Astrocytes in primary culture have chemically activated sodium channels.

The effects of two neurotoxins, veratridine and alpha-scorpion toxin II, on the resting potential (RMP) of identified astrocytes in primary cell culture were studied using standard electophysiological techniques. Veratridine caused either a series of transient depolarizations or a single sustained depolarization. alpha-Scorpion toxin (II), which alone had no effect on the RMP, increased the duration of the veratridine-induced transient depolarizations. The depolarization caused by veratridine, or veratridine plus alpha-scorpion toxin II, was reversibly inhibited by tetrodotoxin and was reversibly reduced in magnitude by reductions of the external sodium concentration. Cells that were depolarized by veratridine were shown to contain glial fibrillary acidic protein, a marker considered specific for astrocytes. The effect of long-term (10 sec) hyperpolarizing and depolarizing current pulses on the RMP were also studied using two microelectrodes, i.e., dual impalement. In the absence of veratridine, the RMP returned to its original value after termination of the hyperpolarizing current, and the current-voltage relationship was found to be linear over a wide range of membrane potentials. In the presence of veratridine, termination of the hyperpolarizing current produced a transient depolarization that was sensitive to tetrodotoxin. Depolarizing current pulses were without effect. These results show that astrocytes in primary culture have a chemically inducible Na+ channel that appears to be voltage-dependent.