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G Falk

Publications and source records attributed to G Falk.

101 records · Page 6Linked to original sources
PubMed1966

Rapid hydrogen ion uptake of rod outer segments and rhodopsin solutions on illumination.

1. Flash illumination of a suspension of frog rod outer segments or rhodopsin solution in contact with a platinum electrode produces a rapidly developing negative displacement of potential of the electrode (with respect to a reversible electrode).2. The amplitude of the potential change varies inversely with the H(+) buffering capacity of the medium. It is inferred that the response is due to an uptake of H(+) by the rod outer segments or rhodopsin, with the platinum surface acting as a pH electrode.3. Determination of the action spectrum shows that the response depends on the absorption of light by rhodopsin.4. In frog rods one acid-binding group with a pK of about 7.9 is produced for each molecule of rhodopsin bleached, consistent with a rhodopsin concentration in frog rods of 1.7 mM.5. It is suggested that the time course of the response with rhodopsin solutions reflects the kinetics of the conversion of metarhodopsin I to metarhodopsin II.6. A slower time course of voltage change observed for suspensions of outer segments is attributable to the time required for the diffusion of H(+) buffer out of the rods.

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Responses of rod bipolar cells isolated from dogfish retinal slices to concentration-jumps of glutamate.

Rod on-bipolar cell light responses are mediated by a class of metabotropic glutamate receptor which is coupled via a G-protein to the control of a cGMP cascade, with cGMP acting to open cation channels, whilst off-bipolar cells possess ionotropic glutamate receptors. Whole-cell voltage-clamp recordings were obtained from on- and off-bipolar cells of dark-adapted dogfish retinal slices, identified by their light responses. Isolated cells were exposed to concentration-jumps of glutamate. At negative voltage-clamp potentials, on-bipolar cells responded to glutamate with outward currents with a mean delay of 10.8 ms, whilst off-bipolar cells responded with inward currents without any delay. Neither cell type showed desensitization to applied steps of glutamate. The dose-response relation for on-bipolar cells showed no gradual saturation, but increased linearly with a sharp cutoff above 200 microM glutamate. This dose-response relation could be fitted with a theoretical expression assuming Michaelis-Menten kinetics for the action of glutamate on receptors and a linear relation between the concentration of receptors bound to glutamate and the fall in cGMP this induces. The dose-response relation of off-bipolar cells showed saturation with a limiting slope of 2 at low glutamate concentrations, suggesting that two molecules of glutamate are required to open each channel by a cooperative mechanism. The glutamate receptor coupled cGMP cascade of rod on-bipolar cells can account for high synaptic voltage gain.

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PubMedDate not supplied

Contribution of rod, on-bipolar, and horizontal cell light responses to the ERG of dogfish retina.

Simultaneous extracellular ERG and intracellular recordings from horizontal and ON-bipolar cells were obtained from the dark-adapted retina of the dogfish. The light intensity-peak response relation (IR) and time course of on-bipolar cell responses closely resembled that of the ERG b-wave, but only at low light intensities [<10 rhodopsin molecules bleached per rod (Rh*)]. Block of on-bipolar cell responses with 50 microM 2-amino-4-phosphonobutyrate (APB) abolished the b-wave and unmasked a vitreal-negative wave. Subtraction from the control ERG resulted in the isolation of a vitreal-positive ERG with an IR which matched that of on-bipolar cells over the full range of light intensities. The D.C. component of the ERG arises as a result of sustained depolarization of on-bipolar cells in response to long (>0.5 s) dim light stimuli, or following bright light flashes. The IR of horizontal cells and the vitreal-negative wave unmasked by APB could be matched by scaling at low light intensities (<5 Rh*). However, horizontal cell responses saturated at about 30 Rh*, while the vitreal-negative wave continued to increase in amplitude. The time course of horizontal cell membrane current with dim flashes could be matched to the rising phase of the vitreal-negative wave, assuming that the delay in generating the voltage response in horizontal cells is due to their long (100 ms) membrane time constant. Blocking post-photoreceptor activity resulted in a much smaller vitreal-negative wave than that unmasked by APB alone. We conclude that the b-wave arises from on-bipolar cell depolarization, while the leading edge of the a-wave is a composite of the change in extracellular voltage drop across the rod layer and a component (proximal PIII) reflecting a decrease in extracellular K+ as horizontal cell synaptic channels close with light.

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