Prolonged depolarization of isolated, voltage-clamped skate retinal horizontal cells produces an outward current that exhibit a late onset and develops slowly with time. This current, which we refer to as the Q-current, is associated with an increase in membrane conductance, and is present when other voltage-gated conductances have been pharmacologically blocked. The reversal potential for the Q-current, obtained using tail current analysis, was close to 0 mV. The magnitude of the current was greatly reduced by superfusion with 25 mM acetate, and by 4 mM cobalt chloride, 2 mM 1-octanol, and a saturated solution of the general anesthetic halothane. In addition, the low-molecular weight fluorescent dye Lucifer yellow, applied extracellularly, entered the cells during activation of the Q-current, whereas a 3 kD dextran-fluorescein complex did not cross the cell membrane. The effects of divalent cations, the non-specific nature of the ionic current suggested by its reversal potential, the entry of Lucifer yellow, and the ability of acetate, halothane, cobalt, and octanol to block the current lead us to hypothesize that the Q-current results from the opening of hemi-gap junctional channels that mediate electrical coupling between skate horizontal cells.

In the retinae of many vertebrates, there are classes of horizontal cell that probably utilize r-aminobutyric acid (GABA) as a neurotransmitter. As with other amino acid transmitter agents, the postsynaptic action of GABA is thought to be terminated by uptake into neurons and glia surrounding the release site. The present study examined whether an uptake system for GABA could be detected in isolated skate horizontal cells by means of electrophysiological methods. Pressure ejection of GABA onto voltage-clamped horizontal cells produced an inward current that showed no sign of desensitization regardless of the GABA concentration. The dose-response relationship followed simple Michaelis-Menten kinetics, with a half-maximal response elicited at =110 ,AM. Nipecotic acid produced a similar current and reduced the responses to GABA when introduced in the bath solution prior to the GABA pulse.On the other hand, application of 500 ,uM muscimol or 1 mM baclofen, GABAA and GABAB receptor agonists, respectively, were completely without effect. The GABA-induced current was not blocked by superfusion with 500 jAM bicuculline, 500 ,uM picrotoxin, or 500 ,uM phaclofen. However, the responses to GABA were abolished when the cells were superfused in Ringer's solution in which choline or lithium had been substituted for sodium, and were reduced when the extracellular chloride concentration was decreased from 266 mM to 16 mM. Current-voltage data showed a maximal response to GABA when the cells were held at or below their resting potential. At more depolarized levels, the inward current became progressively smaller until, near +50 mV, it could no longer be detected; over the range tested (-90 to +50 mV), the response never reversed into an outward current. These findings suggest that the GABA-induced currents in skate horizontal cells are mediated by an electrogenic uptake mechanism.

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