Publication Date
4-1-2023
Journal
Vision Research
DOI
10.1016/j.visres.2023.108187
PMID
36758452
PMCID
PMC11349081
PubMedCentral® Posted Date
8-27-2024
PubMedCentral® Full Text Version
Author MSS
Published Open-Access
yes
Keywords
Animals, Mice, Retinal Ganglion Cells, Amacrine Cells, Retina, Strychnine, Chlorides, Cations, Sustained and transient ganglion cells, ON, OFF and ON-OFF ganglion cells, glycineregic amacrine cells, narrow-field amacrine cells, light-evoked cation and chloride currents, light-evoked spike responses, feedforward synapse, feedback synapse, strychnine
Abstract
By analyzing light-evoked spike responses, cation currents (ΔIC) and chloride currents (ΔICl) of over 100 morphologically-identified retinal ganglion cells (GCs) in dark-adapted mouse retina, we found there are at least 14 functionally- and morphologically-distinct types of RGCs. These cells can be divided into 5 groups based on their patterns of spike response to whole field light steps (SRWFLS), a GC identification scheme commonly used in studies with extracellular recording techniques. We also found that all GCs in the mouse retina express strychnine-sensitive glycine receptors, and receive light-elicited chloride current (ΔICl) accompanied by a conductance increase from narrow-field, glycinergic amacrine cells. As the dark membrane potential of RGC are near the chloride-equilibrium potential, mouse GCs’ spike responses are mediated primarily by bipolar cells inputs, and modulated by “shunting inhibition” from narrow-field amacrine cells. Analysis of strychnine actions on light-evoked cation current ΔIC (bipolar cell inputs) in GCs suggests that narrow-field amacrine cells modulate GCs by sending ON-OFF crossover feedback signals to presynaptic bipolar cell axon terminals via sign-inverting glycinergic synapses, and the feedback signals are synergistic to the bipolar cell light responses. Therefore narrow-field amacrine cells enhance light-evoked bipolar cell inputs to GCs by presynaptic “synergistic addition”, besides the abovementioned postsynaptic “shunting inhibition” in GCs.