Purchase this article with an account.
Z. Sun, D.–Q. Zhang, D.G. McMahon; Zinc Modulation of Hemi Gap Junction Channels in Bass Horizontal Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):388.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Hemi gap junction (HGJ) channels are expressed in bass retinal horizontal cells (HCs), where they may play important roles in modulating the synaptic connections between adjacent neurons. Zinc, an endogenous neuromodulator, is released onto HCs from photoreceptors. Although evidence indicates that zinc released from nerve terminals can modulate postsynaptic receptors and voltage–gated channels, the effects on HGJ channels have not been explored extensively. In the present study, we sought to examine the effect of zinc on the currents mediated by the HGJ of bass HCs.
Cultured bass HCs were recorded using the conventional whole–cell patch clamp configuration.
It is known that currents mediated by hemichannels can be induced in positive holding potentials in calcium free medium but are blocked by physiological concentrations of calcium. In the present study, we found that HGJ currents were also inhibited by external application of zinc. In the presence of 5 uM zinc, the magnitude of the HGJ currents was suppressed by 19 ± 2% (mean ± standard error, n=4). 30 uM zinc reduced the HGJ currents by 33 ± 1% (n=4), and 100 uM zinc reduced HGJ currents by 77 ± 1% (n=4), an amount comparable to the physiological concentration of calcium. HGJ currents were also sensitive to external pH and substantially decreased when the pH was switched from 7.4 to 6.0. Further studies revealed that the effects on HGJ currents by zinc and calcium were additive.
These results provide a possible mechanism by which zinc located in synaptic clefts may regulate the HCs function by modulating hemichannel currents. The actions of zinc and calcium appear to be independent.
This PDF is available to Subscribers Only