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D. A. Protti, V. A. Nguyen; Phasic and Tonic Neurotransmitter-Gated Currents in Mouse Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4186.
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© ARVO (1962-2015); The Authors (2016-present)
The operational range of retinal ganglion cells (RGCs) is limited to ~2.5 log units and it matches large fluctuations in environmental light levels (~14 log units) via various adaptation mechanisms in the retinal circuit, among them changes in the gain of RGCs. Gain control is strongly influenced by the balance of spontaneous excitatory and inhibitory inputs, which can be either fast (phasic) or slow (tonic) acting. The aim of this study was to examine the relationship between the spontaneous excitatory and inhibitory inputs onto RGCs in order to understand how this activity may influence RGCs integration properties.
Mice were dark-adapted for at least an hour before dissection; all procedures were carried out in the dark under infrared illumination. The retina was mounted in a recording chamber with photoreceptor side down. Recordings were obtained from RGCs which were whole-cell voltage-clamped at -70, -40 and 0 mV. Light-evoked postsynaptic currents (LEPSCs) were recorded in response to centre and surround stimulation of the receptive field. The effect of the GABA uptake blocker NO-711, GABA blockers and ionotropic glutamate receptor blockers on spontaneous synaptic activity and LEPSCs was investigated.
A subset of RGCs exhibited spontaneous postsynaptic currents (PSCs) that were reduced by ionotropic glutamate receptor blockers. This treatment not only abolished fast PSCs but also reduced the baseline current, consistent with the presence of tonic excitatory input. In these cells, PSCs and tonic currents were also enhanced by GABA blockers and reduced by NO-711, suggesting that these drugs act presynaptically to attenuate and enhance inhibition respectively. Another subset of RGCs displayed PSCs that were blocked by GABA blockers and enhanced by NO-711. These treatments also revealed the presence of an inhibitory tonic current. NO-711 strongly suppressed excitatory LEPSCs and diminished inhibitory LEPSCs for all cells tested.
These results show that RGCs receive both phasic and tonic synaptic inputs, which may modulate gain in RGCs. In addition, enhancement of inhibitory synaptic transmission by NO-711 affects light-evoked excitatory input onto ganglion cells more potently than light-evoked inhibitory input, suggesting that presynaptic inhibitory mechanisms play a more significant role modulating RGCs output.
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