Purchase this article with an account.
J. Petit–Jacques, B. Volgyi, B. Rudy, S. Bloomfield; Spontaneous Oscillatory Membrane Currents in Starburst Amacrine Cells in Mouse Retina . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4268.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: To study the membrane currents of starburst amacrine cells in mouse retina. Methods: Patch clamp recordings were obtained from displaced starburst amacrine cells visualized with infrared illumination in a mouse retina–scleral preparation. The patch pipette contained biocytin, which allowed for subsequent morphological identification. Results: Spontaneous postsynaptic currents were recorded at a holding potential of –70 mV. They appeared as slow, oscillatory inward currents riding on top of lower amplitude, high frequency miniature synaptic currents. The oscillatory currents were virtually eliminated by application of 10 µM CNQX, indicating that they were generated by activation of AMPA/Kainate glutamate receptors. Surprisingly, the oscillatory currents were affected by application of TEA, a potassium channel blocker. Application of TEA increased the amplitude of these currents and slightly diminished their frequency. In contrast, the oscillatory currents were abolished by application of 200 µM cadmium, a non–specific blocker of calcium channels. They were also virtually eliminated by the application of 30 µM nifedipine, a specific blocker of L–type calcium channels. These data suggest that TEA, by blocking potassium channels, depolarize presynaptic cells, likely bipolar cells. In this scheme, the depolarization of bipolar cells, triggered by TEA, stimulates the opening of L–type calcium channels and an increased release of glutamate onto starburst cells. Application of the metabotropic glutamate receptor agonist, AP4 (50 µM), abolished the glutamate–activated currents in the starburst amacrine cells, although the inhibition was only transient. This suggests that glutamate was released from on–center bipolar cells that synapse onto displaced starburst amacrine cells. Glutamate–activated currents prestimulated with TEA had significantly larger amplitudes in the presence of the GABA receptor antagonists, picrotoxin or bicucculline. This could be due to direct inhibition via GABAA receptors and/or a GABAC receptor–mediated feedback inhibition that regulates glutamate release from bipolar cells. Conclusions: Our data suggest that presynaptic cyclic release of glutamate from on–center bipolar cells result in spontaneous oscillatory postsynaptic currents in displaced starburst amacrine cells by activation of AMPA/Kainate glutamate receptors. The frequency of these excitatory glutamate currents might subsequently control the release of GABA and/or ACh from starburst amacrine cells.
This PDF is available to Subscribers Only