Calmodulin gene expression in an immortalized striatal gabaergic cell line.

We have demonstrated the presence of the mRNAs transcribed from the three calmodulin (CaM) genes in the GABAergic cell line M26-1F derived from embryonic rat striatal cells and immortalized by oncogene transduction. Similarly as in the rat striatum in vivo, these clonal cells express CaM I, CaM II and CaM III mRNAs differently, the CaM I mRNA population being the most abundant, followed in sequence by the CaM II and CaM III mRNA populations. The proportions of these transcripts resemble those in the adult striatum. The possibility of deriving immortalized cell lines from primary neuronal tissue which exhibit characteristics similar to those of the tissue of origin could provide an important tool in many types of in vitro studies.

beta-Amyloid[1-40]-induced early hyperpolarization in M26-1F cells, an immortalized rat striatal cell line.

The short-term (20-minute) action of beta[1-40]-amyloid on the resting transmembrane potential was investigated by means of flow-cytofluorimetric studies in M26-1F cells, an immortalized rat striatal cell line, using the potential-sensitive fluorescent probe bis-oxonol. The distribution of the individual cell-associated probe fluorescence was found to be shifted to lower levels in cells treated with beta-amyloid[1-40] for 20 minutes as compared with that of their untreated counterparts. A change in the same direction was caused by valinomycin, a hyperpolarizing ionophore, whereas gramicidin, a depolarizing ionophore, induced a shift to higher fluorescence intensities. These findings, together with the reported behaviour of this particular fluorescent probe at different transmembrane potential levels, indicate that beta-amyloid[1-40] is capable of inducing early hyperpolarization in M26-1F cells. This is one of the earliest cell physiological effect of beta-amyloid peptides that has been reported so far. Moreover, our findings indicate an ionophore-like action of amyloid peptides.