Abstract
Purpose: :
The expression of functional nicotinic acetylcholine receptors (nAChRs) by retinal ganglion cells has been well-documented. Retinal ganglion cells express a number of different nAChR subtypes, and activation of these nAChRs differentially influences ganglion cell response properties. There is indirect evidence that activation of nAChRs expressed by upstream cells also influences ganglion cell response properties. For example, the responses of ganglion cells to the application of cholinergic agents differs before and after synaptic isolation, immunohistochemical evidence suggests that subsets of On cone bipolar cells express alpha7 nAChRs, and subsets of glycinergic and GABAergic amacrine cells express alpha7 and/or non-alpha7 nAChRs. Because to date there has been no direct evidence that nAChR immunoreactivity in the inner nuclear layer (INL) represents functional nAChRs, this project was designed to directly test whether or not functional nAChRs are expressed by amacrine cells in rabbit retina.
Methods: :
Rabbit retina slices and eyecups were used for whole cell patch clamp recordings to test the responses of amacrine cells to cholinergic agonists and antagonists. Whole cell configuration was obtained under visual control and cell morphology was confirmed with fluorescent dye injection.
Results: :
Cells in the innermost 1 or 2 tiers of cells in the INL were tested for responses to application of nicotine and or choline. Inward currents reversed at 0 mV, indicating the activation of non-specific cation channels. Outward currents were also observed in amacrine and ganglion cells, indicating that nAChR activation resulted in the release of inhibitory neurotransmitters. In some cases, responses were blocked bymethyllycaconitine, indicating the presence of functional alpha7 nAChRs on INL neurons.
Conclusions: :
These data represent the first direct demonstration of functional nAChRs by amacrine cells in rabbit retina. These data also indicate that more than one nAChR subtype may play a role in the modulation of ganglion cell responses by amacrine cells.
Keywords: acetylcholine • neurotransmitters/neurotransmitter systems • receptors: pharmacology/physiology