Na⁺ channels of Müller (glial) cells isolated from retinae of various mammalian species including man

Abstract

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 (1 microM), and by exposure to sodium-free extracellular solution; typically, they were demonstrable only after blocking most of the K+ conductance by Ba2+ (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 estimated number of sodium channels per cell was low (about 1,500 channels per 7,500 microns 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 current clamp. Modelling estimations show that triggering of glial Na+ currents under physiological conditions, if any, can at best occur by emhaptic transmission at perinodal sites of optic axons. It is speculated that glial Na+ channels might be involved in neuroglial signalling events.

The Müller (Glial) Cell in Normal and Diseased Retina: A Case for Single-Cell Electrophysiology

“…Na+ channels ( fig. 7) [22]. We had then specu lated that the function of these channels might be related to the functional activity of retinal neurons.…”

“…thus, improve visual acuity [21], It is more difficult to understand the func tional significance of voltage-gated Na+ chan nels which have been observed in Müller cells from various mammalian species [22], They arc activated only by strong depolarizations which have never been measured at somatic Müller cell membranes under physiological conditions. Assuming that (i) the Na+ chan nels of Müller cells are located in thin fingerlike processes abutting node-like specializa tions of optic axons in the nerve fiber layer, (ii) these thin processes are elcctrotonically 'isolated' from the soma and stem process and (iii) axonal action potentials may cause cphaptic depolarization of these glial 'finger' membranes, it has been hypothesized that the glial Na+ channels may act as 'sensors' of reti nal ganglion cell activity [22], These few examples may show that there is a growing body of data concerning the proper ties, and the possible physiological impor tance, of ion channels, receptors and uptake carriers in Müller cell membranes. Neverthe less, the regulation of their expression and their possible involvement in pathophysiolog ical mechanisms are not well understood.…”

“…Neverthe less, the regulation of their expression and their possible involvement in pathophysiolog ical mechanisms are not well understood. There might be considerable differences be tween Müller cells from different mammalian species [14,22] which cannot be easily ex plained. There is also recent evidence of changes in membrane properties of Müller cells due to retinal degeneration [23][24][25].…”

Ion Conductances in Supporting Cells Isolated From the Mouse Vomeronasal Organ

“…These properties enable Müller cells to control the activity of retinal neurons by regulating the extracellular concentration of neuroactive substances such as K ϩ , GABA and glutamate. In addition, it has been proposed that voltage-gated Na ϩ channels in these cells could be activated by the functioning of adjacent neurons: this way, glial cells could sense the activity of neighboring neurons (Chao et al 1994). In short, supporting cells seem to be key elements for controlling the transduction and signaling in excitable tissues.…”

Electrophysiological Properties of Human Astrocytic Tumor Cells In Situ: Enigma of Spiking Glial Cells

“…These speculations include tion. We speculate that inwardly rectifying K / channels are expressed in differentiated, nondividing astrocytes, whereas roles in fueling the Na / /K / -ATPase (Sontheimer et al 1994), ephaptic coupling to neurons (Chao et al 1994), or they are down-regulated in dividing cells for unknown reasons. Indeed, this was observed in numerous cell types, inchannel biosynthesis and transfer to neurons (Bevan et al 1987).…”