The authors also performed experiments that tested whether the activation of the chloride channels was dependent on the membrane potential. They found that the chloride channels that they activated were not activated at the resting potential and were only activated when the membrane potential was stepped to a positive membrane potential. They also found that the activation of the chloride channels was dependent on calcium and calmodulin, which are known to regulate many types of ion channels. These results indicate that the activation of the chloride channels that they observed was not due to an artifact of the assay they used. They also showed that the activation of the chloride channels was not due to light-induced chloride efflux. This is based on the observation that stimulating the neurons at a positive membrane potential with continuous light did not increase the light-induced chloride current. Finally, the authors were able to demonstrate that the light-induced chloride current is indeed mediated by chloride channels, since inhibiting chloride channels with either the chloride channel blocker NPPB or the chloride channel opener DIDS blocked the light-induced chloride current. Although this is not the first demonstration of light-induced chloride conductance in neurons, this work is one of the first demonstrations of light-induced chloride conductance in brainstem neurons, and it provides a step forward in understanding the biology of how neurons communicate with one another.
“The article does a good job of showing that there are many different ways to activate channels in neurons, and the particular way that we decided to activate the channels in the cells is elegant,” says first author Sarah C. Malyshev, Ph.D., a research associate in Robert R. Redfield’s laboratory. “It is a simple idea that led us to a surprising and highly unexpected result.”
The light-induced chloride conductance might be physiologically relevant in the brain. The authors found that the effect of this chloride conductance depends on the chloride channel subunits that are expressed in the neurons. Chloride conductances are known to be involved in synaptic transmission and regulation of excitability in neurons. For example, activation of chloride conductances has been shown to increase the frequency of spontaneous action potentials in hippocampal neurons in vitro (Chen et al., 2011), increase the frequency of spontaneous GABA-induced inhibitory postsynaptic currents in olfactory bulb neurons (Chen et al.
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