Influence of retinoic acid and of cyclic AMP on the expression of choline acetyltransferase and of vesicular acetylcholine transporter in NG108-15 cells

Detection of choline transporter‐like 1 protein CTL1 in neuroblastoma × glioma cells and in the CNS, and its role in choline uptake

“…Unlike either of the parental cell lines, rat C6 glioma cells or the mouse N18 neuroblastoma cells, the hybrid NG108-15 cell line is considered a model cholinergic cell line as it is able to both synthesize and release ACh (Hamprecht 1977). However, these cells are not able to properly store ACh because they do not express vesicular ACh transporter protein (Diebler et al 1998;Doležal et al 2001). In line with this finding, the reduction of choline uptake resulted in a decrease of steady state concentration of free cellular choline and ACh.…”

Vitamin A deficiency induces motor impairments and striatal cholinergic dysfunction in rats

“…In fact, previous reports have demonstrated that retinoic acid regulates the expression of ChAT, the enzyme synthesizing ACh, and the vesicular acetylcholine transporter in cell culture (Berrard et al, 1993(Berrard et al, , 1995Kobayashi et al, 1994;Berse and Blusztajn, 1995;Diebler et al, 1998).…”

“…Furthermore, given the fundamental role of DA in basal ganglia-mediated motor behaviors, we studied the integrity of dopaminergic transmission in VAD rats by measuring in the striatum the rate of synthesis and extracellular levels of DA and the integrity of DA D1 and D2 receptors by means of mRNA level evaluation. Moreover, since retinoic acid has been shown to regulate the expression of choline acetyltransferase (ChAT) in cell cultures (Berrard et al, 1995;Berse and Blusztajn, 1995;Diebler et al, 1998) we measured the striatal content of ACh.…”

Asymmetric regulation by estrogen at the cholinergic gene locus in differentiated NG108-15 neuronal cells

“…The NG108-15 cells are a hybrid cell line constructed by somatic fusion of rat C6 glioma cells and mouse N18TG2 neuroblastoma cells. N18TG2 cells themselves do not express the differentiated phenotypes in the presence of RA (Bignami et al 1997), but NG108-15 and N18TG2 treated with a medium conditioned over C6 cells can differentiate by retinoic acid into functional cholinergic cells (Diebler et al 1998;Dolezal et al 2001;Castell et al 2002), indicating that the differentiation of N18TG2 neuroblastoma requires the cooperation of C6 glioma. The possibility remains that E 2 acted directly or indirectly on differentiation-inducing factor(s) derived from C6 glioma, and prompted further increase of ChAT gene expression.…”