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Two separate Ni 2+ ‐sensitive voltage‐gated Ca 2+ channels modulate transretinal signalling in the isolated murine retina
Author(s) -
Alnawaiseh Maged,
Albanna Walid,
Chen ChienChang,
Campbell Kevin P.,
Hescheler Jürgen,
Lüke Matthias,
Schneider Toni
Publication year - 2011
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2011.02167.x
Subject(s) - retina , erg , biophysics , electroretinography , electrophysiology , retinal , chemistry , biology , physics , anatomy , biochemistry , neuroscience
. Purpose: Light‐evoked responses from vertebrate retinas were recorded as an electroretinogram (ERG). The b‐wave is the most prominent component of the ERG, and in the bovine retina its NiCl 2 ‐sensitive component was attributed to reciprocal signalling by pharmacoresistant R‐type voltage‐gated Ca 2+ channels, which similar to other voltage‐dependent Ca 2+ channels trigger and control neurotransmitter release. The murine retina has the great advantage that the effect of gene inactivation for Ni 2+ ‐sensitive Ca 2+ channels can be analysed to prove or disprove that any of these Ca 2+ channels is involved in retinal signalling. Methods: Superfused retinas from different murine genotypes lacking either one or both highly Ni 2+ ‐sensitive voltage‐gated Ca 2+ channels were used to record their ex vivo ERGs. Results: The isolated retinas from mice lacking Ca v 2.3 R‐type or Ca v 3.2 T‐type or both voltage‐gated Ca 2+ channels were superfused with a NiCl 2 (15 μ m ) containing nutrient solution. The change in the b‐wave amplitude and implicit time, caused by NiCl 2 , was calculated as a difference spectrum and compared to data from control animals. From the results, it can be deduced that Ca v 2.3 contributes rather to a later component in the b‐wave response, while in the absence of Ca v 3.2 the gain of Ni 2+ ‐mediated increase in the b‐wave amplitude is significantly increased, probably due to a loss of reciprocal inhibition to photoreceptors. Thus, each of the Ni 2+ ‐sensitive Ca 2+ channels contributes to specific features of the b‐wave response. Conclusion: Both high‐affinity Ni 2+ ‐sensitive Ca 2+ channels contribute to transretinal signalling. Based on the results from the double knockout mice, additional targets for NiCl 2 must contribute to transretinal signalling, which will be most important for the structurally similar physiologically more important heavy metal cation Zn 2+ .