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We have established two immortalized cell lines from dorsal root ganglia of normal (G4b) and trisomy 16 mice (GTI), a model for Down syndrome. By immunohistochemistry, both cell lines exhibit neuronal traits and lack glial markers. GTI cells exhibited greater [ 3 H]choline uptake than G4b cells. K + and nicotine-mediated acetylcholine release was greater in GTI cells. Basal intracellular Ca 2+ concentration ([Ca 2+ ] i ) was significantly lower in GTI cells. More GTI cells responded to neurotransmitters with a transient [Ca 2+ ] i increase compared to G4b cells, but both cell types showed similar amplitudes of [Ca 2+ ] i responses. The results show that both cell lines retain neuronal characteristics and respond to specific neurotransmitter stimuli. Altered GTI cell responses could be related to neuronal pathophysiology in Down's syndrome.

WE established two immortalized cell lines from cerebral cortex of normal (CNh) and trisomy 16 (CTb) mouse fetuses, an animal model of human trisomy 21. Those cells loaded with the fluorescent Ca 2+ dyes, Indo-1 and Fluo-3, exhibited increments of intracellular Ca 2+ ([Ca 2+ ] i ) in response to external glutamate, NMDA, AMPA and kainate. CTb cells exhibited higher basal Ca 2+ concentrations and had higher amplitude and slower time-dependent kinetics in the decay than CNh cells, suggesting an impaired Ca 2+ buffering capacity in the trisomy 16-derived cell line. Nicotine also induced increments of [Ca 2+ ] i . The CTb cell line could represent a model for studying cellular alterations related to Down syndrome.