HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chappell, R. L. Articles by Ripps, H. Search for Related Content PubMed Articles by Chappell, R. L. Articles by Ripps, H.

Histidine Suppresses Zinc Modulation of Connexin Hemichannels Expressed in Xenopus Oocytes

¹ Marine Biological Laboratory, Woods Hole, Massachusetts
² Hunter College and The Graduate Center, CUNY, New York, New York
³ University of Illinois College of Medicine, Chicago, Illinois

We showed previously that zinc modulates hemichannel currents of connexins (Cx35 and Cx38) expressed in Xenopus oocytes. In both cases the effects were biphasic; low concentrations of zinc enhanced, whereas higher concentrations decreased, current response magnitudes. The present study was designed to determine the effects of zinc on hemichannels formed by Cx26, a connexin expressed on dendrites of carp horizontal cells. In addition, we examined whether histidine, a zinc chelator, blocked the action of zinc or exerted a direct effect on Cx26 hemichannel currents.

Unlike results obtained with Cx35 or Cx38, the I-V curves of Cx26 hemichannels were constitutively open, gave large currents in response to both hyperpolarizing and depolarizing voltages, and had no evidence of outward rectification. Nevertheless, hemichannel currents mediated by Cx26 exhibited similar biphasic effects in response to increasing zinc concentrations, but with different sensitivities to zinc. Cx26 hemichannel currents were larger in 1 µM zinc than in control solutions, but progressively suppressed at higher concentrations. Current recovery after zinc application was very slow, taking up to 15 min following 1 mM zinc. Moreover, the zinc chelator histidine (1 mM) completely blocked the action of zinc (100 µM) but had no direct effect on hemichannel currents.

A recent hypothesis based on evidence from carp retina holds that currents through Cx26 hemichannels on horizontal cell dendritic processes serve to modulate calcium currents and related photoreceptor transmitter release via an ephaptic current within the synaptic region. The process is presumed to play a significant role in center-surround organization of distal neurons. We suggest that, if these channels were modulated by zinc as described here, the vesicular co-release of zinc and glutamate presumed to occur at the photoreceptor terminal could contribute to adaptive processes that involve the slow components of visual adaptation. Similar mechanisms involving zinc modulation of hemichannels may be important elsewhere in the nervous system as well.

Support: Fight for Sight, PSC/CUNY Grant 66257-0035, and NCRR/NIH RCMI Award RR-03037 (RLC); NIH Grants EY-06516 (HR), EY-12028 (HQ), and RPB (HR).

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chappell, R. L. Articles by Ripps, H. Search for Related Content PubMed Articles by Chappell, R. L. Articles by Ripps, H.