The small-and large-field (cone)

Light-evoked membrane currents were recorded with suction electrodes from the outer segments of individual photoreceptors enzymatically dissociated from the skate retina. The intensity-response relation of dark-adapted cells closely followed a Michaelis function for which a half-saturating response was elicited by a flash intensity that produced about 36 photoisomerizations. Dim-light responses, as well as the early rising phase of the responses to a wide range of flash intensities, could be described by a reaction scheme that involved a series of four first-order delay stages. The number of delay stages required to model the rising phase of the photocurrents did not change in light adaptation. However, background illumination that reduced sensitivity by 1.5 log units, or a bleaching exposure that resulted in a nearly equivalent desensitization, shortened significantly the time scale of the responses. In both instances there were two-to threefold increases in the rate constants of the transitional delays, and almost complete suppression of the tail current that characterized the response of the dark-adapted cell. These findings suggest that although light adaptation alters the gain and kinetics of the transduction mechanism, the nature of the intervening processes is the same in dark-and light-adapted photoreceptors. Moreover, the results show clearly that there is no need to postulate the existence of a second class of conelike rods to account for the remarkable ability of skate photoreceptors to respond to incremental stimuli presented on "saturating" background fields or after exposure to an intense bleaching light.

GABA receptors of bipolar cells from the skate retina: actions of zinc on GABA-mediated membrane currents. J. Neurophysiol. 78: 2402-2412, 1997. gamma-Aminobutyric acid (GABA)-induced currents were recorded from isolated bipolar cells of the skate retina using perforated patch-clamp methodology. Pharmacological analysis of the responses, using selective agonists and antagonists of the major classes of GABA receptor, revealed the presence of both GABAA and GABAC receptors at both the dendrites and axon terminals of the bipolar cells. The two receptor types showed very different reactions to zinc, a divalent metallic cation that was detected in the synaptic terminal region of skate photoreceptors. Currents mediated by the activation of GABAC receptors were down-regulated by zinc, a feature that is typical of the action of zinc on GABAC receptors. On the other hand, the effects of zinc on GABAA receptor-mediated activity was highly dependent on zinc concentration. Unlike the GABAA receptors on other neurons, responses mediated by activation of the GABAA receptor of skate bipolar cells were significantly enhanced by zinc concentrations in the range of 0. 1-100 mu M; at higher concentrations of zinc (>100 mu M), response amplitudes were suppressed below control levels. The enhancement of GABAA receptor activity on skate bipolar cells showed little voltage dependence, suggesting that zinc is acting on the extracellular domain of the GABAA receptor. In the presence of 10 mu M zinc, the dose-response curve for 4,5,6, 7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP; a GABAA agonist that suppresses GABAC-activated currents) was shifted to the left of the curve obtained in the absence of zinc, but without a significant change in the response maximum. This finding indicates that the enhancing effect of zinc is due primarily to its ability to increase the sensitivity of the GABAA receptor. The novel enhancement of neuronal GABAA receptor activity by zinc, observed previously in the GABAA-mediated responses of skate Müller (glial) cells, may reflect the presence of a unique subtype of GABAA receptor on the bipolar and Müller cells of the skate retina.