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S. Lee, K. Kim, Z. J. Zhou; The Organization and Mechanism of Cholinergic and GABAergic Synaptic Transmission Between Starburst Amacrine and DS Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5801.
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© ARVO (1962-2015); The Authors (2016-present)
Despite a critical involvement of the starburst amacrine cell (SAC) in direction selectivity, the underlying circuitry between SACs and a direction selective ganglion cell (DSGC) is not fully understood and the synaptic mechanism underlying ACh and GABA release by SACs is essentially unknown in the mature retina. Here we investigated the synaptic organization and function of SACs in relation to visual processing.
Paired voltage-clamp recording was used to dissect the synaptic organization between SACs and DSGCs and the mechanism of corelease of ACh and GABA by SACs in functionally mature rabbit retina (postnatal 2-5 week old). Pharmacology was used to analyze the components of synaptic inputs to the DSGC during light stimulation.
Dual patch clamp revealed the basic synaptic connectivity between SACs and DSGCs. Robust GABA-A receptor mediated currents in DSGCs were evoked by null-side SACs, while little or no response was evoked by prefer-side SACs, consistent with previous report (Fried et al. 2002). However, DSGCs also received nicotinic receptor-mediated inputs from overlapping SACs regardless of their relative directional configuration, although inputs from prefer-side SACs were slightly larger. Sequential application of nicotinic receptor blocker, hexamethonium and NMDA receptor antagonist CPP during moving light stimulation revealed that the excitatory synaptic inputs were mediated by nicotinic, NMDA and AMPA/KA receptors. These excitatory inputs, especially, nicotinic and NMDA inputs were noticeably facilitated by apparent motion stimulation. The release of ACh and GABA from a SAC was completely blocked by 500 µM CdCl2 or by removing extracellular calcium, thus consistent with our previous findings of calcium-dependent ACh/GABA co-release between SACs in the developing retina. Notably, the release of ACh and GABA had different sensitivity to calcium concentration. ACh release required over 500 µM extracelluar calcium, whereas GABA release clearly occurred at 200 µM extracellular calcium under our stimulation conditions.
Our results revealed two different synaptic organization schemes and release mechanisms for ACh and GABA release. First, GABA synapses on DSGCs are formed mainly with null-side SACs, indicating that the GABAergic input encodes directional information. Second, nicotinic synapses are formed with virtually all overlapping SACs, and ACh release is dependent on a higher calcium concentration and is facilitated by calcium accumulation, suggesting that the nicotinic input encodes motion information.
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