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836 records · Page 47Linked to original sources
PubMed1981

Mechanisms of the mucosa-negative transepithelial potential produced by amphotericin B in gallbladder epithelium.

Exposure of the apical (luminal) surface of gallbladder epithelium to the polyene antibiotic amphotericin B produces a mucosa-negative change of the transepithelial potential. The mechanism of this effect has been studied by both electrophysiologic techniques and tracer flux measurements. The main effect of amphotericin B appears to be an increase in the permeability of the apical membrane to small monovalent cations. During exposure to Na-Cl-Ringer's, this results in cell depolarization and in K loss and Na uptake by the cells. The loss of apical membrane K selectivity appears to account for most of the change in the transepithelial potential. Accumulation of K in the mucosal un-stirred layers can contribute to this change as well. The evidence for stimulation of an electrogenic basolateral Na pump (by the net Na entry caused by amphotericin B) is not conclusive due to a) indirect effects of the polyene antibiotic on the resistance of basolateral membrane, b) lack of reduction of the amphotericin B-dependent change of transepithelial potential when the pump is inhibited, and c) lack of effect of NaCl addition on basolateral membrane potential in tissues preincubated in high K-media and exposed to amphotericin B on the luminal side.

Amphotericin B↗
PubMed1998

Action potentials are required for the lateral transmission of glycinergic transient inhibition in the amphibian retina.

Transient lateral inhibition (TLI), the suppression of responses of a ganglion cell to light stimuli in the receptive field center by changes in illumination in the receptive field surround, was studied in light-adapted mud puppy and tiger salamander retinas using both eyecup and retinal slice preparations. In the eyecup, TLI was measured in on-off ganglion cells as the ability of rotating, concentric windmill patterns of 500-1200 micron inner diameter to suppress the response to a small spot stimulus in the receptive field center. Both the suppression of the spot response and the hyperpolarization produced in ganglion cells by rotation of the windmill were blocked in the presence of 2 microM strychnine or 500 nM tetrodotoxin (TTX), but not by 150 microM picrotoxin. In the slice preparation in which GABA-mediated currents were blocked with picrotoxin, IPSCs elicited by diffuse illumination were blocked by strychnine and strongly reduced by TTX. The TTX-resistant component was probably attributable to illumination of the receptive field center. TTX had a much greater effect in reducing the glycinergic inhibition elicited by laterally displaced stimulation versus nearby focal electrical stimulation. Strychnine enhanced light-evoked excitatory currents in ganglion cells, but this was not mimicked by TTX. The results suggest that local glycinergic transient inhibition does not require action potentials and is mediated by synapses onto both ganglion cell dendrites and bipolar cell terminals. In contrast, the lateral spread of this inhibition (at least over distances >250 micron) requires action potentials and is mainly onto ganglion cell dendrites.

Action Potentials↗