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Na + channels of Müller (glial) cells isolated from retinae of various mammalian species including man
Author(s) -
Chao T. Ivo,
Skachkov Sergey N.,
Eberhardt Wolfgang,
Reichenbach Andreas
Publication year - 1994
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440100304
Subject(s) - conductance , biophysics , biology , neuroglia , patch clamp , extracellular , sodium channel , electrophysiology , sodium , retina , neuroscience , microbiology and biotechnology , physics , central nervous system , chemistry , organic chemistry , condensed matter physics
Within the last few years, the expression of voltage‐dependent, TTX‐sensitive Na + channels has been demonstrated in several types of neuroglial cells such as astrocytes and Schwann cells. Recently, we reported the occurrence of such Na + currents in retinal Müller (glial) cells from dog and cat. This paper deals with the description of the properties of Na + currents in Müller cells isolated from retinae of several mammalian species, as well as from human retinae. These Na + currents were eliminated by TTX (1μM), and by exposure to sodium‐free extracellular solution; typically, they were de‐monstrable only after blocking most of the K + conductance by Ba 2+ (1 mM). Voltage‐dependent activation and inactivation characteristics and time constants of the Na + currents were similar to those of currents carried by neuronal Na + channels. The esti‐mated number of sodium channels per cell was low (about 1,500 channels per 7,500μm 2 ), and the K + conductance exceeded the peak Na + conductance by an average factor of 5. Thus, the cells were incapable of generating action‐potential‐like responses under cur‐rent clamp. Modelling estimations show that triggering of glial Na + currents under physiological conditions, if any, can at best occur by ephaptic transmission at perinodal sites of optic axons. It is speculated that glial Na + channels might be involved in neuro‐glial signalling events. © 1994 Wiley‐Liss, Inc.