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Patch‐clamp Recording of Human Retinal Photoreceptors and Bipolar Cells †
Author(s) -
Ohkuma Mahito,
Kawai Fusao,
Horiguchi Masayuki,
Miyachi EiIchi
Publication year - 2007
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/2006-06-15-ra-923
Subject(s) - depolarization , current clamp , tetrodotoxin , sodium channel , membrane potential , patch clamp , biophysics , retina , voltage clamp , retinal , electrophysiology , chemistry , neuroscience , sodium , biology , biochemistry , organic chemistry
Photoreceptors and retinal bipolar cells are considered as nonspiking neurons; however, we recently showed that human rod photoreceptors can generate sodium action potentials in response to membrane depolarization from membrane potentials of −60 or −70 mV (Kawai et al. , Neuron 30 [2001] 451). We performed patch‐clamp recording of human cone photoreceptors and retinal bipolar cells to examine whether functional voltage‐gated sodium channels are expressed in these cells as well as rod photoreceptors. Under current‐clamp conditions, the injection of depolarizing current steps into a cone photoreceptor‐induced marked action potentials. These action potentials were blocked by 1 µ M tetrodotoxin, a voltage‐gated sodium channel blocker. Under voltage‐clamp conditions, depolarizing voltage steps‐induced a fast transient inward current in several bipolar cells ( n = 4/78). This current was activated from −70 to +20 mV (maximal at −10 mV) and inactivated within 5 ms. The 10–90% rise time of this current was shorter than another inward current (less than one‐hundredth). These results indicate that human cones and bipolar cells express voltage‐gated sodium channels as rod photoreceptors. Sodium channels may serve to amplify the release of a neurotransmitter and to accelerate the light–dark change in photosignals.