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Sun-Sook Paik, Myung-Hoon Chun, In-Beom Kim; A Ca2+-Dependent Cl- Current in the Axon Terminals of Mouse Rod Bipolar Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1162.
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Rod bipolar cells in the mouse retina have two types of Ca2+ channel with different kinetics. L-type Ca2+ channels are located in rod bipolar terminals and play a role in regulating neurotransmitter release. Ca2+ influx through these channels can also activate a Ca2+-dependent Cl- channel (CaCC). This Ca2+-dependent Cl- channel current has been well-documented in cones. However, it has not been clearly identified and characterized in bipolar cells. Here, we report that a CaCC is present in mouse rod bipolar cells and present further details about its electrophysiological properties.
Retinal slices and dissociated cells were prepared from the C57BL/6 mouse. Membrane currents were recorded in the whole-cell recording configuration. All recorded cells were morphologically identified by filling with Lucifer Yellow and Neurobiotin.
In rod bipolar cells isolated from the mouse retina, a very slow inward tail current was observed following a depolarizing voltage step, during which two types of inward Ca2+ current were elicited. In most cases (20 out of 24), a fast and transient Ca2+ current (considered as T-type) was not detectable. A tail current was present with a very small amplitude and long inactivation time. The properties of the tail current were identified by the following tests: 1. the application of a Ca2+ channel blocker (Cd2+) and an L-type Ca2+ channel antagonist (nifedipine), 2. The reversal potential of the tail current, 3. The effect of a Cl- channel blocker. Cd2+ blocked the inward Ca2+ current as well as the tail current, indicating that the tail current was dependent on intracellular Ca2+ influx. When [Cl-]o was reduced from 100% to 20% , the reversal potential shifted towards the predicted value of ECl. The extracellular application of 200 µM niflumic acid blocked the tail current but not the calcium current. This selective action is strong evidence that the tail current consists of a Cl- conductance activated by intracellular Ca2+ influx.
These results demonstrate that rod bipolar cells have a slowly declining inward tail current due to a Ca2+-dependent Cl- conductance. The slow and sustained gating properties of the Cl- current reflect the changing intracellular Ca2+ concentration. The CaCC current may stabilize the membrane potential of rod bipolar cells during synaptic activity.
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