Contrast Adaptation in Retina Ganglion Cells
Adaptation is essential for signal detection, since natural stimulus has a large dynamic range whereas the viable responses of neurons are limited. It has been proposed that organisms adapt to both the mean and contrast of the stimuli so that the entire response range is utilized. The mechanisms or sites of such a phenomenon, however, requires more investigation. In the first paper linked below, the authors investigate the possible sites for temporal contrast adaptation in the retina. Contrast adaptation differs from mean adaptation in the location in which it takes place – while mean adaptation involves photoreceptors, contrast adaptation doesn’t, and it extends well beyond the retina into cortical regions. This paper mainly focuses on adaptaion in the ganglion cell, whereas another one with an identical topic focuses on the bipolar cell, which is linked below for an interested reader (second link).
The authors had three main findings: a) desensitization of the input currents to the ganglion cell resulting from a high contrast input has two distinct time scales, while recovery of sensitivity only has one; b) the degree of adaptation of the input current is not enough to explain the extent of adaptation in the spiking of the ganglion cell, suggesting that there is also an adaptation mechanism intrinsic to the ganglion cell; c) OFF pathways adapt to contrast changes more than ON pathways. In other words, adaptation occurs in both the input current (i.e. bipolar-to-ganglion synapse) and the ganglion cell itself. The latter adapts much stronger than the former, and voltage-activated sodium channels are being suspected to play a role in it.
In the third paper linked below, the authors proposed a model that further explains adaptation in the input current. They proposed a divisive suppression model, which pinpoints the inhibition from amacrine cells along with STD (short-term depression) as the mechanisms responsible for adaptation. This model consists of two linear-nonlinear models, with one acting as an inhibitory signal that interacts with the other excitatory pathway in a divisive manner. The resulting fitted model could predict the activities of the ganglion cells to a millisecond precision, whereas commonly used single linear-nonlinear models could not.
In conclusion, contrast adaptation is found to occur both in the bipolar-to-ganglion synapse and the ganglion cell itself. Possible mechanisms for the former include inhibition from amacrine cells and vesicle depletion. Possible mechanisms for the latter include a modification related to the voltage-activated sodium channels.
Written by: Pei-Hsien Liu
Original papers:
[1] Kim, K. J., & Rieke, F. (2001). Temporal Contrast Adaptation in the Input and Output Signals of Salamander Retinal Ganglion Cells. The Journal of Neuroscience,21(1), 287-299. doi:10.1523/jneurosci.21-01-00287.2001
[2] Rieke, F. (2001). Temporal Contrast Adaptation in Salamander Bipolar Cells. The Journal of Neuroscience,21(23), 9445-9454. doi:10.1523/jneurosci.21-23-09445.2001
[3] Cui, Y., Wang, Y. V., Park, S. J., Demb, J. B., & Butts, D. A. (2016). Divisive suppression explains high-precision firing and contrast adaptation in retinal ganglion cells. ELife,5. doi:10.7554/elife.19460
The authors had three main findings: a) desensitization of the input currents to the ganglion cell resulting from a high contrast input has two distinct time scales, while recovery of sensitivity only has one; b) the degree of adaptation of the input current is not enough to explain the extent of adaptation in the spiking of the ganglion cell, suggesting that there is also an adaptation mechanism intrinsic to the ganglion cell; c) OFF pathways adapt to contrast changes more than ON pathways. In other words, adaptation occurs in both the input current (i.e. bipolar-to-ganglion synapse) and the ganglion cell itself. The latter adapts much stronger than the former, and voltage-activated sodium channels are being suspected to play a role in it.
In the third paper linked below, the authors proposed a model that further explains adaptation in the input current. They proposed a divisive suppression model, which pinpoints the inhibition from amacrine cells along with STD (short-term depression) as the mechanisms responsible for adaptation. This model consists of two linear-nonlinear models, with one acting as an inhibitory signal that interacts with the other excitatory pathway in a divisive manner. The resulting fitted model could predict the activities of the ganglion cells to a millisecond precision, whereas commonly used single linear-nonlinear models could not.
In conclusion, contrast adaptation is found to occur both in the bipolar-to-ganglion synapse and the ganglion cell itself. Possible mechanisms for the former include inhibition from amacrine cells and vesicle depletion. Possible mechanisms for the latter include a modification related to the voltage-activated sodium channels.
Written by: Pei-Hsien Liu
Original papers:
[1] Kim, K. J., & Rieke, F. (2001). Temporal Contrast Adaptation in the Input and Output Signals of Salamander Retinal Ganglion Cells. The Journal of Neuroscience,21(1), 287-299. doi:10.1523/jneurosci.21-01-00287.2001
[2] Rieke, F. (2001). Temporal Contrast Adaptation in Salamander Bipolar Cells. The Journal of Neuroscience,21(23), 9445-9454. doi:10.1523/jneurosci.21-23-09445.2001
[3] Cui, Y., Wang, Y. V., Park, S. J., Demb, J. B., & Butts, D. A. (2016). Divisive suppression explains high-precision firing and contrast adaptation in retinal ganglion cells. ELife,5. doi:10.7554/elife.19460
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