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S. Lee, K. Kim, Z.J. Zhou; Detection of Functional Cholinergic and GABAergic Communications Between Starburst Amacrine Cell and Direction Selective Ganglion Cell . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2676.
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© ARVO (1962-2015); The Authors (2016-present)
ACh release from starburst amacrine cell (SAC) affects the light response properties of many ganglion cells, including the direction selective ganglion cell (DSGC). However, the exact function of ACh in the mature retina remains obscured, in part because cholinergic transmission has never been detected directly at the synaptic level. Thus, it is unclear whether ACh functions locally at well defined synapses or diffuses broadly to affect many cells without generating a resolvable quantal effect.
Paired patch recordings were made from DSGCs and SACs in functionally matured rabbit retinal wholemounts. Light and voltage stimulations were used together with pharmacological interventions to determine the functional connectivity between DSGCs and SACs and the properties of ACh release.
Dual voltage–clamp recordings revealed functional communication between SACs and DSGCs. GABA–receptor mediated inhibitory synaptic inputs to DSGC were evoked mainly by SACs on the null side as previously reported. In addition, we found that voltage–step stimulation of a SAC reliably evoked nicotinic postsynaptic responses in the neighboring DSGC, regardless whther the SAC was on the preferred or the null side. The nicotinic currents consisted of a large fast component, followed by a small prolonged component. These components were regulated differently by various stimulus patterns. Application of the acetylcholine esterase inhibitor, neostigmine, profoundly enhanced the nicotinic transmission between SACs and DSGCs. Neostigmine also greatly enhanced the amplitude and duration of light–evoked excitatory inputs to DSGC by increasing postsynaptic nicotinic currents. The degree of directional asymmetry in the excitatory inputs to DSGCs appeared to be slightly reduced by neostigmine. In the presence of neostigmine, light–evoked inhibitory synaptic inputs to DSGC were slightly reduced, but the directional asymmetry in the inhibitory inputs remained intact.
The results demonstrate that ACh does mediate fast synaptic transmission between SACs and DSGCs, though it remains to be determined whether the slow nicotinic component represents perisynaptic or extrasynaptic transmission. We showed that nicotinic input from SACs to DSGCs was non–directional, while the GABAergic input was directional. Neostigmine blocked direction selectivity in DSGCs largely by enhancing the excitatory inputs via nicotinic receptors on DSGCs, but not by reducing the asymmetry of the inhibitory inputs.
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