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.