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C. Hu, M. Slaughter; A Unique Signaling Pathway Formed by T-type Calcium Channels in Rat Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3864.
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Retinal neurons possess several types of voltage-gated calcium currents. Of these, the low-voltage activated T-type currents are particularly distinctive and may be involved in both transmitter release and in the shaping of the light response. T-type calcium channels have been identified in a number of retinas. If T-type channels relay unique visual information, their distribution should reflect this distinction.
Ganglion cells in the rat retinal slice were voltage clamped using whole cell recording techniques. High and low threshold calcium currents were activated with voltage steps or ramps while potassium and sodium currents were blocked. For comparison, similar experiments were performed in the tiger salamander retina.
In rat retina, ganglion cells could be divided into two groups: in one the T-type calcium currents were much larger than the high voltage-activated (HVA) calcium currents while in the second group the HVA currents far exceeded the T-type. In contrast, the T-type current in salamander retina was always far smaller than the HVA current, or completely absent. In most T-type dominant rat ganglion cells, the channel was more permeable to calcium than to barium. However, there was a small subset of ganglion cells with the reverse permeability preference. In voltage clamp experiments on rat retinal ganglion cells, baclofen (an agonist at metabotropic GABA receptors) enhanced the HVA L-type calcium channels but had no direct effect on T-type channels. However, in current clamp experiments baclofen did increase T-type channel currents significantly, leading to calcium spikes. This was due to removal of T-type channel inactivation.
There is a distinct population of rat ganglion cells in which T-type calcium channels predominate and can play an important role in the output neural code, especially in response to near-threshold light signals. Hyperpolarization, such as that produced by activation of GABAB receptors, leads to enhanced T-type channel currents and changes the spike code in response to the same stimulus.
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