Stimulation of endogenous dopamine release and metabolism in amphibian retina by light- and K+-evoked depolarization

Boatright, Jeffrey H; Hoel, Martha; Iuvone, P. Michael

doi:10.1016/0006-8993(89)90555-6

Cited by 116 publications

(90 citation statements)

References 16 publications

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“…In agreement with our results, Myhr et al (1994) show that dopamine release in salamander retina is increased when illumination that predominantly affects cones is increased from dim to bright levels, consistent with biochemical experiments demonstrating that dopamine levels are two to four times higher in light, compared with dark levels (Godley and Wurtman, 1988;Boatright et al, 1989;Puppala et al, 2004). Our preliminary results show that the suppressive effects of bright light on bipolar sodium currents developed over several minutes, similar to other forms of dopamine-dependent light adaptation (Myhr et al, 1994).…”

Section: Dopamine and Bright Light Contribute To Network Adaptation Bsupporting

confidence: 90%

“…Extracellular dopamine levels are low in dim conditions and are high in bright conditions (Boatright et al, 1989). Because the activity of voltage-gated sodium channels in other parts of the CNS is modulated by dopamine (Cantrell et al, 1997;Hayashida and Ishida, 2004), and dopamine receptors are present on bipolar cells (Veruki and Wassle, 1996;NguyenLegros et al, 1997;Mora-Ferrer et al, 1999), we investigated whether dopamine mediated the light-dependent modulation of the sodium channel activity by activating dopamine receptors in dim light with agonist applications.…”

Section: Dopamine Mimicked the Effects Of Light On Voltage-gated Sodimentioning

confidence: 98%

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Ambient Light Regulates Sodium Channel Activity to Dynamically Control Retinal Signaling

Ichinose

Lukasiewicz

2007

J. Neurosci.

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The retinal network increases its sensitivity in low-light conditions to detect small visual inputs and decreases its sensitivity in brightlight conditions to prevent saturation. However, the cellular mechanisms that adjust visual signaling in the retinal network are not known. Here, we show that voltage-gated sodium channels in bipolar cells dynamically control retinal light sensitivity. In dim conditions, sodium channels amplified light-evoked synaptic responses mediated by cone pathways. Conversely, in bright conditions, sodium channels were inactivated by dopamine released from amacrine cells, and they did not amplify synaptic inputs, minimizing signal saturation. Our findings demonstrate that bipolar cell sodium channels mediate light adaptation by controlling retinal signaling gain.

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Section: Dopamine and Bright Light Contribute To Network Adaptation Bsupporting

confidence: 90%

Section: Dopamine Mimicked the Effects Of Light On Voltage-gated Sodimentioning

confidence: 98%

Ambient Light Regulates Sodium Channel Activity to Dynamically Control Retinal Signaling

Ichinose

Lukasiewicz

2007

J. Neurosci.

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“…Two possible explanations for the higher value detected in our study were the more intact preparation and the higher concentration of nomifensine in the superfusate Endogenous dopamine was also released from the rabbit retina under dim, red light, and because rabbits do not have long wavelength sensitive cones, this stimulus was probably equivalent to darkness (Godley & Wurtman, 1988). Endogenous dopamine is also released from retinas of Xenopus (Boatright et al, 1989(Boatright et al, , 1994Witkovsky et al, 1993), rats (Gibson, 1990(Gibson, , 1992, and macaques in darkness. Retinal dopamine turns over in darkness (Parkinson & Rando, 1983), and 0.5 to 1% of the preloaded tritiated dopamine is released per minute in darkness (Bauer et al, 1980).…”

Section: Dopamine Releasementioning

confidence: 53%

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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“…In the Xenopus retina, exposure to light increases dopamine release (Boatright et al, 1989;Witkovsky et al, 1993), which presumably will result in increased rod-cone coupling in lightadapted retinas, as reported for the salamander retina by Yang and Wu (1989). Similarly, in the turtle retina, rod-cone coupling is greater when rods are slightly desensitized (Schwartz, 1975) compared with fully dark-adapted rods (Copenhagen and Owen, 1976).…”

Section: Presence and Mechanism Of Rod-cone Coupling In Vertebrate Rementioning

confidence: 67%

Dopamine D2 receptor‐mediated modulation of rod‐cone coupling in the Xenopus retina

Križaj¹,

Gábriel²,

Owen³

et al. 1998

J. Comp. Neurol.

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We studied the responses of rod photoreceptors that were elicited with light flashes or sinusoidally modulated light by using intracellular recording. Dark-adapted Xenopus rod photoreceptors responded to sinusoidally modulated green lights at temporal frequencies between 1 Hz and 4 Hz. In normal Ringer's solution, 57% of the rods tested could follow red lights that were matched for equal rod absorbance to frequencies >5 Hz, indicating an input from red-sensitive cones. Quinpirole (10 μM), a D2 dopamine agonist, increased rod-cone coupling, whereas spiperone (5 μM), a selective D2 antagonist, completely suppressed it. D1 dopamine ligands were without effect. Neurobiotin that was injected into single rods diffused into neighboring rods and cones in quinpirole-treated retinas but only diffused into rods in spiperone-treated retinas. A subpopulation of rods (ca. 10% total rods) received a very strong cone input, which quickened the kinetics of their responses to red flashes and greatly increased the bandpass of their responses to sinusoidally modulated light. Based on electron microscopic examination, which showed that rod-rod and cone-cone gap junctions are common, whereas rod-cone junctions are relatively rare, we postulate that cone signals enter the rod network through a minority of rods with strong cone connections, from which the cone signal is further distributed in the rod network. A semiquantitative model of coupling, based on measures of gapjunction size and distribution and estimates of their conductance and open times, provides support for this assumption. The same network would permit rod signals to reach cones. Keywords gap junction; photoreceptor; retina; neuromodulation When rod photoreceptors are fully dark-adapted, they respond reliably to the absorbance of a single quantum of light (Yau et al., 1977). Rods continue to function when they are desensitized by background lights (Fain, 1976) or by prior exposure to light, and, in those circumstances, the effective stimuli for rods can be sufficiently bright to also activate cone photoreceptors, allowing for the possibility of interactions between rod signals and cone signals. (Raviola and Gilula, 1973), and functional rod-cone coupling in primate retina has been reported (Schneeweis and Schnapf, 1995).The main experimental question of the present study is whether the conductances of photoreceptor gap junctions are subject to neuromodulation. We focus on the intrinsic retinal neurochemical, dopamine (Haggendal and Malmfors, 1965), which is known to modulate the gap-junctional conductance of retinal second-order neurons (Piccolino et al., 1984) and to augment information flow in cone circuits while suppressing that in rod circuits (Witkovsky and Dearry, 1991). Photoreceptors have dopamine receptors of the D2/D4 subtypes (Cohen et al., 1992;Muresan and Besharse, 1993). In the present study, we found that a D2 dopamine agonist, but not a D1 agonist, increases rod-cone coupling in the Xenopus retina, resulting in altered rod light-evoked response k...

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Stimulation of endogenous dopamine release and metabolism in amphibian retina by light- and K+-evoked depolarization

Cited by 116 publications

References 16 publications

Ambient Light Regulates Sodium Channel Activity to Dynamically Control Retinal Signaling

Ambient Light Regulates Sodium Channel Activity to Dynamically Control Retinal Signaling

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

Dopamine D2 receptor‐mediated modulation of rod‐cone coupling in the Xenopus retina

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