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Two types of calcium currents of the mouse bipolar cells recorded in the retinal slice preparation
Author(s) -
De La Villa Pedro,
Vaquero Cecilia F.,
Kaneko Akimichi
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00051.x
Subject(s) - retina , depolarization , chemistry , biophysics , axon terminal , amacrine cell , axon , inner plexiform layer , voltage dependent calcium channel , membrane potential , neuroscience , calcium , biology , biochemistry , organic chemistry
In the vertebrate retina, the bipolar cell makes reciprocal synapses with amacrine cells at the axon terminal. It has been postulated that amacrine cells may control the transmitter release from bipolar cells by modulating their calcium currents ( I Ca ). To clarify this possibility calcium currents were studied in bipolar cells of the mouse retina using a slice preparation. I Ca was identified by voltage clamp protocols, ionic substitution and pharmacological tools. Depolarization to –30 mV from a holding voltage of –80 mV induced an inward current consisting of an initial transient and a long‐lasting sustained component. The transient component was inactivated by holding the membrane at more positive voltages. Addition of 100 μ m nifedipine suppressed the sustained component, leaving the transient component almost intact. The sustained component was enhanced when external solution contained 0.1 μ m Bay K 8644 or when the external Ca 2+ was substituted by equimolar Ba 2+ . Omega‐conotoxin (10 μ m ω‐ctxn GVIA) did not alter either component. We concluded that the transient component is a low‐voltage activated T‐type I Ca , while the sustained component is a high‐voltage activated L‐type I Ca . T‐type I Ca was recorded in all cells tested, while L‐type I Ca was found only in cells that retained axon terminals ramifying in the inner plexiform layer. Thus, it is highly likely that L‐type I Ca is generated at the axon terminal and contributes to the transmitter release from the bipolar cell. The present results confirm that in addition to the T‐type I Ca that had been previously described, bipolar cells of the mammalian retina also contain L‐type I Ca similar to the one that has been reported in bipolar cells of the goldfish. The use of retinal slice preparation allowed us to record this current that was not seen previously in the dissociated mouse bipolar cells.