Zn2+ differentially modulates signals from red- and short wavelength-sensitive cones to horizontal cells in carp retina

Dong Gen Luo, Xiong Li Yang

Research output: Contribution to journalArticle


The effects of Zn2+ were studied while recording intracellularly from L-type horizontal cells (LHCs) in the isolated, superfused carp retina. In darkness, 25 μM Zn2+ hyperpolarized LHCs and potentiated responses of these cells to 500 nm flashes, but decreased those to 680 nm flashes. Zn2+ did not change photopic electroretinographic P III responses. The differential modulation by Zn2+ persisted when the Zn2+-induced membrane hyperpolarization was compensated by lowering Ca2+ concentration in the perfusate, but it was abolished in the presence of background illumination. Furthermore, the differential modulation no longer existed in the presence of bicuculline, suggesting the involvement of γ-aminobutyric acidA (GABAA) receptors. We speculate that the differential modulation may be a consequence of multiple changes caused by Zn2+. Decreased glutamate release from the cone terminal by Zn2+ results in a reduction of cone signals. Zn2+ antagonizes GABA receptors on LHCs, leading to cone signal reduction. On the other hand, Zn2+ may reduce the strength of the negative feedback from LHCs to cones by downregulating the activity of GABA receptors on the cone terminal, which causes a potentiation of LHC light responses. Cone- or wavelength-relevance of the Zn2+-induced feedback strength change may account for the differential modulation.

Original languageEnglish (US)
Pages (from-to)95-102
Number of pages8
JournalBrain research
Issue number1
StatePublished - May 4 2001



  • Cone input
  • Horizontal cell
  • Retina
  • Zinc
  • γ-aminobutyric acid receptor

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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