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M Wilson, JM Hurtado, S Borges; Transmitter Release from Amacrine Cells Uses Ca2+ Released from Presynaptic ER . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1947.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:To examine the control of [Ca2+]i within the dendrites of amacrine cells. Methods:Isolated amacrine cells cultured from the embryonic chick retina were examined using either Fura-2 or OGB-1 as Ca2+ indicators. Small segments of dendrite were examined while the cell was depolarized either in voltage clamp or else unclamped with the application of a high K+ puff. Results: With Na+-Ca2+ exchange disabled by removing Na+o, [Ca2+]i transients induced by brief depolarization were prolonged in all cells. Concomitantly, synaptic transmission was prolonged. This prolongation was not the result of reverse mode Na+-Ca2+ exchange since removal of Ca2+o immediately after depolarization did not abbreviate the [Ca2+]i transients. Evidence that the majority of the [Ca2+]i increase came from internal stores was provided by experiments in which the ER was depleted of Ca2+ with thapsigargin. In this condition [Ca2+] transients in dendrites were greatly reduced in both duration and amplitude but unchanged when Na+-Ca2+ exchange was disabled.With Na+-Ca2+ exchange disabled, [Ca2+]i transients induced by brief depolarization in some cells were seen to form stable patterns of higher and lower [Ca2+] over µm length scales. Similar hotspots for [Ca2+] lasting many seconds after depolarization could also be seen in normal conditions and are thought to be produced by local CICR. Conclusion: Although Na+-Ca2+ exchange has an important role in controlling [Ca2+] dynamics in dendrites it appears to contribute little to the actual clearance of Ca2+ from the bulk of dendritic cytoplasm. Instead it controls CICR by moderating the positive feedback of the Ca2+ amplifier.
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