Development of G protein-mediated Ca2+ channel regulation in mouse embryonic stem cell-derived neurons

Garsten Strutting*, Jürgen Rohwedel, G. Ahnert-Hilger, Bertram Wiedenmann, Jrgen Hescheler, A.M. Wobus

*Corresponding author for this work
23 Citations (Scopus)


Besides other mechanisms, the influx of Ca2+ into embryonic neurons controls growth and differentiation processes. To study the expression and regulation of voltage-gated Ca2+ channels during early neurogenesis, we measured whole-cell Ca2+ currents (ICa) in neurons developing from pluripotent embryonic stem cells. Various receptor agonists, including somatostatin and baclofen, reversibly inhibited lca in embryonic stem cell-derived neurons. The effects of somatostatin and baclofen were abolished by pretreatment of cells with pertussis toxin and mimicked by intracellular infusion of guanosine 5′-O-(3-thiotriphosphate), suggesting the involvement of pertussis toxin-sensitive G proteins in ICa inhibition. Investigations at different stages of neuronal differentiation showed that somatostatin efficiently suppressed L- and N-type Ca2+ channels in immature as well as mature neurons. In contrast, inhibition of L- and N-type channels by baclofen was rarely observed at the early stage. In terminally differentiated neurons, responses to baclofen were as prominent as those to somatostatin but were confined to N-type Ca2+ channels. The stage-dependent sensitivity of voltage-gated Ca2+ channels to somatostatin and baclofen was not due to differential expression of Goto isoforms, as revealed by reverse transcription-polymerase chain reaction and immunofluorescence microscopy. These findings demonstrate that specific neurotransmitters such as somatostatin regulate voltage-gated Ca2+ channels via G proteins during the early stages of neurogenesis, thus providing a mechanism for the epigenetic control of neuronal differentiation.

Original languageEnglish
JournalEuropean Journal of Neuroscience
Issue number4
Pages (from-to)824-832
Number of pages9
Publication statusPublished - 01.12.1997

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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