This article addresses whether TRPC1 or TRPC6 is an essential component of a mammalian stretch-activated mechano-sensitive Ca(2+) permeable cation channel (MscCa). We have transiently expressed TRPC1 and TRPC6 in African green monkey kidney (COS) or Chinese hamster ovary (CHO) cells and monitored the activity of the stretch-activated channels using a fast pressure clamp system. Although both TRPC1 and TRPC6 are highly expressed at the protein level, the amplitude of the mechano-sensitive current is not significantly altered by overexpression of these subunits. In conclusion, although several TRPC channel members, including TRPC1 and TRPC6, have been recently proposed to form MscCa in vertebrate cells, the functional expression of these TRPC subunits in heterologous systems remains problematic.

L-glutamic acid (L-Glu) and L-aspartic acid (L-Asp) are considered to be major excitatory amino acid transmitters, causing depolarization and excitation of neurones in the mammalian central nervous system (CNS). These responses have been thought to be an exclusively neuronal property as the excitatory amino acids either did not affect the potential of electrophysiologically unresponsive glial cells, or when an effect was seen, it was attributed to changes in external [K+] (refs 5, 6). Here we report that L-Glu directly depolarizes immunocytochemically-identified astrocytes in primary culture. L- or D-Asp and kainic acid (KA) also depolarized these cells while none or minimal changes in the resting membrane potentials were found in response to N-methyl-D-aspartate, D-glutamate, taurine, L-glutamine or to the inhibitory amino acids gamma-aminobutyric acid (GABA) and glycine. We conclude that the membrane potential of astrocytes can no longer be thought of as being responsive only to K+ and that the electrophysiological effects of excitatory amino acids in situ may not be exclusively a neuronal property.

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