PMC

A: Electron microscopic view of a gap junction between inner segments of a rod (R) and a cone (C). Scale bar is 0.5 μm. B: Higher magnification of a rod-cone gap junction. Scale bar = 0.1 μm.

Simultaneously recorded HC pair. A: Control response to 200 msec 650 nm flash. B: 30-minute ionophoresis from intracellular pipettes filled with 0.5 M cAMP creates a light-adapted phenotype in the injected cell.

Simultaneously recorded HC pair. Stimulation with a sinusoidal 650 nm 1–15 Hz flicker ramp at two intensities differing by 1.8 log units. The control cell responded well to the dim red flicker and became saturated with the bright red flicker. On the contrary, the cAMP-injected cell was relatively insensitive to the dim flicker, responding vigorously to the bright flicker. Note that the injected cell, unlike the control cell, responded from the middle of its dynamic range.

Flicker responses of a mesopic HC to sinusoidal stimulus of 660 nm light. Top: HC exposed to steady 650 nm (logQ=13.80) background light. At 3–5 Hz a prominent second peak in the HC flicker response is observed (arrow). The peak disappears at 6 Hz. Middle: HC under a steady 527 nm background (logQ=12.8). The second peak disappears under these conditions leaving only the peak with the faster kinetics. Bottom: The flicker stimulus.

Effect of dopamine on L-HC responses to kainate. Isolated HC was whole cell-clamped at −60 mV. Top: Control. A 300-msec puff of 50 μM kainate elicited an inward current. The slow decay of the current is due to the absence of saline wash. A 1.3-second puff of 0.5 μM dopamine was applied between the two top traces, and the test pulse of kainate was applied each 30 seconds thereafter. At 1 and 2 minutes, the KA-induced current was larger than control, but recovered to control amplitude by 4 minutes.

Aa–d: Simultaneous recording from a rod and an L-HC in the mesopic state (9.88; 10.72; 11.55; 12.38 logQ). Stimulus markers are 200 msec. Note that the strongest flash induces a suppression of the rod tail in the HC but not in the rod itself (arrow). Bc₁–d ₁: Scaled and superimposed responses from Ac–d. Whereas the responses of the rod and HC in c are remarkably similar (note in particular the kinetics of the onset and the offset of the cells’ light responses), both their amplitude and kinetics are dramatically changed with the stronger flash in d/d₁.

Intracellular recording from rod photoreceptors. Aa: “Ordinary” rod responses to green (567 nm) and red (667 nm) steps of light matched for equal absorbance by the rods. Stimulus marker is 300 msec. Ab: Responses to sinusoidally modulated green (567 nm; 11.56 log quanta cm⁻² s⁻¹) and red (660 nm; 13.63 log quanta cm⁻² s⁻¹). Cells were exposed to a flicker ramp with frequencies from 1 to 8 Hz. Note that the fusion frequency for this cell is below 4 Hz for both red and green stimuli. Ba: “Gatepost” rod responses to green and red steps of light. Note that the red, but not the green, flash evokes a transient response in the rod strongly resembling the cone light response (arrow). Stimulus marker is 200 msec. Bb: Flicker responses of the gatepost rod peter out before 4 Hz whereas responses to red flicker are maintained even at 8Hz.

The effect of the dopamine D1 agonist SKF 38393 on the HC. Left: Responses of an HC in the rod-dominated mesopic state to 200 msec 650 nm flash (12.0 logQ) before (A) and after (B) exposure to SKF38393. The waveform of the cell under control conditions shows a slow afterhyperpolarizing tail that is abolished by SKF. Right: HC flicker responses to green (567 nm) and red (660 nm) flicker 1–15 Hz ramps. Under control conditions, the HC in A responds to both red and green flicker to ~ 5Hz. Following exposure to 40 μM SKF38393, the response to green flicker in the same cell is completely suppressed, whereas the red flicker follows well up to 15 Hz. Note that in A the cell hyperpolarizes to its Vmax when hit by the flicker, whereas after SKF treatment it repolarizes to about the middle of its operating range.