Transient activation of specific neurons in mice by selective expression of the capsaicin receptor

The ability to control the electrical activity of a neuronal subtype is a valuable tool in deciphering the role of discreet cell populations in complex neural circuits. Recent techniques that allow remote control of neurons are either labor intensive and invasive or indirectly coupled to neural elec...

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Veröffentlicht in:Nature communications 2012-03, Vol.3 (1), p.746-746, Article 746
Hauptverfasser: Güler, Ali D., Rainwater, Aundrea, Parker, Jones G., Jones, Graham L., Argilli, Emanuela, Arenkiel, Benjamin R., Ehlers, Michael D., Bonci, Antonello, Zweifel, Larry S., Palmiter, Richard D.
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Sprache:eng
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Zusammenfassung:The ability to control the electrical activity of a neuronal subtype is a valuable tool in deciphering the role of discreet cell populations in complex neural circuits. Recent techniques that allow remote control of neurons are either labor intensive and invasive or indirectly coupled to neural electrical potential with low temporal resolution. Here we show the rapid, reversible and direct activation of genetically identified neuronal subpopulations by generating two inducible transgenic mouse models. Confined expression of the capsaicin receptor, TRPV1, allows cell-specific activation after peripheral or oral delivery of ligand in freely moving mice. Capsaicin-induced activation of dopaminergic or serotonergic neurons reversibly alters both physiological and behavioural responses within minutes, and lasts ~10 min. These models showcase a robust and remotely controllable genetic tool that modulates a distinct cell population without the need for invasive and labour-intensive approaches. The ability to spatially and temporally control excitation of neurons in vivo is an invaluable tool. By expressing the TRPV1 receptor in specific neuronal populations, Güler et al . have developed a rapid and noninvasive method to stimulate neuronal activity by the simple administration of capsaicin.
ISSN:2041-1723
2041-1723
DOI:10.1038/ncomms1749