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J. Petit-Jacques, S. A. Bloomfield; Dopamine Regulates the Light-Evoked Responses of Starburst Amacrine Cells in the Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5788. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To study the influence of dopaminergic synaptic inputs on the light responses of starburst amacrine cells in the mouse retina.
Patch clamp recordings were obtained from starburst amacrine cells visualized in the ganglion cell layer under infrared illumination in a dark-adapted mouse retina-scleral preparation. The patch pipette solution contained biocytin, which allowed for subsequent morphological identification. Computer-generated light stimuli were produced by a DLP projector onto a coherent fiber optic and then delivered to the retina through the microscope objective.
Postsynaptic currents were usually recorded at a holding potential of -70 mV. As shown previously (Petit-Jacques and Bloomfield, ARVO 2007) the typical response of a displaced starburst amacrine cell to small diameter spots of dim light (70 µm) consisted of a large transient peak of inward current at light onset followed by smaller amplitude oscillatory currents that were maintained for the duration of the light stimulus. We showed at last year’s ARVO meeting that both response components are dependent on the release of glutamate from presynaptic ON bipolar cells. Since bipolar cells express dopamine D1 receptors (Nguyen-Legros et al., 1997), it is likely that dopamine will influence glutamate release and the responses of postsynaptic starburst cells. Therefore, we recorded light-evoked responses of starburst cells in the presence of dopaminergic agonists and antagonists . The dopaminergic D1 receptor agonist SKF (10 µM) increased the maximal amplitude of the transient peak by 84 %, but increased the frequency of the subsequent oscillations by only 5%. Consistent with this effect, application of the D1 receptor antagonist SCH (10 µM) decreased the maximal amplitude of the transient component by 51% and reduced the frequency of the oscillatory component by 21% when compared to control conditions. In addition to the light-evoked oscillations, starburst cells also show robust spontaneous oscillatory activity in the dark. However, neither the D1 agonist nor the antagonist had a significant effect on the starburst spontaneous oscillations recorded in the dark.
Our results indicate that the light-dependent transient and oscillatory glutamate release from presynaptic ON bipolar cells is regulated by dopaminergic inputs. The data obtained with SCH suggest that a basal dopaminergic input increases the release of glutamate from ON bipolar cells, thereby amplifying the responses of postsynaptic starburst amacrine cells.
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