PubMed · 9627640
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S M Archer. 1998. Prism Adaptation Study.. https://doi.org/10.1016/s0161-6420(98)96047-x
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1. This investigation was to determine the extent to which retinal 'on' bipolar cells contribute to the adaptive changes that occur with light, which enable the rod visual system to operate over a wide range of ambient light intensities, and to elucidate the underlying adaptive mechanism. 2. Whole-cell voltage clamp recordings were obtained from bipolar cells in dark-adapted dogfish retinal slices. Current responses to brief flashes and steps of light were analysed. 'On' bipolar cell inward current light responses are mediated by a metabotropic glutamate receptor linked to the control of a cGMP cascade, with cGMP opening cation channels. Outward current responses to light of 'off' bipolar cells are mediated by the closure of ionotropic glutamate receptor channels. 3. When Ca2+ buffer was omitted from the patch pipette solution, 'on' bipolar cells rapidly desensitized to steps of light as dim as one rhodopsin molecule bleached per rod per second (1 Rh* s-1), whereas 'off' bipolar cells did not desensitize. Responses of 'on' bipolar cells to flashes in the presence of dim backgrounds recovered after a delay, but with diminished sensitivity, i.e. the cells adapted. 4. With the Ca2+ chelator BAPTA in the patch pipette solution, step responses of 'on' bipolar cells were sustained and flash responses following steps showed rapid recovery. Buffering Ca2+ in the patch pipette solution to 1 microM prevented desensitization, whereas 50 microM free Ca2+ reduced the 'on' bipolar cell flash responses, suppressed inward dark current and decreased input conductance. 5. We conclude that a major component of adaptation of the visual system is due to a reduction in gain at the rod-'on' bipolar cell synapse as a result of Ca2+ loading of the dendrites when their cGMP-gated cation channels open with light.
Light activation of Drosophila photoreceptors leads to the generation of a depolarizing receptor potential via opening of transient receptor potential and transient receptor potential-like cationic channels. Counteracting the light-activated depolarizing current are two voltage-gated K+ conductances, IA and IK, that are expressed in these sensory neurons. Here we show that Drosophila photoreceptors IA and IK are regulated by calcium-calmodulin (Ca2+/calmodulin) via a Ca2+/calmodulin-dependent protein kinase (CaM kinase), with IK being far more sensitive than IA. Inhibition of Ca2+/calmodulin by N-(6 aminohexyl)-5-chloro-1-naphthalenesulfonamide or trifluoperazine markedly reduced the K+ current amplitudes. Likewise, inhibition of CaM kinases by KN-93 potently depressed IK and accelerated its C-type inactivation kinetics. The effect of KN-93 was specific because its structurally related but functionally inactive analog KN-92 was totally ineffective. In Drosophila photoreceptor mutant ShKS133, which allows isolation of IK, we demonstrate by current-clamp recording that inhibition of IK by quinidine or tetraethylammonium increased the amplitude of the photoreceptor potential, depressed light adaptation, and slowed down the termination of the light response. Similar results were obtained when CaM kinases were blocked by KN-93. These findings place photoreceptor K+ channels as an additional target for Ca2+/calmodulin and suggest that IK is well suited to act in concert with other components of the signaling machinery to sharpen light response termination and fine tune photoreceptor sensitivity during light adaptation.
A shaky hand holding a video camera invariably turns a treasured moment into an annoying, jittery momento. More recent consumer cameras thoughtfully offer stabilization mechanisms to compensate for our unsteady grip. Our eyes face a similar challenge in that they are constantly making small movements even when we try to maintain a fixed gaze. What should be substantial, distracting jitter passes completely unseen. Position changes from large eye movements (saccades) seem to be corrected on the basis of extraretinal signals such as the motor commands sent to the eye muscle, and the resulting motion responses seem to be simply switched off. But this approach is impracticable for incessant, small displacements, and here we describe a novel visual illusion that reveals a compensation mechanism based on visual motion signals. Observers were adapted to a patch of dynamic random noise and then viewed a larger pattern of static random noise. The static noise in the unadapted regions then appeared to 'jitter' coherently in random directions. Several observations indicate that this visual jitter directly reflects fixational eye movements. We propose a model that accounts for this illusion as well as the stability of the visual world during small and/or slow eye movements such as fixational drift, smooth pursuit and low-amplitude mechanical vibrations of the eyes.