al., 1999). In the retina, neuronally released K ϩ , water, and glutamate are cleared from the extracellular space mainly by the radial glial (Müller) cells. Retinal glial cells display a complex pattern of K ϩ channel expression in their plasma membranes that directs the flow of neuronally released K ϩ into the glial cell bodies and farther into the vitreous and the blood vessels (Kofuji et al., 2002). Parallel water fluxes were suggested to be coupled to the transglial K ϩ fluxes (Nagelhus et al., 1999). The K ϩ and water fluxes, generated by neuronal activity and mediated by glial cells, are accompanied by swelling of cells and shrinkage of the extracellular space caused by the decreased extracellular osmolality (Dietzel et al., 1980;Jendelová and Syková, 1991;Syková, 1991). Cell volume alterations are important, particularly under pathological conditions such as ...

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A Dopamine- and Protein Kinase A-Dependent Mechanism for Network Adaptation in Retinal Ganglion Cells

Cited by 58 publications

References 82 publications

HCN4-like immunoreactivity in rat retinal ganglion cells

HCN4-like immunoreactivity in rat retinal ganglion cells

Dopaminergic modulation of tracer coupling in a ganglion-amacrine cell network

Glutamate-Evoked Alterations of Glial and Neuronal Cell Morphology in the Guinea Pig Retina

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